1

UI  - 16

AU  - Barrionuevo M

AU  - Aguirre N

AU  - Del Rio JD

AU  - Lasheras B

AD  - Department of Pharmacology, University of Navarra, Pamplona, Spain

TI  - Serotonergic deficits and impaired passive-avoidance learning in rats by MDEA: a comparison with MDMA

AB  - The serotonergic deficits induced by 3,4-methylenedioxyethamphetamine (MDEA, "eve"), were examined and compared with 3,4 methylenedioxymethamphetamine (MDMA, "ecstasy"). A single dose of MDEA (10, 20, or 40 mg/kg IP) induced a dose-related hyperthermia, but only the highest dose significantly reduced 5-HT content and 5-HT transporter density in the frontal cortex and in the hippocampus 7 days later. Long-term serotonergic deficits were much more marked when MDEA was given repeatedly (40 mg/kg IP., b.i.d., for 4 consecutive days). Single or repeated administration of MDEA induced no change on 5-HT1A receptor density in the frontal cortex, brain stem, or hippocampus, although 3 h after both treatments plasma corticosterone levels were significantly increased. MDEA (5-20 mg/kg, IP) produced significant retention deficits in a passive-avoidance learning task. Conversely, 7 days after the repeated administration of MDEA (40 mg/kg b.i.d., for 4 consecutive days) no effect on passive-avoidance performance was observed unless rats were treated again with another dose of MDEA (20 mg/kg IP) 30 min before the training trial. The 5-HT1A receptor antagonist, WAY 100635, prevented the impairment in retention performance induced by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH- DPAT), but not by MDEA or MDMA, indicating that the effect of these amphetamine derivates was not mediated by 5-HT1A receptor activation. The results suggest the risk of serotonergic dysfunction associated with MDEA abuse in humans

MH  - Animal

MH  - Avoidance Learning

MH  - drug effects

MH  - Carrier Proteins

MH  - metabolism

MH  - Designer Drugs

MH  - pharmacology

MH  - Frontal Lobe

MH  - Hippocampus

MH  - Male

MH  - Membrane Glycoproteins

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Paroxetine

MH  - Rats

MH  - Rats,Wistar

MH  - Receptors,Serotonin

MH  - Serotonin

MH  - Serotonin Agents

MH  - Serotonin Uptake Inhibitors

MH  - Support,Non-U.S.Gov't

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 20135529LA - EngRN - 0 (serotonin transporter)RN - 0 (Carrier Proteins)RN - 0 (Designer Drugs)RN - 0 (Membrane Glycoproteins)RN - 0 (Receptors, Serotonin)RN - 0 (Serotonin Agents)RN - 0 (Serotonin Uptake Inhibitors)RN - 112692-38-3 (serotonin 1A receptor)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 61869-08-7 (Paroxetine)RN - 82801-81-8 (3,4-methylenedioxyethamphetamine)PT - JOURNAL ARTICLEDA - 20000314IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 200005

UR  - PM:0010672974

SO  - Pharmacol Biochem Behav 2000 Feb ;65(2):233-240

 

2

UI  - 2

AU  - Boot BP

AU  - McGregor IS

AU  - Hall W

AD  - Faculty of Medicine, University of Sydney, NSW, Australia

TI  - MDMA (Ecstasy) neurotoxicity: assessing and communicating the risks [In Process Citation]

RP  - NOT IN FILE

NT  - UI - 20290449LA - EngDA - 20000530IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SRO - O:099

UR  - PM:0010832852

SO  - Lancet 2000 May 20 ;355(9217):1818-1821

 

3

UI  - 13

AU  - Chang L

AU  - Grob CS

AU  - Ernst T

AU  - Itti L

AU  - Mishkin FS

AU  - Jose-Melchor R

AU  - Poland RE

AD  - Department of Neurology, UCLA School of Medicine, Harbor-UCLA Medical Center, 1000 W. Carson Street, B-4, Torrance, CA 90509, USA. linda_chang@humc.edu

TI  - Effect of ecstasy [3,4-methylenedioxymethamphetamine (MDMA)] on cerebral blood flow: a co-registered SPECT and MRI study

AB  - 3,4-methylenedioxymethamphetamine (MDMA), an illicit recreational drug, damages serotonergic nerve endings. Since the cerebrovasculature is regulated partly by the serotonergic system, MDMA may affect cerebral blood flow (CBF) in humans. We evaluated 21 abstinent recreational MDMA users and 21 age- and gender-matched healthy subjects with brain SPECT and MRI. Ten of the MDMA subjects also had repeat SPECT and MRI after receiving two doses of MDMA. Abstinent MDMA users showed no significantly different global or regional CBF (rCBF) compared to the control subjects. However, within 3 weeks after MDMA administration, rCBF remained decreased in the visual cortex, the caudate, the superior parietal and dorsolateral frontal regions compared to baseline rCBF. The decreased rCBF tended to be more pronounced in subjects who received the higher dosage of MDMA. Two subjects who were scanned at 2- 3 months after MDMA administration showed increased rather than decreased rCBF. Low-dose recreational MDMA use does not cause detectable persistent rCBF changes in humans. The lack of long-term rCBF changes may be due to a non-significant effect of serotonergic deficits on rCBF, or regeneration of serotonergic nerve terminals. The subacute decrease in rCBF after MDMA administration may be due to the direct effect of MDMA on the serotonergic system or the indirect effects of its metabolites on the dopaminergic system; the preliminary data suggest these effects may be transient

MH  - Adult

MH  - Brain

MH  - drug effects

MH  - pathology

MH  - radionuclide imaging

MH  - Case-Control Studies

MH  - Cerebrovascular Circulation

MH  - Dose-Response Relationship,Drug

MH  - Female

MH  - Human

MH  - Magnetic Resonance Imaging

MH  - Male

MH  - Middle Age

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - administration & dosage

MH  - adverse effects

MH  - Radiopharmaceuticals

MH  - diagnostic use

MH  - Serotonin Agents

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

MH  - Technetium Tc 99m Exametazime

MH  - Time Factors

MH  - Tomography,Emission-Computed,Single-Photon

RP  - NOT IN FILE

NT  - UI - 20175743LA - EngRN - 0 (Radiopharmaceuticals)RN - 0 (Serotonin Agents)RN - 0 (Technetium Tc 99m Exametazime)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEID - DA00280/DA/NIDAID - MO1 RR00425/RR/NCRRID - MH00534/MH/NIMHDA - 20000509IS - 0165-1781SB - MCY - IRELANDJC - QC4AA - AuthorEM - 200007

UR  - PM:0010708923

SO  - Psychiatry Res 2000 Feb 28 ;98(1):15-28

 

4

UI  - 17

AU  - de la TR

AU  - Farre M

AU  - Ortuno J

AU  - Mas M

AU  - Brenneisen R

AU  - Roset PN

AU  - Segura J

AU  - Cami J

AD  - Pharmacology Research Unit, Institut Municipal d'Investigacio Medica (IMIM), Universitat Pompeu Fabra and Universitat Autonoma de Barcelona, Spain. rtorre@imim.es

TI  - Non-linear pharmacokinetics of MDMA ('ecstasy') in humans

AB  - AIMS: 3,4-Methylenedioxymethamphetamine (MDMA, commonly called ecstasy) is a synthetic compound increasingly popular as a recreational drug. Little is known about its pharmacology, including its metabolism and pharmacokinetics, in humans in controlled settings. A clinical trial was designed for the evaluation of MDMA pharmacological effects and pharmacokinetics in healthy volunteers. METHODS: A total of 14 subjects were included. In the pilot phase six received MDMA at 50 (n=2), 100 (n=2), and 150 mg (n=2). In the second phase eight received MDMA at both 75 and 125 mg (n=8). Subjects were phenotyped for CYP2D6 activity and were classified as extensive metabolizers for substrates, such as MDMA, whose hepatic metabolism is regulated by this enzyme. Plasma and urine samples were collected throughout the study for the evaluation of MDMA pharmacokinetics. Body fluids were analysed for the determination of MDMA and its main metabolites 3,4-methylenedioxyamphetamine (MDA), 4- hydroxy-3-methoxy-methamphetamine (HMMA) and 4-hydroxy-3-methoxy- amphetamine (HMA). RESULTS: As the dose of MDMA administered was increased, volunteers showed rises in MDMA concentrations that did not follow the same proportionality which could be indicative of nonlinearity. In the full range of doses tested the constant recovery of HMMA in the urine combined with the increasing MDMA recovery seems to point towards a saturation or an inhibition of MDMA metabolism (the demethylenation step). These observations are further supported by the fact that urinary clearance was rather constant while nonrenal clearance was dose dependent. CONCLUSIONS: It has previously been postulated that individuals genetically deficient for the hepatic enzyme CYP2D6 (about 10% of the Caucasian people) were at risk of developing acute toxicity at moderate doses of MDMA because the drug would accumulate in the body instead of being metabolized and inactivated. The lack of linearity of MDMA pharmacokinetics (in a window of doses compatible with its recreational use) is a more general phenomenon as it concerns the whole population independent of their CYP2D6 genotype. It implies that relatively small increases in the dose of MDMA ingested are translated to disproportionate rises in MDMA plasma concentrations and hence subjects are more prone to develop acute toxicity

MH  - Adult

MH  - Area Under Curve

MH  - Blood Pressure

MH  - drug effects

MH  - Cross-Over Studies

MH  - Deoxyepinephrine

MH  - analogs & derivatives

MH  - urine

MH  - Diastole

MH  - Dose-Response Relationship,Drug

MH  - Double-Blind Method

MH  - Hallucinogens

MH  - blood

MH  - pharmacokinetics

MH  - Human

MH  - Hydrogen-Ion Concentration

MH  - Male

MH  - Metabolic Clearance Rate

MH  - Methamphetamine

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Pilot Projects

MH  - Support,Non-U.S.Gov't

MH  - Time Factors

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 20137822LA - EngRN - 0 (Hallucinogens)RN - 117652-28-5 (4-hydroxy-3-methoxymethamphetamine)RN - 15398-87-5 (alpha-methylepinine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 501-15-5 (Deoxyepinephrine)RN - 537-46-2 (Methamphetamine)PT - CLINICAL TRIALPT - JOURNAL ARTICLEPT - RANDOMIZED CONTROLLED TRIALDA - 20000302IS - 0306-5251SB - MCY - ENGLANDJC - AU9AA - AuthorEM - 200005

UR  - PM:0010671903

SO  - Br J Clin Pharmacol 2000 Feb ;49(2):104-109

 

5

UI  - 6

AU  - Erdtmann-Vourliotis M

AU  - Mayer P

AU  - Riechert U

AU  - Hollt V

AD  - Institute for Pharmacology and Toxicology, Otto-von-Guericke Universitat, Leipziger Str. 44, 39120, Magdeburg, Germany

TI  - Prior experience of morphine application alters the c-fos response to MDMA ('ecstasy') and cocaine in the rat striatum [In Process Citation]

AB  - Repeated morphine application usually leads to the development of tolerance but under certain circumstances sensitization may arise simultaneously. This phenomenon becomes obvious in behavioral tests as increasing locomotor activity and increasing drug self-administration during a course of chronic morphine application. It was suggested recently that sensitization could contribute to addiction. The molecular mechanisms of sensitization may include the long lasting increase in neuronal responsiveness to morphine which was observed in defined brain areas after repeated morphine injections. In this work, we studied whether morphine-sensitized Wistar rats also display an enhanced neuronal activity in response to other drugs of abuse (so called co-sensitization). The substances to be tested were injected as single doses 4 weeks after completion of a 10-day morphine pretreatment. MDMA (3, 4-methylenedioxymethamphetamine, 6 mg/kg) as a single test dose yielded a c-fos response in a wide range of brain areas. In the caudate putamen, the expression pattern of c-fos was clearly altered if the rats had received repeated morphine application previously. In this case, the MDMA-induced c-fos expression was markedly confined to the centromedial, mesolimbic aspect of the striatum whereas it had a diffuse appearance in rats not exposed to the opiate earlier. Cocaine application (50 mg/kg) elicited an intense c- fos expression in the medial striatum if the animals were morphine- pretreated; it was virtually absent in drug-naive rats after the same cocaine dose. Ten mg/kg cocaine had a similar but weaker effect. No difference in the c-fos expression pattern between morphine and saline pretreated animals was observed in the case of a THC (Delta(9)- tetrahydrocannabinol, 25 mg/kg) or an LSD (lysergic acid diethylamide, 1 mg/kg) test application. These findings imply that morphine sensitizes the brain towards other addicting drugs. In consequence, morphine sensitization obviously does not solely reflect alterations in &mgr;-opioid receptor signaling. Rather, it seems to reflect further rearrangements within the mesolimbic system

RP  - NOT IN FILE

NT  - UI - 20276033LA - EngDA - 20000617IS - 0169-328XSB - MCY - NETHERLANDSJC - MBRAA - AUTHORRO - O:099

UR  - PM:0010814832

SO  - Brain Res Mol Brain Res 2000 Apr 14 ;77(1):55-64

 

6

UI  - 9

AU  - Fischer HS

AU  - Zernig G

AU  - Schatz DS

AU  - Humpel C

AU  - Saria A

AD  - Division of Neurochemistry, Department of Psychiatry, Anichstrasse 35, A-6020 Innsbruck, Austria

TI  - MDMA ('ecstasy') enhances basal acetylcholine release in brain slices of the rat striatum [In Process Citation]

AB  - The pharmacological basis of acute (+/-)-MDMA (3, 4- methylenedioxymethamphetamine) intoxication still awaits full characterization. According to present knowledge, MDMA enhances the release of serotonin and dopamine in striatal slices and interacts with different types of receptors such as 5-HT2 (5-hydroxytryptamine or serotonin), M1 and M2 muscarinic acetylcholine (ACh), and histamine H1 receptors. Currently, no information is available about the influence of (+/-)-MDMA on striatal cholinergic neurotransmission. In the present study, we used the in vitro perfusion technique to investigate the effect of (+/-)-MDMA on ACh release in rat striatal slices. Perfusions with (+/-)-MDMA (10-300 &mgr;M) resulted in a dose-dependent increase of spontaneous ACh release (EC50 approximately 30 &mgr;M). The effect was reversible and Ca++- and tetrodotoxin-sensitive. To determine the neurochemical pathways underlying this response, we perfused with (+/-)- MDMA in the presence of various inhibitors of neurotransmitter receptors. Blockade of glutamate or muscarinic ACh receptors as well as 5-HT1, 5-HT2, 5-HT3C or dopamine D2 receptors did not modulate (+/-)- MDMA-induced ACh release. However, the presence of histamine H1 receptor antagonists in the perfusion medium abolished (+/-)-MDMA- induced ACh release. The present data clearly demonstrate that (+/-)- MDMA enhances the activity of striatal cholinergic neurons and suggest an involvement of histamine H1 receptors. The effect is not mediated by glutamate and does not involve the activation of receptors of dopamine D2, 5-HT1, 5-HT2, 5-HT3C or muscarinic ACh. Considering the relatively high affinity of (+/-)-MDMA for the H1 histamine receptor (Ki 6 &mgr;M), a direct activation of this type of receptor might represent a plausible mechanism for (+/-)-MDMA-induced ACh release

RP  - NOT IN FILE

NT  - UI - 20225557LA - EngDA - 20000511IS - 0953-816XSB - MCY - FRANCEJC - BYGAA - AUTHORRO - O:099

UR  - PM:0010762366

SO  - Eur J Neurosci 2000 Apr ;12(4):1385-1390

 

7

UI  - 23

AU  - Horan B

AU  - Gardner EL

AU  - Ashby CR

AD  - PHS Department, College of Pharmacy and Allied Health Professions, St. John's University, Jamaica, New York 11439, USA

TI  - Enhancement of conditioned place preference response to cocaine in rats following subchronic administration of 3, 4- methylenedioxymethamphetamine (MDMA)

AB  - In this study, we measured conditioned place preference (CPP) responses to cocaine following subchronic administration of the recreationally abused drug (+/-)-3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") in male Sprague-Dawley rats. Animals were given either vehicle (1 ml/kg of distilled water, s.c.) or MDMA (20 mg/kg, s.c.) twice a day for 4 consecutive days. Two weeks later, CPP responses to cocaine (5, 10, or 20 mg/kg, i.p.) were measured. The MDMA-treated animals showed a significantly greater CPP response to cocaine than the vehicle-treated animals. Since conditioned place preference is believed to be a measure of appetitive behavior, these results suggest that MDMA abuse could lead to an increased vulnerability to the rewarding actions of cocaine and, hence, to increased vulnerability to cocaine addiction and dependence. Copyright 2000 Wiley-Liss, Inc

MH  - Animal

MH  - Appetite

MH  - drug effects

MH  - physiology

MH  - Choice Behavior

MH  - Cocaine

MH  - pharmacology

MH  - Conditioning,Operant

MH  - Dose-Response Relationship,Drug

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Reward

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 20079332LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-36-2 (Cocaine)PT - JOURNAL ARTICLEID - R29MH55155/MH/NIMHDA - 20000217IS - 0887-4476SB - MCY - UNITED STATESJC - VFLAA - AuthorEM - 200004

UR  - PM:0010611642

SO  - Synapse 2000 Feb ;35(2):160-162

 

8

UI  - 5

AU  - Iravani MM

AU  - Asari D

AU  - Patel J

AU  - Wieczorek WJ

AU  - Kruk ZL

AD  - Department of Pharmacology, Queen Mary & Westfield College, University of London, UK. m.iravani@kcl.ac.uk

TI  - Direct effects of 3,4-methylenedioxymethamphetamine (MDMA) on serotonin or dopamine release and uptake in the caudate putamen, nucleus accumbens, substantia nigra pars reticulata, and the dorsal raphe nucleus slices

AB  - We examined the effects of pressure ejected 3, 4- methylenedioxymethamphetamine (MDMA) from a micropipette on direct chemically stimulated release, and on electrically stimulated serotonin (5-HT) or dopamine (DA) release in the caudate putamen (CPu), nucleus accumbens (NAc), substantia nigra pars reticulata (SNr), and the dorsal raphe nucleus (DRN) brain slices of rat, using fast cyclic voltammetry (FCV). MDMA is electroactive, oxidising at +1100 mV. When the anodic input waveform was reduced from +1.4 to +1.0 volt, MDMA was not electroactive. Using this waveform, pressure ejection of MDMA did not release 5-HT or DA in brain slices prepared from any of the nuclei studied. MDMA significantly potentiated electrically stimulated 5-HT release in the SNr and DA release in CPu. In the DRN or in the NAc, MDMA was without effect on peak electrically stimulated 5-HT or DA release. The rates of neurotransmitter uptake, expressed as t(1/2), were in all cases significantly decreased after MDMA. The results indicate that MDMA, unlike (+)amphetamine, is not as a releaser of DA or 5-HT, it is a potent inhibitor of both DA and 5-HT uptake. Copyright 2000 Wiley-Liss, Inc

MH  - Amphetamine

MH  - pharmacology

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - Caudate Nucleus

MH  - Dopamine

MH  - Electric Stimulation

MH  - Electrochemistry

MH  - In Vitro

MH  - Injections,Jet

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Nucleus Accumbens

MH  - Raphe Nuclei

MH  - Rats

MH  - Rats,Wistar

MH  - Serotonin

MH  - Substantia Nigra

RP  - NOT IN FILE

NT  - UI - 20280163LA - EngRN - 300-62-9 (Amphetamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)PT - JOURNAL ARTICLEDA - 20000606IS - 0887-4476SB - MCY - UNITED STATESJC - VFLAA - AuthorEM - 200008

UR  - PM:0010819905

SO  - Synapse 2000 Jun 15 ;36(4):275-285

 

9

UI  - 19

AU  - Jurado C

AU  - Gimenez MP

AU  - Soriano T

AU  - Menendez M

AU  - Repetto M

AD  - Instituto Nacional de Toxicologia, Sevilla, Spain. quim@sev.inaltox.es

TI  - Rapid analysis of amphetamine, methamphetamine, MDA, and MDMA in urine using solid-phase microextraction, direct on-fiber derivatization, and analysis by GC-MS

AB  - A rapid, sensitive, and solvent-free procedure for the simultaneous determination of amphetamine, methamphetamine, 3,4- methylenedioxyamphetamine (MDA), and 3,4-methylenedioxymethamphetamine (MDMA) in urine was developed using solid-phase microextraction (SPME) and gas chromatography-mass spectrometry (GC-MS) in the selected ion monitoring mode. A headspace vial containing the urine sample, NaOH, NaCl, and amphetamine-d3 as the internal standard was heated at 100 degrees C for 20 min. A polydimethylsiloxane fiber was maintained in the vial headspace for 10 min in order to adsorb the amphetaminic compounds, which were subsequently derivatized by exposing the fiber to trifluoroacetic anhydride for 20 min in the headspace of another vial maintained at 60 degrees C for 20 min. The trifluoroacetyl derivatives were desorbed in the GC injection port for 5 min. Several parameters were considered during the method optimization process. These included a comparison of SPME with or without headspace, the required derivatization procedure, and the influence of temperature on the headspace extraction and derivatization methods. The optimized method was validated for the four compounds tested. Calibration curves showed linearity in the range 50-1000 ng/mL (r = 0.9946-0.9999). Recovery data were 71.89-103.24%. The quantitation limits were 10 ng/mL for amphetamine and methamphetamine and 20 ng/mL for MDA and MDMA. All of these data recommend the applicability of the method for use in the analytical routine of a forensic laboratory

MH  - Amphetamine

MH  - urine

MH  - Comparative Study

MH  - Dimethylpolysiloxanes

MH  - chemistry

MH  - Human

MH  - Mass Fragmentography

MH  - Methamphetamine

MH  - Microchemistry

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Reproducibility of Results

MH  - Sensitivity and Specificity

MH  - Substance Abuse Detection

MH  - methods

MH  - Sympathomimetics

MH  - Temperature

MH  - Time Factors

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 20118724LA - EngRN - 0 (Dimethylpolysiloxanes)RN - 0 (Sympathomimetics)RN - 300-62-9 (Amphetamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 537-46-2 (Methamphetamine)PT - JOURNAL ARTICLEDA - 20000309IS - 0146-4760SB - MCY - UNITED STATESJC - K4RAA - AuthorEM - 200005

UR  - PM:0010654563

SO  - J Anal Toxicol 2000 Jan ;24(1):11-16

 

10

UI  - 10

AU  - Liechti ME

AU  - Baumann C

AU  - Gamma A

AU  - Vollenweider FX

AD  - Psychiatric University Hospital Zurich. Research Department, P.O. Box 68, CH-8029, Zurich, Switzerland. mliechti@bli.unizh.ch

TI  - Acute psychological effects of 3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy") are attenuated by the serotonin uptake inhibitor citalopram

AB  - 3,4-Methylenedioxymethamphetamine (MDMA, "Ecstasy") is a recreational drug that has been shown to release serotonin (5-HT) and dopamine (DA) in animals. The effect of MDMA on 5-HT release can be blocked by 5-HT uptake inhibitors such as citalopram, suggesting that MDMA interacts with the 5-HT uptake site. It is unknown whether this mechanism is also responsible for the psychological effects of MDMA in humans. We investigated the effect of citalopram pretreatment (40 mg iv) on the psychological effects of MDMA (1.5 mg/kg po) in a double-blind placebo- controlled psychometric study in 16 healthy human volunteers. MDMA produced an emotional state with heightened mood, increased self- confidence and extroversion, moderate derealization, and an intensification of sensory perception. Most of these effects were markedly reduced by citalopram. This finding suggests that the psychological effects of MDMA are mediated via action at the 5-HT uptake site to increase 5-HT release through the carrier, as expected from animal studies

MH  - Adult

MH  - Amphetamine-Related Disorders

MH  - drug therapy

MH  - physiopathology

MH  - psychology

MH  - Brain

MH  - drug effects

MH  - Citalopram

MH  - administration & dosage

MH  - Double-Blind Method

MH  - Female

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Neuropsychological Tests

MH  - Nootropic Agents

MH  - Serotonin Uptake Inhibitors

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 20197909LA - EngRN - 0 (Hallucinogens)RN - 0 (Nootropic Agents)RN - 0 (Serotonin Uptake Inhibitors)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 59729-33-8 (Citalopram)PT - CLINICAL TRIALPT - CONTROLLED CLINICAL TRIALPT - JOURNAL ARTICLEDA - 20000509IS - 0893-133XSB - MCY - UNITED STATESJC - ADQAA - AuthorEM - 200007

UR  - PM:0010731626

SO  - Neuropsychopharmacology 2000 May ;22(5):513-521

 

11

UI  - 1

AU  - Maldonado E

AU  - Navarro JF

AD  - Area de Psicobiologia, Facultad de Psicologia, Universidad de Malaga, Spain

TI  - Effects of 3,4-methylenedioxy-methamphetamine (MDMA) on anxiety in mice tested in the light-dark box [In Process Citation]

AB  - 1. The effects of acute administration of 3,4- methylenedioxymethamphetamine (MDMA; "ecstasy") on anxiety tested in the light/dark box were examined in albino male mice of the OF.1 strain. 2. Animals were evaluated in the light/dark test 30 min after injection of MDMA (1, 8, and 15 mg/kg, i.p) or saline. The following parameters were recorded (for 5 min); (a) number of exploratory rearings in the light and dark sections; (b) number of transitions between the lit and dark areas; (c) time spent in the light and dark areas; (d) latency of the initial movement from the light to the dark area, and (e) locomotor activity in light area. 3. MDMA (8 and 15 mg/kg) produced a significant reduction in exploratory activity (rearings and transitions), without decreasing motility, in comparison with saline-treated mice. However, time spent in lit/dark compartments was not significantly affected by the drug, which could be a consequence of the anti-exploratory properties of MDMA. 4. Overall, the behavioral profile found in the light/dark test indicates an anxiogenic- like activity of MDMA in mice. It is suggested, however, that animal models of anxiety which emphasize a social interaction could be more sensitive to the effects of this substance

RP  - NOT IN FILE

NT  - UI - 20294482LA - EngDA - 20000601IS - 0278-5846SB - MCY - ENGLANDJC - Q45AA - AUTHORRO - O:099

UR  - PM:0010836493

SO  - Prog Neuropsychopharmacol Biol Psychiatry 2000 Apr ;24(3):463-472

 

12

UI  - 11

AU  - McGuire P

AD  - Section of Neuroimaging, Institute of Psychiatry and GKT School of Medicine, London, UK. p.mcguire@iop.kcl.ac.uk

TI  - Long term psychiatric and cognitive effects of MDMA use

AB  - Clinical case reports suggest that regular MDMA use can be associated with chronic psychiatric symptoms which persist after the cessation of drug use. Neuropsychological comparisons of regular MDMA users and controls also suggest that MDMA use may lead to memory deficits, with other cognitive processes relatively unaffected. This paper reviews these studies and discusses a number of methodological issues that impact on the interpretation of the findings. Methods for examining the biological effects of MDMA use in man are also outlined. Future research should clarify whether MDMA use has long term psychological effects, and if these are related to changes in central serotonergic function

MH  - Chronic Disease

MH  - Cognition Disorders

MH  - chemically induced

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Memory Disorders

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Neuropsychology

MH  - Psychopathology

MH  - Recall

MH  - drug effects

MH  - Serotonin Agents

RP  - NOT IN FILE

NT  - UI - 20187900LA - EngRN - 0 (Hallucinogens)RN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 20000504IS - 0378-4274SB - MSB - XCY - NETHERLANDSJC - VXNAA - AuthorEM - 200007

UR  - PM:0010720725

SO  - Toxicol Lett 2000 Mar 15 ;112-113():153-156

 

13

UI  - 4

AU  - Parrott AC

AU  - Sisk E

AU  - Turner JJ

AD  - Department of Psychology, University of East London, E15 4LZ, London, UK

TI  - Psychobiological problems in heavy 'ecstasy' (MDMA) polydrug users [In Process Citation]

AB  - Twelve heavy recreational ecstasy drug users (30-1000 occasions), 16 light ecstasy users (1-20 occasions) and 22 non ecstasy user controls, with group mean ages around 21 years, were compared. Three self-rating questionnaires were completed when drug-free: the SCL-90 (an outpatient psychiatric symptom checklist), the impulsiveness venturesomeness and empathy (IVE) scale; and the uplifts, hassles, stresses and cognitive failures questionnaire. Heavy Ecstasy users reported significantly higher scores than controls on the following SCL-90 factors: paranoid ideation, psychoticism, somatisation, obsessionality, anxiety, hostility, phobic anxiety, altered appetite and restless sleep, together with greater IVE impulsiveness. Light ecstasy users generally produced intermediate scores, with significantly higher scores than controls on two factors and significantly lower scores than heavy ecstasy users on another two. Previous reports have described various psychiatric and psychobiological disorders in recreational ecstasy users, but it is not known how typical they are, being mainly based on individual case studies. This is the first study to describe psychological problems in a non clinical sample of young recreational ecstasy users. However, our ecstasy users were polydrug users, with both groups showing significantly greater usage of amphetamine, LSD and cocaine, than the controls. These other illicit drugs probably contributed to their adverse psychobiological profiles, while there is also the possibility of pre-existing differences between ecstasy users and non users. However, since repeated MDMA can cause serotonergic neurotoxicity in laboratory animals and man, these problems may reflect reduced serotonin activity induced by regular ecstasy use

RP  - NOT IN FILE

NT  - UI - 20283515LA - EngDA - 20000614IS - 0376-8716SB - MCY - IRELANDJC - EBSAA - AUTHORRO - O:099

UR  - PM:0010821995

SO  - Drug Alcohol Depend 2000 Jul 1 ;60(1):105-110

 

14

UI  - 12

AU  - Ricaurte GA

AU  - McCann UD

AU  - Szabo Z

AU  - Scheffel U

AD  - Department of Neurology, Johns Hopkins Medical Institutions, 5501 Hopkins Bayview Circle, Baltimore, MD, USA. ricaurte@jhmi.edu

TI  - Toxicodynamics and long-term toxicity of the recreational drug, 3, 4- methylenedioxymethamphetamine (MDMA, 'Ecstasy')

AB  - The recreational drug, (+/-)3,4-methylenedioxymethamphetamine (MDMA, 'Ecstasy'), is a potent serotonin (5-HT) neurotoxin in animals. Whether humans who use MDMA incur 5-HT neural injury is unknown. The present studies utilized positron emission tomography (PET) in conjunction with the 5-HT transporter ligand, [11C]McN-5652 to assess the status of brain 5-HT neurons in human MDMA users. Like nonhuman primates treated with neurotoxic doses of MDMA, humans with a history of MDMA use showed lasting decrements in global brain [11C]McN-5652 binding, with decreases in [11C]McN-5652 binding positively correlated to the extent of previous MDMA use. These results suggest that human MDMA use results in brain 5-HT neurotoxicity

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - Chromatography,High Pressure Liquid

MH  - Female

MH  - Human

MH  - Isoquinolines

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - blood

MH  - pharmacology

MH  - toxicity

MH  - Neurons

MH  - Papio

MH  - Serotonin Agents

MH  - Serotonin Antagonists

MH  - Support,U.S.Gov't,P.H.S.

MH  - Tomography,Emission-Computed

RP  - NOT IN FILE

NT  - UI - 20187898LA - EngRN - 0 (Isoquinolines)RN - 0 (Serotonin Agents)RN - 0 (Serotonin Antagonists)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 96795-90-3 (McN 5652)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALID - DA05707/DA/NIDAID - DA06275/DA/NIDADA - 20000504IS - 0378-4274SB - MSB - XCY - NETHERLANDSJC - VXNAA - AuthorEM - 200007

UR  - PM:0010720723

SO  - Toxicol Lett 2000 Mar 15 ;112-113():143-146

 

15

UI  - 14

AU  - Schroeder B

AU  - Brieden S

AD  - Department of Ophthalmology, Philipps-University, Germany. schroed2@mailer.uni-marburg.de

TI  - Bilateral sixth nerve palsy associated with MDMA ("ecstasy") abuse

AB  - PURPOSE:To report the association of methylenedioxymetamphetamine (MDMA, "ecstasy") abuse and bilateral sixth nerve palsy. METHODS: Case report. RESULTS: A 17-year-old male presented with horizontal diplopia in all directions of gaze after having taken MDMA tablets at 5-day to 7- day intervals during a 2-month period. Examination showed bilateral sixth nerve palsy. Ocular motility returned to normal within 5 days without use of MDMA and with no other treatment. CONCLUSION: Methylenedioxymetamphetamine "ecstasy" abuse should be considered in the differential diagnosis in otherwise unexplained sixth nerve palsy

MH  - Abducens Nerve Diseases

MH  - chemically induced

MH  - Adolescence

MH  - Case Report

MH  - Diplopia

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Substance-Related Disorders

MH  - etiology

MH  - Visual Fields

RP  - NOT IN FILE

NT  - UI - 20170775LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 20000404IS - 0002-9394SB - ASB - MCY - UNITED STATESJC - 3OQAA - AuthorEM - 200006

UR  - PM:0010704573

SO  - Am J Ophthalmol 2000 Mar ;129(3):408-409

 

16

UI  - 7

AU  - Tuchtenhagen F

AU  - Daumann J

AU  - Norra C

AU  - Gobbele R

AU  - Becker S

AU  - Pelz S

AU  - Sass H

AU  - Buchner H

AU  - Gouzoulis-Mayfrank E

AD  - Department of Psychiatry and Psychotherapy, Medical Faculty of the University of Technology, Pauwelsstrasse 30, D-52074, Aachen, Germany

TI  - High intensity dependence of auditory evoked dipole source activity indicates decreased serotonergic activity in abstinent ecstasy (MDMA) users

AB  - Neurotoxic damage of central serotonergic systems has been demonstrated in numerous animal studies after exposure to methylenedioxyamphetamines (ecstasy). A high intensity dependence of auditory evoked potentials and, particularly, of the tangential N1/P2 source activity has been associated with low levels of serotonergic neurotransmission in humans. We performed an auditory evoked potentials study in 28 abstinent recreational ecstasy users and two equally sized groups of cannabis users and nonusers. The ecstasy users exhibited an increase of the amplitude of the tangential N1/P2 source activity with higher stimulus intensities; whereas, both control groups failed to exhibit this feature. These data are in line with the hypothesis that abstinent ecstasy users present with diminished central serotonergic activity. This feature of information processing is probably related to the well- recognized neurotoxic potential of ecstasy. Our data indicate that recreational ecstasy use may cause long-term alterations in the function (and possibly structure) of the human brain

MH  - Adolescence

MH  - Adult

MH  - Analysis of Variance

MH  - Brain

MH  - drug effects

MH  - physiology

MH  - Brain Mapping

MH  - Evoked Potentials,Auditory

MH  - Female

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - Receptors,Serotonin

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 20250716LA - EngRN - 0 (Receptors, Serotonin)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEDA - 20000602IS - 0893-133XSB - MCY - UNITED STATESJC - ADQAA - AuthorEM - 200008

UR  - PM:0010788760

SO  - Neuropsychopharmacology 2000 Jun ;22(6):608-617

 

17

UI  - 3

AU  - Wareing M

AU  - Fisk JE

AU  - Murphy PN

AD  - Centre for Studies in the Social Sciences, Edge Hill College of Higher Education, Ormskirk, UK

TI  - Working memory deficits in current and previous users of MDMA ('ecstasy') [In Process Citation]

AB  - Current and previous users of the drug MDMA ('ecstasy') were tested on measures of central executive functioning, information processing speed, and on self-report measures of arousal and anxiety. The results were compared with those for a control group who did not use MDMA. Relative to the control group, both user groups were found to be impaired in some aspects of central executive functioning. Also, there were significant group differences on the measures of anxiety (users were more anxious) and on arousal (previous users scoring higher on the arousal measure relative to current users). Users processed information as quickly as non-users but less accurately. Some possible mediators of the above group differeces are discussed

RP  - NOT IN FILE

NT  - UI - 20291984LA - EngDA - 20000530IS - 0007-1269SB - MCY - ENGLANDJC - B1SAA - AUTHORRO - O:099

UR  - PM:0010832513

SO  - Br J Psychol 2000 May ;91 (Pt 2)():181-188

 

18

UI  - 22

AU  - Aguirre N

AU  - Barrionuevo M

AU  - Ramirez MJ

AU  - Del Rio J

AU  - Lasheras B

AD  - Department of Pharmacology, School of Medicine, University of Navarra, Pamplona, Spain

TI  - Alpha-lipoic acid prevents 3,4-methylenedioxy-methamphetamine (MDMA)- induced neurotoxicity

AB  - A single administration of 3,4-methylenedioxymethamphetamine (MDMA, 20 mg/kg, i.p.), induced significant hyperthermia in rats and reduced 5- hydroxytryptamine (5-HT) content and [3H]paroxetine-labeled 5-HT transporter density in the frontal cortex, striatum and hippocampus by 40-60% 1 week later. MDMA treatment also increased glial fibrillary acidic protein (GFAP) immunoreactivity in the hippocampus. Repeated administration of the metabolic antioxidant alpha-lipoic acid (100 mg/kg, i.p., b.i.d. for 2 consecutive days) 30 min prior to MDMA did not prevent the acute hyperthermia induced by the drug; however, it fully prevented the serotonergic deficits and the changes in the glial response induced by MDMA. These results further support the hypothesis that free radical formation is responsible for MDMA-induced neurotoxicity

MH  - Animal

MH  - Antioxidants

MH  - pharmacology

MH  - Astrocytes

MH  - drug effects

MH  - metabolism

MH  - Binding Sites

MH  - Carrier Proteins

MH  - Fever

MH  - chemically induced

MH  - Frontal Lobe

MH  - cytology

MH  - Glial Fibrillary Acidic Protein

MH  - analysis

MH  - Hippocampus

MH  - Hypothermia

MH  - Male

MH  - Membrane Glycoproteins

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - antagonists & inhibitors

MH  - toxicity

MH  - Neostriatum

MH  - Neuroprotective Agents

MH  - Paroxetine

MH  - Pyramidal Cells

MH  - Rats

MH  - Rats,Wistar

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

MH  - Thioctic Acid

RP  - NOT IN FILE

NT  - UI - 20084683LA - EngRN - 0 (serotonin transporter)RN - 0 (Antioxidants)RN - 0 (Carrier Proteins)RN - 0 (Glial Fibrillary Acidic Protein)RN - 0 (Membrane Glycoproteins)RN - 0 (Neuroprotective Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 61869-08-7 (Paroxetine)RN - 62-46-4 (Thioctic Acid)PT - JOURNAL ARTICLEDA - 20000119IS - 0959-4965SB - MCY - ENGLANDJC - A6MAA - AuthorEM - 200003

UR  - PM:0010619665

SO  - Neuroreport 1999 Nov 26 ;10(17):3675-3680

 

19

UI  - 18

AU  - Bailly D

AD  - Clinique de la Charite, Centre Hospitalier Regional Universitaire, Lille

TI  - [Neuropsychiatric disorders induced by MDMA ("Ecstasy")]

AB  - If neurotoxicity of MDMA (ecstasy) is now well documented in animals, it is not the same in humans. MDMA intoxication puts the problem of its possible link with the serotonin syndrome and the neuroleptic malignant syndrome. Neuropathological consequences following MDMA intake have been reported, including hemorrhaging and cerebral infarction, cerebral venous sinus thrombosis, and acute inflammatory CNS disease. However, the physiopathology of these complications remains unclear. In the same way, there have been various reports that have attributed MDMA to precipitating the onset of a wide range of psychiatric disorders including sleep disorders, cognitive disorders, panic attacks, depression, flashbacks, psychosis and severe paranoia. Findings suggest that these psychiatric manifestations might be consequences of MDMA induced brain serotonin neurotoxic lesions. All these data are examined from a critical review of the literature

MH  - Cerebral Hemorrhage

MH  - chemically induced

MH  - Cerebral Veins

MH  - drug effects

MH  - Dopamine

MH  - metabolism

MH  - English Abstract

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Mental Disorders

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Paranasal Sinuses

MH  - blood supply

MH  - Serotonin Agents

MH  - Sleep Disorders

MH  - Venous Thrombosis

RP  - NOT IN FILE

NT  - UI - 20133782LA - FreRN - 0 (Hallucinogens)RN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 51-61-6 (Dopamine)PT - JOURNAL ARTICLEDA - 20000317IS - 0013-7006SB - MCY - FRANCEJC - EFBAA - AuthorEM - 200005

UR  - PM:0010668603

SO  - Encephale 1999 Nov ;25(6):595-602

 

20

UI  - 31

AU  - Chang L

AU  - Ernst T

AU  - Grob CS

AU  - Poland RE

AD  - Department of Neurology, UCLA School of Medicine, Harbor-UCLA Medical Center, Torrance, California 90502, USA. Linda_Chang@humc.edu

TI  - Cerebral (1)H MRS alterations in recreational 3, 4- methylenedioxymethamphetamine (MDMA, "ecstasy") users

AB  - 3,4-methylenedioxymethamphetamine (MDMA) is an illicit drug that has been associated with serotonergic axonal degeneration in animals. This study evaluates neurochemical abnormalities in recreational MDMA users. Twenty-two MDMA users and 37 normal subjects were evaluated with magnetic resonance imaging (MRI) and proton magnetic resonance spectroscopy ((1)H MRS) in the mid-frontal, mid-occipital, and parietal brain regions. (1)H MRS showed normal N-acetyl (NA) compounds in all brain regions. The myo-inositol (MI) concentration (+16.3%, P = 0.04) and the MI to creatine (CR) ratio (+14.1%, P = 0. 01) were increased in the parietal white matter of MDMA users. The cumulative lifetime MDMA dose showed significant effects on [MI] in the parietal white matter and the occipital cortex. The normal NA concentration suggests a lack of significant neuronal injury in recreational MDMA users. However, the usage-related increase in MI suggests that exposure to MDMA, even at recreational doses, may cause increased glial content. J. Magn. Reson. Imaging 1999;10:521-526. Copyright 1999 Wiley-Liss, Inc

MH  - Adult

MH  - Aged

MH  - Aged,80 and over

MH  - Aspartic Acid

MH  - analogs & derivatives

MH  - analysis

MH  - Brain

MH  - drug effects

MH  - pathology

MH  - Brain Chemistry

MH  - Choline

MH  - Creatine

MH  - Female

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Inositol

MH  - Magnetic Resonance Imaging

MH  - Male

MH  - Middle Age

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Nuclear Magnetic Resonance

MH  - Substance-Related Disorders

MH  - metabolism

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 99437942LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 56-84-8 (Aspartic Acid)RN - 57-00-1 (Creatine)RN - 62-49-7 (Choline)RN - 6917-35-7 (Inositol)RN - 997-55-7 (N-acetylaspartate)PT - JOURNAL ARTICLEID - DA00280/DA/NIDAID - MO1 RR00425/RR/NCRRID - MH00534/MH/NIMHDA - 19991115IS - 1053-1807SB - MCY - UNITED STATESJC - BEOAA - AuthorEM - 200001

UR  - PM:0010508318

SO  - J Magn Reson Imaging 1999 Oct ;10(4):521-526

 

21

UI  - 38

AU  - Colado MI

AU  - Granados R

AU  - O'Shea E

AU  - Esteban B

AU  - Green AR

AD  - Department of Pharmacology, Faculty of Medicine, Complutense University, Madrid, Spain. colado@eucmax.sim.ucm.es

TI  - The acute effect in rats of 3,4-methylenedioxyethamphetamine (MDEA, "eve") on body temperature and long term degeneration of 5-HT neurones in brain: a comparison with MDMA ("ecstasy")

AB  - Administration of a single dose of the recreationally used drug 3,4- methylenedioxyethamphetamine (MDEA or "eve") to Dark Agouti rats resulted in an acute dose-dependent hyperthermic response. The peak effect and duration of hyperthermia of a dose of MDEA of 35 mg/kg intraperitoneally was similar to a dose of 3,4- methylenedioxymethamphetamine (MDMA or "ecstasy") of 15 mg/kg intraperitoneally. Seven days later this dose of MDMA produced a marked (approximately 50%) loss of 5-HT and its metabolite 5-HIAA in cortex, hippocampus and striatum and a similar loss of [3H]-paroxetine binding in cortex: these losses reflecting the MDMA-induced neurotoxic degeneration of 5-HT nerve endings. In contrast, administration of MDEA (15, 25 or 35 mg/kg), even at the highest dose, produced only a 20% loss in cortex and hippocampus and no decrease in striatum. The neurotoxic effect of MDEA was only weakly dose-dependent. Neither MDEA (35 mg/kg) nor MDMA (15 mg/kg) altered striatal dopamine content 7 days later. MDEA appeared to have about half the potency of MDMA in inducing acute hyperthermia and 25% of the potency in inducing degeneration of cerebral 5-HT neurones. However since higher doses of MDEA (compared to MDMA) are probably necessary to induce mood changing effects, these data do not support any contention that this compound is a "safer" recreational drug than MDMA in terms of either acute toxicity or long term neurodegeneration

MH  - Amphetamines

MH  - toxicity

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - Cerebral Cortex

MH  - Comparative Study

MH  - Dose-Response Relationship,Drug

MH  - Fever

MH  - chemically induced

MH  - Hippocampus

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Nerve Endings

MH  - Paroxetine

MH  - analysis

MH  - Rats

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

MH  - Time Factors

MH  - Visual Cortex

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 99328154LA - EngRN - 0 (Amphetamines)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 61869-08-7 (Paroxetine)RN - 82801-81-8 (3,4-methylenedioxyethamphetamine)PT - JOURNAL ARTICLEDA - 19990901IS - 0901-9928SB - MCY - DENMARKJC - PHTAA - AuthorEM - 199911

UR  - PM:0010401727

SO  - Pharmacol Toxicol 1999 Jun ;84(6):261-266

 

22

UI  - 43

AU  - Colado MI

AU  - Esteban B

AU  - O'Shea E

AU  - Granados R

AU  - Green AR

AD  - Departamento de Farmacologia, Facultad de Medicina, Universidad Complutense, Madrid, Spain. colado@eucmax.sim.ucm.es

TI  - Studies on the neuroprotective effect of pentobarbitone on MDMA-induced neurodegeneration

AB  - Administration of a dose of 15 mg/kg of the recreationally used drug 3,4-methylenedioxymethamphetamine (MDMA or "ecstasy") to Dark Agouti rats resulted in an acute hyperthermic response which was followed 7 days later by a marked (approximately 45%) loss of 5-HT and its metabolite 5-HIAA in cortex, hippocampus and striatum and a similar loss of [3H]-paroxetine binding in cortex. These losses reflect the MDMA-induced neurotoxic degeneration of 5-HT nerve endings. Administration of pentobarbitone (40 mg/kg) concurrently with MDMA produced a significant attenuation of the neurotoxic damage, but also acute hypothermia. When the temperature of the MDMA plus pentobarbitone- treated group was kept elevated to that of the MDMA-treated group by the use of a homeothermic blanket, the neuroprotective effect of pentobarbitone was lost. These data demonstrate that pentobarbitone appears to possess no intrinsic neuroprotective activity and the previously reported activity is due to a hypothermic action of the drug

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - Brain

MH  - pathology

MH  - Gaba

MH  - physiology

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - toxicity

MH  - Neuroprotective Agents

MH  - pharmacology

MH  - Paroxetine

MH  - metabolism

MH  - Pentobarbital

MH  - Rats

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 99244074LA - EngRN - 0 (Neuroprotective Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 56-12-2 (GABA)RN - 61869-08-7 (Paroxetine)RN - 76-74-4 (Pentobarbital)PT - JOURNAL ARTICLEDA - 19990610IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199908

UR  - PM:0010229068

SO  - Psychopharmacology (Berl) 1999 Mar ;142(4):421-425

 

23

UI  - 44

AU  - Colado MI

AU  - O'Shea E

AU  - Esteban B

AU  - Granados R

AU  - Green AR

AD  - Departamento de Farmacologia, Facultad de Medicina, Universidad Complutense, Madrid, Spain. colado@eucmax.sim.ucm.es

TI  - In vivo evidence against clomethiazole being neuroprotective against MDMA ('ecstasy')-induced degeneration of rat brain 5-HT nerve terminals by a free radical scavenging mechanism

AB  - Clomethiazole is an effective neuroprotective agent against the degeneration of 5-HT neurones that follows administration of 3,4- methylenedioxymethamphetamine (MDMA or 'ecstasy'). Since there is good evidence that free radical formation resulting from auto-oxidation of MDMA metabolites is responsible for the degeneration we have examined whether clomethiazole is a free radical scavenger. MDMA (15 mg/kg i.p.) increased the formation of 2,3- and 2,5-dihydroxybenzoic acids (2,3- DHBA and 2,5-DHBA) from salicylic acid perfused through a microdialysis tube implanted in the hippocampus, indicating increased free radical formation. Clomethiazole (50 mg/kg i.p.) administered 5 min prior and 55 min post MDMA prevented both the acute MDMA-induced hyperthermia and the rise in 2,3- and 2,5-DHBA. However, when the temperature of the MDMA + clomethiazole treated rats was kept elevated to that of the MDMA treated rats with a homeothermic blanket there was no inhibition of the MDMA-induced increase in 2,3-DHBA or 2,5-DHBA. These data suggest firstly that free radical formation is inhibited when the acute MDMA- induced hyperthermia is prevented. Secondly the data further indicate that clomethiazole has no free radical scavenging activity since the drug produces substantial neuroprotection when MDMA + clomethiazole treated rats are kept hyperthermic. This conclusion was strengthened by our observation that clomethiazole is a weak inhibitor (IC50 > 1 mM) of lipid peroxidation in synaptosomes when it had been induced by addition of FeCl2 + ascorbic acid

MH  - Animal

MH  - Biotransformation

MH  - Body Temperature

MH  - drug effects

MH  - Brain

MH  - metabolism

MH  - Cerebral Cortex

MH  - Chlormethiazole

MH  - pharmacology

MH  - Corpus Striatum

MH  - Free Radical Scavengers

MH  - Hippocampus

MH  - Hydroxybenzoic Acids

MH  - Hydroxyindoleacetic Acid

MH  - Kinetics

MH  - Male

MH  - Microdialysis

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - toxicity

MH  - Nerve Degeneration

MH  - chemically induced

MH  - pathology

MH  - prevention & control

MH  - Nerve Endings

MH  - Neuroprotective Agents

MH  - Paroxetine

MH  - pharmacokinetics

MH  - Rats

MH  - Salicylic Acid

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 99233241LA - EngRN - 0 (Free Radical Scavengers)RN - 0 (Hydroxybenzoic Acids)RN - 0 (Neuroprotective Agents)RN - 303-38-8 (2-pyrocatechuic acid)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 490-79-9 (2,5-dihydroxybenzoic acid)RN - 50-67-9 (Serotonin)RN - 533-45-9 (Chlormethiazole)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 61869-08-7 (Paroxetine)RN - 69-72-7 (Salicylic Acid)PT - JOURNAL ARTICLEDA - 19990624IS - 0028-3908SB - MCY - ENGLANDJC - NZBAA - AuthorEM - 199908

UR  - PM:0010218873

SO  - Neuropharmacology 1999 Feb ;38(2):307-314

 

24

UI  - 51

AU  - Colado MI

AU  - O'Shea E

AU  - Granados R

AU  - Esteban B

AU  - Martin AB

AU  - Green AR

AD  - Departamento de Farmacologia, Facultad de Medicina, Universidad Complutense, Madrid, Spain

TI  - Studies on the role of dopamine in the degeneration of 5-HT nerve endings in the brain of Dark Agouti rats following 3,4- methylenedioxymethamphetamine (MDMA or 'ecstasy') administration

AB  - 1. We investigated whether dopamine plays a role in the neurodegeneration of 5-hydroxytryptamine (5-HT) nerve endings occurring in Dark Agouti rat brain after 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') administration. 2. Haloperidol (2 mg kg(-1) i.p.) injected 5 min prior and 55 min post MDMA (15 mg kg(-1) i.p.) abolished the acute MDMA-induced hyperthermia and attenuated the neurotoxic loss of 5-HT 7 days later. When the rectal temperature of MDMA + haloperidol treated rats was kept elevated, this protective effect was marginal. 3. MDMA (15 mg kg(-1)) increased the dopamine concentration in the dialysate from a striatal microdialysis probe by 800%. L-DOPA (25 mg kg(-1) i.p., plus benserazide, 6.25 mg kg(-1) i.p.) injected 2 h after MDMA (15 mg kg(-1)) enhanced the increase in dopamine in the dialysate, but subsequent neurodegeneration was unaltered. L-DOPA (25 mg kg(-1)) injected before a sub-toxic dose of MDMA (5 mg kg(-1)) failed to induce neurodegeneration. 4. The MDMA-induced increase in free radical formation in the hippocampus (indicated by increased 2,3- and 2,5- dihydroxybenzoic acid in a microdialysis probe perfused with salicylic acid) was unaltered by L-DOPA. 5. The neuroprotective drug clomethiazole (50 mg kg(-1) i.p.) did not influence the MDMA-induced increase in extracellular dopamine. 6. These data suggest that previous observations on the protective effect of haloperidol and potentiating effect of L-DOPA on MDMA-induced neurodegeneration may have resulted from effects on MDMA-induced hyperthermia. 7. The increased extracellular dopamine concentration following MDMA may result from effects of MDMA on dopamine re-uptake, monoamine oxidase and 5-HT release rather than an 'amphetamine-like' action on dopamine release, thus explaining why the drug does not induce degeneration of dopamine nerve endings

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - Brain

MH  - metabolism

MH  - Dopamine

MH  - physiology

MH  - Free Radicals

MH  - Haloperidol

MH  - pharmacology

MH  - Levodopa

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - toxicity

MH  - Neurodegenerative Diseases

MH  - chemically induced

MH  - Paroxetine

MH  - Rats

MH  - Serotonin

MH  - analysis

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 99208114LA - EngRN - 0 (Free Radicals)RN - 0 (Levodopa)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 52-86-8 (Haloperidol)RN - 61869-08-7 (Paroxetine)PT - JOURNAL ARTICLEDA - 19990525IS - 0007-1188SB - MCY - ENGLANDJC - B00AA - AuthorEM - 199907

UR  - PM:0010193771

SO  - Br J Pharmacol 1999 Feb ;126(4):911-924

 

25

UI  - 36

AU  - Dafters RI

AU  - Duffy F

AU  - O'Donnell PJ

AU  - Bouquet C

AD  - Psychology Department, Glasgow University, UK. dick@psy.gla.ac.uk

TI  - Level of use of 3,4-methylenedioxymethamphetamine (MDMA or Ecstasy) in humans correlates with EEG power and coherence

AB  - RATIONALE: Despite animal studies implicating 3,4- methylenedioxymethamphetamine (MDMA or Ecstasy) in serotonergic neurotoxicity, there is little direct evidence of changes in neural function in humans who use MDMA as a recreational drug. OBJECTIVE: The present study investigated whether there is a correlation between quantitative EEG variables (spectral power and coherence) and cognitive/mood variables, and level of prior use of MDMA. METHODS: Twenty-three recreational MDMA users were studied. Resting EEG was recorded with eyes closed, using a 128-electrode geodesic net system, from which spectral power, peak frequency and coherence levels were calculated. Tests of intelligence (NART), immediate and delayed memory, frontal function (card sort task), and mood (BDI and PANAS scales) were also administered. Pearson correlation analyses were used to examine the relationship between these measures and the subject's consumption of MDMA during the previous 12-month period. Partial correlation was used to control for the use of other recreational drugs. RESULTS: MDMA use was positively correlated with absolute power in the alpha (8-12 Hz) and beta (12-20 Hz) frequency bands, but not with the delta (1-3 Hz) or theta (4-7 Hz) bands. MDMA use was negatively correlated with EEG coherence, a measure of synchrony between paired cortical locations, in posterior brain sites thought to overly the main visual association pathways of the occipito-parietal region. MDMA use did not correlate significantly with any of the mood/cognitive measures except the card sort task, with which it was weakly negatively correlated. CONCLUSIONS: Alpha power has been shown to be inversely related to mental function and has been used as an indirect measure of brain activation in both normal and abnormal states. Reduced coherence levels have been associated with dysfunctional connectivity in the brain in disorders such as dementia, white-matter disease and normal aging. Our results may indicate altered brain function correlated with prior MDMA use, and show that electroencephalography may be a cheap and effective tool for examining neurotoxic effects of MDMA and other drugs

MH  - Adolescence

MH  - Adult

MH  - Affect

MH  - drug effects

MH  - Alpha Rhythm

MH  - Cognition

MH  - Electroencephalography

MH  - Hallucinogens

MH  - administration & dosage

MH  - adverse effects

MH  - pharmacology

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Street Drugs

MH  - Substance-Related Disorders

MH  - diagnosis

RP  - NOT IN FILE

NT  - UI - 99372548LA - EngRN - 0 (Hallucinogens)RN - 0 (Street Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19990914IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199911

UR  - PM:0010445376

SO  - Psychopharmacology (Berl) 1999 Jul ;145(1):82-90

 

26

UI  - 57

AU  - de la TR

AU  - Ortuno J

AU  - Mas M

AU  - Farre M

AU  - Segura J

TI  - Fatal MDMA intoxication [letter; comment]

MH  - Anti-HIV Agents

MH  - poisoning

MH  - Cytochrome P-450 CYP2D6

MH  - metabolism

MH  - Drug Interactions

MH  - Hallucinogens

MH  - pharmacokinetics

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Ritonavir

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 99151468LA - EngRN - EC 1.14.99.- (Cytochrome P-450 CYP2D6)RN - 0 (Anti-HIV Agents)RN - 0 (Hallucinogens)RN - 0 (Ritonavir)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - COMMENTPT - LETTERDA - 19990311IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199905RO - M:LC1

UR  - PM:0010029010

SO  - Lancet 1999 Feb 13 ;353(9152):593

 

27

UI  - 28

AU  - Fineschi V

AU  - Centini F

AU  - Mazzeo E

AU  - Turillazzi E

AD  - Unit of Legal Medicine, University of Bari, Italy. vfinesc@tin.it

TI  - Adam (MDMA) and Eve (MDEA) misuse: an immunohistochemical study on three fatal cases

AB  - Three fatal cases of MDMA/MDEA misuse have been examined. These referred to white males between 19 and 20 years of age, in which post- mortem toxicology showed the presence of MDMA (in one case), MDEA (in one case) and both (in one case). The clinical data were analysed and the histopathological findings were studied following immunohistochemical investigations. A complete immunohistochemical study has made it possible to demonstrate rhabdomyolysis and myoglobinuria with alterations of the organs typical of a DIC. Clinical, histopathological and toxicological data suggest that severe or fatal complications following ecstasy ingestion could be related to idiosyncratic response

MH  - Adult

MH  - Case Report

MH  - Disseminated Intravascular Coagulation

MH  - chemically induced

MH  - pathology

MH  - therapy

MH  - Fatal Outcome

MH  - Forensic Medicine

MH  - Hallucinogens

MH  - chemistry

MH  - poisoning

MH  - Human

MH  - Male

MH  - Mass Fragmentography

MH  - Myoglobinuria

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rhabdomyolysis

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 20003472LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 82801-81-8 (3,4-methylenedioxyethamphetamine)PT - JOURNAL ARTICLEDA - 19991130IS - 0379-0738SB - MCY - IRELANDJC - F49AA - AuthorEM - 200002

UR  - PM:0010533279

SO  - Forensic Sci Int 1999 Sep 30 ;104(1):65-74

 

28

UI  - 34

AU  - Gijsman HJ

AU  - Verkes RJ

AU  - van Gerven JM

AU  - Cohen AF

TI  - MDMA study [letter; comment]

MH  - Animal

MH  - Clinical Trials

MH  - standards

MH  - Ethics,Medical

MH  - Hallucinogens

MH  - adverse effects

MH  - toxicity

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Neurons

MH  - drug effects

MH  - metabolism

MH  - pathology

MH  - Receptors,Serotonin

MH  - Serotonin

RP  - NOT IN FILE

NT  - UI - 99411457LA - EngRN - 0 (Hallucinogens)RN - 0 (Receptors, Serotonin)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - COMMENTPT - LETTERDA - 19991008IS - 0893-133XSB - MCY - UNITED STATESJC - ADQEM - 199912RO - M:LC2

UR  - PM:0010481843

SO  - Neuropsychopharmacology 1999 Oct ;21(4):597

 

29

UI  - 15

AU  - Gouzoulis-Mayfrank E

AU  - Hermle L

AU  - Kovar KA

AU  - Sass H

TI  - [Comment on R. Thomasius, M. Schmolke, D. Kraus: MDMA ("Ecstasy") use-- an overview of psychiatric and medical sequelae (letter; comment)]

MH  - Drug Contamination

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Substance-Related Disorders

MH  - diagnosis

RP  - NOT IN FILE

NT  - UI - 20147377LA - GerRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - COMMENTPT - LETTERDA - 20000324IS - 0720-4299SB - MCY - GERMANYJC - F67EM - 200006RO - M:CNR

UR  - PM:0010683753

SO  - Fortschr Neurol Psychiatr 1999 Dec ;67(12):574-576

 

30

UI  - 29

AU  - Harrington RD

AU  - Woodward JA

AU  - Hooton TM

AU  - Horn JR

AD  - Department of Medicine, School of Medicine, University of Washington, Seattle, USA. rdh@u.washington.edu

TI  - Life-threatening interactions between HIV-1 protease inhibitors and the illicit drugs MDMA and gamma-hydroxybutyrate

AB  - Human immunodeficiency virus 1 (HIV-1) protease inhibitors have dramatically reduced the morbidity and mortality due to HIV-1 infection. However, most of these antiretrovirals are also potent inhibitors (and occasionally inducers) of hepatic and intestinal cytochrome P450 systems and, therefore, have the potential to alter the elimination of any substance that utilizes these metabolic pathways. We describe a patient infected with HIV-1 who was treated with ritonavir and saquinavir and then experienced a prolonged effect from a small dose of methylenedioxymetamphetamine (MDMA or ecstacy) and a nearly fatal reaction from a small dose of gamma-hydroxybutyrate (GHB). We also discuss the potential for HIV-1 protease inhibitors to alter the metabolism of other abusable prescribed and illicit substances

MH  - Acquired Immunodeficiency Syndrome

MH  - drug therapy

MH  - Adrenergic Uptake Inhibitors

MH  - adverse effects

MH  - Adult

MH  - Anesthetics

MH  - Case Report

MH  - Drug Synergism

MH  - Hallucinogens

MH  - Human

MH  - HIV Protease Inhibitors

MH  - pharmacology

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Ritonavir

MH  - Saquinavir

MH  - Sodium Oxybate

RP  - NOT IN FILE

NT  - UI - 99454424LA - EngRN - 0 (Adrenergic Uptake Inhibitors)RN - 0 (Anesthetics)RN - 0 (Hallucinogens)RN - 0 (HIV Protease Inhibitors)RN - 0 (Ritonavir)RN - 127779-20-8 (Saquinavir)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 502-85-2 (Sodium Oxybate)PT - JOURNAL ARTICLEDA - 19991027IS - 0003-9926SB - ASB - MSB - XCY - UNITED STATESJC - 7FSAA - AuthorEM - 200001

UR  - PM:0010527300

SO  - Arch Intern Med 1999 Oct 11 ;159(18):2221-2224

 

31

UI  - 30

AU  - Hensley D

AU  - Cody JT

AD  - Clinical Research Squadron, Wilford Hall Medical Center, Lackland AFB, Texas 78236-5319, USA

TI  - Simultaneous determination of amphetamine, methamphetamine, methylenedioxyamphetamine (MDA), methylenedioxymethamphetamine (MDMA), and methylenedioxyethylamphetamine (MDEA) enantiomers by GC-MS

AB  - A method is described for the simultaneous determination of the ratio of l- and d-enantiomers of amphetamine, methamphetamine, 3,4- methylenedioxyamphetamine (MDA), 3,4-methylenedioxymethamphetamine (MDMA), and 3,4-methylenedioxyethylamphetamine (MDEA) in urine. The assay uses liquid-liquid extraction followed by derivatization with trifluoroacetyl-l-prolyl chloride (l-TPC) and analysis by gas chromatography-mass spectrometry. The assay was developed using prepared samples containing varying concentrations of each of the analytes over a range of percentages of each enantiomer. Results showed the method to provide accurate and reliable results in samples containing > or = 10 ng/mL amphetamine and methamphetamine and > or = 25 ng/mL MDA, MDMA, and MDEA. The assay was used to analyze urine samples from subjects of a controlled MDMA study. Results for each of the eight subjects showed a greater percentage of the l-enantiomer of MDMA initially, and the percentage increased with time postdose. Analysis of the metabolite MDA revealed that the proportion of d- enantiomer was initially greater than the l-enantiomer followed by a gradual increase in the proportion of l-enantiomer until it exceeded the amount of the d-enantiomer. In all cases, the l-MDA exceeded the d- MDA within the first 36 h postdose

MH  - Amphetamines

MH  - urine

MH  - Central Nervous System Stimulants

MH  - Human

MH  - In Vitro

MH  - Mass Fragmentography

MH  - Methamphetamine

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Sensitivity and Specificity

MH  - Stereoisomerism

MH  - Substance Abuse Detection

MH  - methods

MH  - Time Factors

MH  - chemistry

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 99445148LA - EngRN - 0 (Amphetamines)RN - 0 (Central Nervous System Stimulants)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 537-46-2 (Methamphetamine)RN - 82801-81-8 (3,4-methylenedioxyethamphetamine)PT - JOURNAL ARTICLEDA - 19991201IS - 0146-4760SB - MCY - UNITED STATESJC - K4RAA - AuthorEM - 200002

UR  - PM:0010517560

SO  - J Anal Toxicol 1999 Oct ;23(6):518-523

 

32

UI  - 58

AU  - Holland J

TI  - Positron emission tomography findings in heavy users of MDMA [letter; comment]

MH  - Brain

MH  - drug effects

MH  - radionuclide imaging

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Tomography,Emission-Computed

RP  - NOT IN FILE

NT  - UI - 99151467LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - COMMENTPT - LETTERDA - 19990311IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199905RO - M:LC1

UR  - PM:0010029009

SO  - Lancet 1999 Feb 13 ;353(9152):592-593

 

33

UI  - 45

AU  - Jansen KL

AU  - Forrest AR

TI  - Toxic effect of MDMA on brain serotonin neurons [letter; comment]

MH  - Brain

MH  - drug effects

MH  - Cocaine

MH  - adverse effects

MH  - Comparative Study

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Patient Selection

MH  - Serotonin

MH  - metabolism

MH  - Serotonin Agents

MH  - Vasoconstrictor Agents

RP  - NOT IN FILE

NT  - UI - 99231457LA - EngRN - 0 (Serotonin Agents)RN - 0 (Vasoconstrictor Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-36-2 (Cocaine)RN - 50-67-9 (Serotonin)PT - COMMENTPT - LETTERDA - 19990513IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199907RO - M:LC2

UR  - PM:0010217105

SO  - Lancet 1999 Apr 10 ;353(9160):1270-1271

 

34

UI  - 55

AU  - Jansen KL

AD  - The Maudsley Hospital, Denmark Hill, London, UK. k@btinternet.com

TI  - Ecstasy (MDMA) dependence

AB  - Methylenedioxymethamphetamine (MDMA) is generally described as non- addictive. However, this report describes three cases in which criteria for dependence were met. A wider understanding that MDMA can be addictive in rare cases is important as very heavy use may cause lasting neuronal changes. This risk could be reduced with effective identification and treatment of dependent persons. In one case dependence was linked with self-medication of post-traumatic stress disorder (PTSD)

MH  - Adult

MH  - Case Report

MH  - Hallucinogens

MH  - adverse effects

MH  - therapeutic use

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Seizures

MH  - chemically induced

MH  - Self Medication

MH  - Stress Disorders,Post-Traumatic

MH  - drug therapy

MH  - Substance-Related Disorders

MH  - diagnosis

RP  - NOT IN FILE

NT  - UI - 99179774LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19990806IS - 0376-8716SB - MCY - IRELANDJC - EBSAA - AuthorEM - 199910

UR  - PM:0010080038

SO  - Drug Alcohol Depend 1999 Jan 7 ;53(2):121-124

 

35

UI  - 52

AU  - Jones AL

AU  - Simpson KJ

AD  - Guy's and St Thomas' Hospital NHS Trust, Medical Toxicology Unit, London, UK

TI  - Review article: mechanisms and management of hepatotoxicity in ecstasy (MDMA) and amphetamine intoxications

AB  - The social use of ecstasy (methylenedioxymethampheta-mine, MDMA) and amphetamines is widespread in the UK and Europe, and they are popularly considered as 'safe'. However, deaths have occurred and hepatotoxicity has featured in many cases of intoxication with amphetamine or its methylenedioxy analogues such as ecstasy. Recreational use of these drugs presents an important but often concealed cause of hepatitis or acute liver failure, particularly in young people. The patterns of liver damage and multiple putative mechanisms of injury are discussed. Recognition of the aetiological agent requires a high index of suspicion. Optimum management of the resultant liver damage, including the controversial role of liver transplantation for fulminant hepatic failure, is also discussed

MH  - Amphetamine

MH  - poisoning

MH  - Human

MH  - Liver

MH  - drug effects

MH  - pathology

MH  - Liver Transplantation

MH  - N-Methyl-3,4-methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 99203776LA - EngRN - 300-62-9 (Amphetamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19990414IS - 0269-2813SB - MCY - ENGLANDJC - A5DAA - AuthorEM - 199906

UR  - PM:0010102941

SO  - Aliment Pharmacol Ther 1999 Feb ;13(2):129-133

 

36

UI  - 46

AU  - Klugman A

AU  - Hardy S

AU  - Baldeweg T

AU  - Gruzelier J

TI  - Toxic effect of MDMA on brain serotonin neurons [letter; comment]

MH  - Adult

MH  - Cognition

MH  - drug effects

MH  - Human

MH  - Memory

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - Psychological Tests

MH  - Serotonin Agents

RP  - NOT IN FILE

NT  - UI - 99231456LA - EngRN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - CLINICAL TRIALPT - COMMENTPT - CONTROLLED CLINICAL TRIALPT - LETTERDA - 19990513IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199907RO - M:LC2

UR  - PM:0010217104

SO  - Lancet 1999 Apr 10 ;353(9160):1269-1270

 

37

UI  - 47

AU  - Kuikka JT

AU  - Ahonen AK

TI  - Toxic effect of MDMA on brain serotonin neurons [letter; comment]

MH  - Binding Sites

MH  - drug effects

MH  - Brain

MH  - Human

MH  - Ligands

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - pharmacokinetics

MH  - Serotonin

MH  - metabolism

MH  - Serotonin Agents

RP  - NOT IN FILE

NT  - UI - 99231455LA - EngRN - 0 (Ligands)RN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - COMMENTPT - LETTERDA - 19990513IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199907RO - M:LC2

UR  - PM:0010217103

SO  - Lancet 1999 Apr 10 ;353(9160):1269-1

 

38

UI  - 27

AU  - Lavelle A

AU  - Honner V

AU  - Docherty JR

AD  - Department of Physiology, Royal College of Surgeons in Ireland, 123 St. Stephen's Green, Dublin 2, Ireland

TI  - Investigation of the prejunctional alpha2-adrenoceptor mediated actions of MDMA in rat atrium and vas deferens

AB  - 1. We have investigated the effects of methylenedioxymethamphetamine (MDMA, 'ecstasy') on peripheral noradrenergic neurotransmission in the rat. 2. In rat atrial slices pre-incubated with [3H]-noradrenaline and in the presence of desipramine (1 micronM) to prevent effects of MDMA on basal outflow of tritium, MDMA (10 micronM) significantly inhibited the release of tritium evoked by short trains of six pulses at 100 Hz every 10 s for 3 min. This effect did not occur in the presence of the alpha2-adrenoceptor antagonist yohimbine (1 micronM). 3. In epididymal portions of rat vas deferens in the presence of nifedipine (10 micronM), MDMA produced a concentration-dependent inhibition of single pulse nerve stimulation-evoked contractions with a pD2 of 5.88+/-0.16 (n=4). Inhibitory effects of MDMA were antagonized by the alpha2- adrenoceptor antagonist yohimbine (0.3 micronM), but not by the 5- hydroxytryptamine receptor antagonist cyanopindolol in a concentration (1 micronM) which markedly antagonized the inhibitory actions of the 5- HT-1 receptor agonist 5-carboxamidotryptamine. 4. In prostatic portions of rat vas deferens in the presence of cocaine (3 micronM), MDMA produced a concentration-dependent inhibition of single pulse nerve stimulation-evoked contractions with a pD2 of 5. 12+/-0.21 (n=4). In the absence of cocaine, only the highest concentration of MDMA (30 micronM) produced an inhibition, but the alpha2-adrenoceptor antagonist yohimbine (0.3 micronM) converted the response to MDMA from inhibition to potentiation of the stimulation-evoked contraction. 5. In radioligand binding studies, MDMA showed similar affinities for alpha2B, alpha2C and alpha2D-adrenoceptor sites, with pKi values of 5.14+/-0.16, 5.11+/-0. 05 and 5.31+/-0.14, respectively. 6 It is concluded that MDMA has significant alpha2-adrenoceptor agonist actions

MH  - Adrenergic Uptake Inhibitors

MH  - pharmacology

MH  - Animal

MH  - Cocaine

MH  - Dopamine Uptake Inhibitors

MH  - Electric Stimulation

MH  - Electrophysiology

MH  - Epididymis

MH  - drug effects

MH  - innervation

MH  - Heart Atrium

MH  - In Vitro

MH  - Kidney

MH  - Ligands

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Neuromuscular Junction

MH  - Prostate

MH  - Radioligand Assay

MH  - Rats

MH  - Rats,Wistar

MH  - Receptors,Adrenergic,alpha-2

MH  - Submandibular Gland

MH  - Support,Non-U.S.Gov't

MH  - Vas Deferens

RP  - NOT IN FILE

NT  - UI - 20025573LA - EngRN - 0 (Adrenergic Uptake Inhibitors)RN - 0 (Dopamine Uptake Inhibitors)RN - 0 (Ligands)RN - 0 (Receptors, Adrenergic, alpha-2)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-36-2 (Cocaine)PT - JOURNAL ARTICLEDA - 20000124IS - 0007-1188SB - MCY - ENGLANDJC - B00AA - AuthorEM - 200003

UR  - PM:0010556934

SO  - Br J Pharmacol 1999 Nov ;128(5):975-980

 

39

UI  - 54

AU  - Lin HQ

AU  - Burden PM

AU  - Christie MJ

AU  - Johnston GA

AD  - Department of Pharmacology, The University of Sydney, NSW, Australia

TI  - The anxiogenic-like and anxiolytic-like effects of MDMA on mice in the elevated plus-maze: a comparison with amphetamine

AB  - Many abused substances have been found to possess anxiogenic-like or/and anxiolytic-like properties. Discrepancies about the effects of MDMA, one of the most popular recreational drugs in recent years, on anxiety have been seen in the literature, and almost all of the data in this respect were derived from retrospective studies. The present study was thus designed to examine the drug's actions by using an animal model of anxiety, the elevated plus-maze test in male mice. Intraperitoneal MDMA at 1 mg/kg was ineffective, at 4 mg/kg decreased the percent of open arm entries (p < 0.01), and increased enclosed entries (p < 0.05), at 12 mg/kg had no significant effect, and at 20 mg/kg induced an increase of percent of open time (p < 0.01). As control drugs, amphetamine (0.5-4 mg/kg, i.p.) produced a dose- dependent, anxiogenic-like effect and diazepam (1 mg/kg, i.p.) induced an anxiolytic-like effect in the test. The results indicate that MDMA has anxiogenic-like properties at lower doses and anxiolytic-like at higher doses. The effects of MDMA and amphetamine on the mouse's responses to the plus-maze are compared. These findings provide a possible explanation for the controversies over MDMA's effects on anxiety in the literature

MH  - Amphetamine

MH  - pharmacology

MH  - Animal

MH  - Anti-Anxiety Agents

MH  - Anti-Anxiety Agents,Benzodiazepine

MH  - Anxiety

MH  - chemically induced

MH  - psychology

MH  - Behavior,Animal

MH  - drug effects

MH  - Comparative Study

MH  - Diazepam

MH  - Dopamine Uptake Inhibitors

MH  - Dose-Response Relationship,Drug

MH  - Hallucinogens

MH  - Male

MH  - Mice

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 99178315LA - EngRN - 0 (Anti-Anxiety Agents)RN - 0 (Anti-Anxiety Agents, Benzodiazepine)RN - 0 (Dopamine Uptake Inhibitors)RN - 0 (Hallucinogens)RN - 300-62-9 (Amphetamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 439-14-5 (Diazepam)PT - JOURNAL ARTICLEDA - 19990517IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199907

UR  - PM:0010080230

SO  - Pharmacol Biochem Behav 1999 Mar ;62(3):403-408

 

40

UI  - 32

AU  - Malpass A

AU  - White JM

AU  - Irvine RJ

AU  - Somogyi AA

AU  - Bochner F

AD  - Department of Clinical & Experimental Pharmacology, University of Adelaide, SA, Australia

TI  - Acute toxicity of 3,4-methylenedioxymethamphetamine (MDMA) in Sprague- Dawley and Dark Agouti rats

AB  - Ingestion of MDMA ("ecstasy") by humans can cause acute toxicity manifested by hyperthermia and death. Demethylenation of MDMA is catalyzed by cytochrome P-450 2D6 (CYP2D6) and cytochrome P-450 2D1 (CYP2D1) in humans and rats, respectively, and is polymorphically expressed. It has been proposed that CYP2D6 deficiency may account for the unexplained toxicity of MDMA. The female Dark Agouti rat is deficient in CYP2D1, and serves as a model for the human poor metabolizer. We investigated thermogenic and locomotor actions of MDMA in adult female Sprague-Dawley (CYP2D1 replete) and Dark Agouti rats. MDMA (2, 5, and 10 mg/kg) and saline were injected subcutaneously at ambient temperatures of 22 and 31 degrees C. There was no difference in core temperature responses between the two rat strains. Hypothermia occurred in the first 30 min and temperature elevation thereafter. MDMA increased locomotor activity in Sprague-Dawley but not in Dark Agouti rats. However, MDMA had pronounced lethal effects at 31 degrees C ambient in the Dark Agouti rats only. We conclude that the poor metaboliser phenotype may predispose to lethality, but the mechanism is as yet unknown

MH  - Animal

MH  - Body Temperature Regulation

MH  - drug effects

MH  - Comparative Study

MH  - Cytochrome P-450

MH  - metabolism

MH  - Cytochrome P-450 CYP2D6

MH  - Female

MH  - Hallucinogens

MH  - toxicity

MH  - Motor Activity

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Species Specificity

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 99423185LA - EngRN - EC 1.14.99.- (Cytochrome P-450 CYP2D6)RN - 0 (cytochrome P-450 CYP2D1)RN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 9035-51-2 (Cytochrome P-450)PT - JOURNAL ARTICLEDA - 19991021IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199912

UR  - PM:0010494994

SO  - Pharmacol Biochem Behav 1999 Sep ;64(1):29-34

 

41

UI  - 39

AU  - Marston HM

AU  - Reid ME

AU  - Lawrence JA

AU  - Olverman HJ

AU  - Butcher SP

AD  - Fujisawa Institute of Neuroscience, Department of Pharmacology, University of Edinburgh, UK. Hugh.Marston@ed.ac.uk

TI  - Behavioural analysis of the acute and chronic effects of MDMA treatment in the rat

AB  - RATIONALE: A variety of animal models have shown MDMA (3,4- methylenedioxymethamphetamine) to be a selective 5-HT neurotoxin, though little is known of the long-term behavioural effects of the pathophysiology. The widespread recreational use of MDMA thus raises concerns over the long-term functional sequelae in humans. OBJECTIVE: This study was designed to explore both the acute- and post-treatment consequences of a 3-day neurotoxic exposure to MDMA in the rat, using a variety of behavioural paradigms. METHODS: Following training to pretreatment performance criteria, animals were treated twice daily with ascending doses of MDMA (10, 15, 20 mg/kg) over 3 days. Body temperature, locomotor activity, skilled paw-reaching ability and performance of the delayed non-match to place (DNMTP) procedure was assessed daily during this period and on an intermittent schedule over the following 16 days. Finally, post mortem biochemical analyses of [3H] citalopram binding and monoamine levels were performed. RESULTS: During the MDMA treatment period, an acute 5-HT-like syndrome was observed which showed evidence of tolerance. Once drug treatment ceased the syndrome abated completely. During the post-treatment phase, a selective, delay-dependent, deficit in DNMTP performance developed. Post-mortem analysis confirmed reductions in markers of 5-HT function, in cortex, hippocampus and striatum. CONCLUSIONS: These results confirm that acutely MDMA exposure elicits a classical 5-HT syndrome. In the long-term, exposure results in 5-HT neurotoxicity and a lasting cognitive impairment. These results have significant implications for the prediction that use of MDMA in humans could have deleterious long- term neuropsychological/psychiatric consequences

MH  - Animal

MH  - Behavior,Animal

MH  - drug effects

MH  - Biogenic Monoamines

MH  - metabolism

MH  - Chromatography,High Pressure Liquid

MH  - Citalopram

MH  - Kinetics

MH  - Male

MH  - Mental Disorders

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Radioligand Assay

MH  - Rats

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 99306294LA - EngRN - 0 (Biogenic Monoamines)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 59729-33-8 (Citalopram)PT - JOURNAL ARTICLEDA - 20000112IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 200003

UR  - PM:0010379626

SO  - Psychopharmacology (Berl) 1999 May ;144(1):67-76

 

42

UI  - 41

AU  - McCann UD

AU  - Mertl M

AU  - Eligulashvili V

AU  - Ricaurte GA

AD  - Unit on Anxiety, Biological Psychiatry Branch, NIMH, Bethesda, MD 20892- 1272, USA. umccann@helix.nih.gov

TI  - Cognitive performance in (+/-) 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") users: a controlled study

AB  - RATIONALE: (+/-) 3,4-Methylenedioxymethamphetamine (MDMA, "ecstasy") is an amphetamine analog and drug of abuse. In animals, MDMA damages brain serotonin (5-HT) neurons at doses that overlap with those used recreationally by some humans. To date, few functional sequelae of MDMA- induced 5-HT damage have been identified. OBJECTIVE: Since serotonin is thought to be involved in cognitive processes, and since previous studies have reported verbal and visual memory deficits in MDMA users, the present study sought to determine whether other cognitive processes are influenced by previous exposure to MDMA. METHODS: Twenty-two MDMA users who had not used MDMA for at least 3 weeks and 23 control subjects were tested repeatedly with a computerized cognitive performance assessment battery while participating in a 5-day controlled inpatient study. Cerebrospinal fluid (CSF) measures of monoamine metabolites were also collected as an index of brain monoaminergic function. RESULTS: MDMA users and controls were found to perform similarly on several cognitive tasks. However, MDMA subjects had significant performance deficits on a sustained attention task requiring arithmetic calculations, a task requiring complex attention and incidental learning, a task requiring short term memory and a task of semantic recognition and verbal reasoning. MDMA users also had significant selective decreases in CSF 5-HIAA. CONCLUSIONS: The present CSF data provide further evidence that MDMA is neurotoxic to brain 5-HT neurons in humans, and the behavioral data suggest that brain 5-HT injury is associated with subtle, but significant, cognitive deficits

MH  - Adult

MH  - Analysis of Variance

MH  - Attention

MH  - drug effects

MH  - Cognition

MH  - Female

MH  - Hallucinogens

MH  - pharmacology

MH  - Human

MH  - Hydroxyindoleacetic Acid

MH  - cerebrospinal fluid

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Neurons

MH  - Recall

MH  - Support,U.S.Gov't,P.H.S.

MH  - Task Performance and Analysis

RP  - NOT IN FILE

NT  - UI - 99293980LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - JOURNAL ARTICLEID - DA05707/DA/NIDAID - DA05938/DA/NIDAID - DA00206/DA/NIDADA - 19990805IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199910

UR  - PM:0010367560

SO  - Psychopharmacology (Berl) 1999 Apr ;143(4):417-425

 

43

UI  - 25

AU  - McCann UD

AU  - Eligulashvili V

AU  - Mertl M

AU  - Murphy DL

AU  - Ricaurte GA

AD  - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892-1272, USA. umccann@helix.nih.gov

TI  - Altered neuroendocrine and behavioral responses to m- chlorophenylpiperazine in 3,4-methylenedioxymethamphetamine (MDMA) users

AB  - RATIONALE: (+/-) 3,4-Methylenedioxymethamphetamine (MDMA, "Ecstasy") is a popular drug of abuse and a brain serotonin neurotoxin in animals. Growing evidence indicates that humans are also susceptible to MDMA's neurotoxic effects, although few functional consequences of MDMA- induced 5-HT damage have been identified. OBJECTIVE: The present study sought to determine whether possible differences between MDMA users and control subjects could be unmasked by utilizing a pharmacological challenge with the mixed 5-HT agonist, meta-chlorophenylpiperazine (m- CPP). It was postulated that 5-HT neurotoxicity in MDMA users would be associated with altered 5-HT responsivity, exemplified by altered physiological and behavioral responses to m-CPP. METHODS: Twenty-five MDMA users who had not taken MDMA for at least 3 weeks and 25 controls received intravenous placebo (normal saline) and m-CPP (0.08 mg/kg) in a fixed order, single blind design. Repeated measures of mood, physical symptoms, and blood samples for neuroendocrine analyses were collected during the 90 min after each infusion. RESULTS: MDMA users reported more positive and fewer negative emotions and physical symptoms following m-CPP than controls, and were significantly less likely to report an m-CPP-induced panic attack. Male MDMA users had diminished cortisol and prolactin responses to m-CPP. CONCLUSIONS: The present data indicate that MDMA users have alterations in 5-HT neuronal function, possibly as a consequence of MDMA-induced brain serotonin neural injury

MH  - Adult

MH  - Affect

MH  - drug effects

MH  - Anxiety

MH  - psychology

MH  - Behavior

MH  - Female

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Hydrocortisone

MH  - blood

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Neurosecretory Systems

MH  - Piperazines

MH  - diagnostic use

MH  - Prolactin

MH  - Serotonin

MH  - physiology

MH  - Serotonin Agonists

MH  - Single-Blind Method

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 20065490LA - EngRN - 0 (Hallucinogens)RN - 0 (Piperazines)RN - 0 (Serotonin Agonists)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-23-7 (Hydrocortisone)RN - 50-67-9 (Serotonin)RN - 6640-24-0 (1-(3-chlorophenyl)piperazine)RN - 9002-62-4 (Prolactin)PT - CLINICAL TRIALPT - JOURNAL ARTICLEID - DA05707/DA/NIDAID - DA05938/DA/NIDAID - DA00206/DA/NIDADA - 20000124IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 200003

UR  - PM:0010591869

SO  - Psychopharmacology (Berl) 1999 Nov ;147(1):56-65

 

44

UI  - 48

AU  - Morgan JF

TI  - Toxic effect of MDMA on brain serotonin neurons [letter; comment]

MH  - Binding Sites

MH  - drug effects

MH  - Brain

MH  - Human

MH  - Mental Disorders

MH  - metabolism

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - Serotonin

MH  - Serotonin Agents

RP  - NOT IN FILE

NT  - UI - 99231454LA - EngRN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - COMMENTPT - LETTERDA - 19990513IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199907RO - M:LC2

UR  - PM:0010217102

SO  - Lancet 1999 Apr 10 ;353(9160):1268-1269

 

45

UI  - 59

AU  - Morgan MJ

AD  - Centre for Substance Abuse Research, Department of Psychology, University of Wales Swansea, UK. m.j.morgan@swansea.ac.uk

TI  - Memory deficits associated with recreational use of "ecstasy" (MDMA)

AB  - Evidence from both animal, and human, studies suggests that repeated administration of 3,4-methylenedioxymethamphetamine (MDMA: "ecstasy") produces lasting decreases in serotonergic activity. Serotonin is believed to play a modulatory role in a variety of psychological processes, including learning and memory. There are recent reports that polydrug users, who have used ecstasy recreationally, exhibit selective impairments in memory. However, these studies did not compare ecstasy users with polydrug users who had not taken ecstasy, leaving open the possibility that the memory deficits may be associated with a history of use of other illicit drugs. The present study used the Rivermead Behavioural Memory test to investigate immediate and delayed recall in: 25 polydrug-users who had taken more than 20 tablets of ecstasy (MDMA group), 22 participants (polydrug controls) who had never taken ecstasy, but, otherwise has personal characteristics (e.g. age, gender, education, height, weight), and illicit drug use histories, that were generally not significantly different from those of the MDMA group, and 19 participants who had not used illicit drugs but who also had similar personal characteristics (non-drug controls). Participants in the MDMA group recalled significantly fewer ideas (approximately 75% of the number of ideas recalled by participants in either of the other two groups), in both immediate and delayed recall conditions. The two illicit drug-using groups did differ in their estimated IQ scores and their duration of use of LSD, but only the latter proved to be a statistically significant covariate, and the difference in recall performance between the MDMA and polydrug controls groups remained statistically significant when this variable was treated as a covariate. The present findings provide the first evidence that deficits in memory performance in recreational ecstasy users are primarily associated with past exposure to ecstasy, rather than with the other legal and illicit drugs consumed by these individuals, and are consistent with reduced serotonergic modulation of mnemonic function as a result of long-term neurotoxic effects of MDMA in humans

MH  - Adult

MH  - Female

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Male

MH  - Memory Disorders

MH  - chemically induced

MH  - Memory,Short-Term

MH  - drug effects

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Recall

MH  - Serotonin

MH  - metabolism

MH  - Street Drugs

RP  - NOT IN FILE

NT  - UI - 99135533LA - EngRN - 0 (Hallucinogens)RN - 0 (Street Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEDA - 19990413IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199906

UR  - PM:0009952062

SO  - Psychopharmacology (Berl) 1999 Jan ;141(1):30-36

 

46

UI  - 40

AU  - Navarro JF

AU  - Maldonado E

AD  - Area de Psicobiologia, Facultad de Psicologia, Universidad de Malaga, Spain. navahuma@uma.es

TI  - Behavioral profile of 3,4-methylenedioxy-methamphetamine (MDMA) in agonistic encounters between male mice

AB  - 1. The effects of acute administration of 3, 4- methylenedioxymethamphetamine (MDMA), a synthetic amphetamine derivative (0.5-20 mg/kg, i.p.) on agonistic behavior elicited by isolation in male mice were examined. 2. Individually housed mice were exposed to anosmic "standard opponents" 30 min after MDMA injection, and the encounters were videotaped and evaluated using an ethologically based analysis. 3. MDMA (5-20 mg/kg) exhibited a behavioral profile characterized by a reduction of aggression (threat and attack) without a concomitant increase of immobility, accompanied by a decrease of social investigation and a increment of exploration from a distance, avoidance/flee and defense/submission behaviors. 4. This ethopharmacological profile might suggest an anxiogenic-like activity of MDMA in albino male mice

MH  - Aggression

MH  - drug effects

MH  - Animal

MH  - Exploratory Behavior

MH  - Hallucinogens

MH  - pharmacology

MH  - Male

MH  - Mice

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Social Behavior

MH  - Social Dominance

RP  - NOT IN FILE

NT  - UI - 99297262LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19990817IS - 0278-5846SB - MCY - ENGLANDJC - Q45AA - AuthorEM - 199910

UR  - PM:0010368873

SO  - Prog Neuropsychopharmacol Biol Psychiatry 1999 Feb ;23(2):327-334

 

47

UI  - 35

AU  - O'Connor A

AU  - Cluroe A

AU  - Couch R

AU  - Galler L

AU  - Lawrence J

AU  - Synek B

AD  - Department of Critical Care Medicine, Auckland Hospital

TI  - Death from hyponatraemia-induced cerebral oedema associated with MDMA ("Ecstasy") use

MH  - Adult

MH  - Brain Edema

MH  - chemically induced

MH  - Case Report

MH  - Fatal Outcome

MH  - Female

MH  - Hallucinogens

MH  - poisoning

MH  - Human

MH  - Hyponatremia

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Overdose

RP  - NOT IN FILE

NT  - UI - 99376214LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19990826IS - 0028-8446SB - MCY - NEW ZEALANDJC - OBQEM - 199910

UR  - PM:0010448984

SO  - N Z Med J 1999 Jul 9 ;112(1091):255-256

 

48

UI  - 20

AU  - Pacifici R

AU  - Zuccaro P

AU  - Farre M

AU  - Pichini S

AU  - Di Carlo S

AU  - Roset PN

AU  - Ortuno J

AU  - Segura J

AU  - de la TR

AD  - Clinical Biochemistry Department, Istituto Superiore di Sanita, Roma, Italy

TI  - Immunomodulating properties of MDMA alone and in combination with alcohol: a pilot study

AB  - Cell-mediated immune response after the administration of MDMA alone and in combination with alcohol was evaluated in a randomized, double- blind, double-dummy, cross-over pilot clinical trial conducted in four healthy MDMA consumers who received single oral doses of 75 mg MDMA (n = 2) or 100 mg MDMA (n = 2), alcohol (0.8 mg/kg), MDMA and alcohol, or placebo. Acute MDMA treatment produced a time-dependent immune dysfunction associated with MDMA plasma concentrations. Although total leukocyte count remained unchanged, there was a decrease in the CD4 T/CD8 T-cell ratio as well as in the percentage of mature T lymphocytes, probably because of a decrease in both the percentage and absolute number of T helper cells. The decrease in CD4 T-cell counts and in the functional responsiveness of lymphocytes to mitogenic stimulation was dose-dependent. The correlation between MDMA pharmacokinetics and the profile of MDMA-induced immune dysfunction suggests that alteration of the immune system may be mediated by the central nervous system. Alcohol consumption produced a decrease in T helper cells, B lymphocytes, and PHA-induced lymphocyte proliferation. Combined MDMA and alcohol produced the greatest suppressive effect on CD4 T-cell count and PHA-stimulated lymphoproliferation. Immune function was partially restored at 24 hours. These results provide the first evidence that recreational use of MDMA alone or in combination with alcohol alters the immunological status

MH  - Adjuvants,Immunologic

MH  - blood

MH  - pharmacology

MH  - pharmacokinetics

MH  - Administration,Oral

MH  - Central Nervous System Depressants

MH  - Cross-Over Studies

MH  - Dose-Response Relationship,Immunologic

MH  - Double-Blind Method

MH  - Drug Synergism

MH  - Ethanol

MH  - Hallucinogens

MH  - Human

MH  - Immunity,Cellular

MH  - drug effects

MH  - Male

MH  - N-Methyl-3,4- methylenedioxyamphetamine

MH  - Pilot Projects

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 20085987LA - EngRN - 0 (Adjuvants, Immunologic)RN - 0 (Central Nervous System Depressants)RN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 64-17-5 (Ethanol)PT - CLINICAL TRIALPT - JOURNAL ARTICLEPT - RANDOMIZED CONTROLLED TRIALDA - 20000119IS - 0024-3205SB - MSB - XCY - ENGLANDJC - L62AA - AuthorEM - 200003

UR  - PM:0010622275

SO  - Life Sci 1999  ;65(26):L309-L316

 

49

UI  - 49

AU  - Reed LJ

AU  - Winstock A

AU  - Cleare AJ

AU  - McGuire P

TI  - Toxic effect of MDMA on brain serotonin neurons [letter; comment]

MH  - Brain

MH  - drug effects

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - Neurons

MH  - metabolism

MH  - Sensitivity and Specificity

MH  - Serotonin

MH  - Serotonin Agents

MH  - Substance-Related Disorders

MH  - Tomography,Emission-Computed

RP  - NOT IN FILE

NT  - UI - 99231453LA - EngRN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - COMMENTPT - LETTERDA - 19990513IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199907RO - M:LC2

UR  - PM:0010217101

SO  - Lancet 1999 Apr 10 ;353(9160):1268-1

 

50

UI  - 37

AU  - Regenthal R

AU  - Kruger M

AU  - Rudolph K

AU  - Trauer H

AU  - Preiss R

TI  - Survival after massive "ecstasy" (MDMA) ingestion [letter]

MH  - Adult

MH  - Case Report

MH  - Hallucinogens

MH  - blood

MH  - poisoning

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Overdose

MH  - diagnosis

RP  - NOT IN FILE

NT  - UI - 99343333LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - LETTERDA - 19990914IS - 0342-4642SB - MCY - UNITED STATESJC - H2JEM - 199911

UR  - PM:0010416925

SO  - Intensive Care Med 1999 Jun ;25(6):640-641

 

51

UI  - 60

AU  - Scearce-Levie K

AU  - Viswanathan SS

AU  - Hen R

AD  - Center for Neurobiology and Behavior, Columbia Unversity, New York, NY 10032, USA

TI  - Locomotor response to MDMA is attenuated in knockout mice lacking the 5- HT1B receptor

AB  - 3,4-Methylenedioxymethamphetamine (MDMA) is a psychoactive drug of abuse which is increasingly popular in human recreational drug use. In rats, the drug has been shown to stimulate locomotion while decreasing exploratory behavior. MDMA acts as an indirect agonist of serotonin (5- HT) receptors by inducing 5-HT release by a 5-HT reuptake transporter- dependent mechanism, although it is not known which 5-HT receptors are important for the behavioral effects of the drug. In order to examine the role of specific 5-HT receptors, we assessed the behavioral effects of MDMA on knockout mice lacking the 5-HT1B receptor. Knockout animals show a reduced locomotor response to MDMA, although delayed locomotor stimulation is present in these animals. This finding indicates that the locomotor effects of MDMA are dependent upon the 5-HT1B receptor, at least in part. In contrast, MDMA eliminates exploratory behavior in both normal and knockout mice, suggesting that the exploratory suppression induced by MDMA occurs through mechanisms other than activation of the 5-HT1B receptor. To confirm these findings, we tested the effects of MDMA on the locomotor and exploratory behavior of wild- type mice pretreated with GR 127935, a 5-HT1B/1D receptor antagonist. These mice had an attenuated locomotor response to MDMA, but still exhibited the drug-induced suppression of exploration

MH  - Animal

MH  - Exploratory Behavior

MH  - drug effects

MH  - physiology

MH  - Human

MH  - Mice

MH  - Mice,Knockout

MH  - Motor Activity

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Rats

MH  - Receptors,Serotonin

MH  - deficiency

MH  - Serotonin Agents

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 99135510LA - EngRN - 0 (serotonin 1B receptor)RN - 0 (Receptors, Serotonin)RN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEID - R01DA09862/DA/NIDADA - 19990413IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199906

UR  - PM:0009952039

SO  - Psychopharmacology (Berl) 1999 Jan ;141(2):154-161

 

52

UI  - 56

AU  - Schwab M

AU  - Seyringer E

AU  - Brauer RB

AU  - Hellinger A

AU  - Griese EU

TI  - Fatal MDMA intoxication [letter; comment]

MH  - Adolescence

MH  - Anti-HIV Agents

MH  - poisoning

MH  - Cytochrome P-450 CYP2D6

MH  - deficiency

MH  - genetics

MH  - Drug Interactions

MH  - Female

MH  - Hallucinogens

MH  - pharmacokinetics

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Ritonavir

RP  - NOT IN FILE

NT  - UI - 99151469LA - EngRN - EC 1.14.99.- (Cytochrome P-450 CYP2D6)RN - 0 (Anti-HIV Agents)RN - 0 (Hallucinogens)RN - 0 (Ritonavir)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - COMMENTPT - LETTERDA - 19990311IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199905RO - M:LC1

UR  - PM:0010029011

SO  - Lancet 1999 Feb 13 ;353(9152):593-594

 

53

UI  - 21

AU  - Semple DM

AU  - Ebmeier KP

AU  - Glabus MF

AU  - O'Carroll RE

AU  - Johnstone EC

AD  - University Department of Psychiatry, Royal Edinburgh Hospital

TI  - Reduced in vivo binding to the serotonin transporter in the cerebral cortex of MDMA ('ecstasy') users

AB  - BACKGROUND: The use of MDMA ('ecstasy') is common among young people in Western countries. Animal models of MDMA toxicity suggest a loss of serotonergic neurons, and potentially implicate in the development of significant psychiatric morbidity in humans. AIMS: To test whether long- term use of MDMA can produce abnormalities in cerebral serotonin, but not dopamine, transporter binding measured by single photon emission computed tomography (SPECT). METHOD: Ten male regular ecstasy users and 10 well-matched controls recruited from the same community sources participated in SPECT with the serotonin transporter (SERT) ligand [123I] beta-CIT. Dopamine transporter binding was determined from scans acquired 23 hours after injection of the tracer. RESULTS: Ecstasy users showed a cortical reduction of SERT binding, particularly prominent in primary sensory-motor cortex, with normal dopamine transporter binding in lenticular nuclei. CONCLUSIONS: This cross-sectional association study provides suggestive evidence for specific, at least temporary, serotonergic neurotoxicity of MDMA in humans

MH  - Adolescence

MH  - Adult

MH  - Carrier Proteins

MH  - drug effects

MH  - metabolism

MH  - Case-Control Studies

MH  - Cerebral Cortex

MH  - Cross-Sectional Studies

MH  - Human

MH  - Male

MH  - Membrane Glycoproteins

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - Psychomotor Performance

MH  - Serotonin Agents

MH  - Support,Non-U.S.Gov't

MH  - Tomography,Emission-Computed,Single-Photon

RP  - NOT IN FILE

NT  - UI - 20087650LA - EngRN - 0 (serotonin transporter)RN - 0 (Carrier Proteins)RN - 0 (Membrane Glycoproteins)RN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 20000124IS - 0007-1250SB - MCY - ENGLANDJC - B1KAA - AuthorEM - 200003

UR  - PM:0010621770

SO  - Br J Psychiatry 1999 Jul ;175():63-69

 

54

UI  - 24

AU  - Shankaran M

AU  - Gudelsky GA

AD  - College of Pharmacy, University of Cincinnati, OH 45267-0004, USA

TI  - A neurotoxic regimen of MDMA suppresses behavioral, thermal and neurochemical responses to subsequent MDMA administration

AB  - RATIONALE: 3,4-Methylenedioxymethamphetamine (MDMA) produces a long- term depletion of serotonin (5-HT) in the rat brain; this depletion may have some functional consequences. OBJECTIVE: The aim of the present study was to evaluate the acute effects of MDMA on the extracellular concentrations of dopamine and 5-HT, body temperature and the 5-HT behavioral syndrome in rats 7 days following a neurotoxic regimen of MDMA. METHODS: One week after the rats were treated with a neurotoxic regimen of MDMA (10 mg/kg, i.p., every 2 h for a total of four injections), the rats were injected with a subsequent injection of MDMA. In vivo microdialysis combined with HPLC was utilized to measure the extracellular concentration of 5-HT and dopamine in the striatum. The increase in body temperature was determined by rectal temperature measurements, and the 5-HT behavioral syndrome was scored using a rating scale following the administration of MDMA. RESULTS: The neurotoxic regimen produced a 45% reduction in brain 5-HT concentrations. The magnitude of the MDMA-induced increase in the extracellular concentration of 5-HT, but not dopamine, in the striatum produced by an acute injection of MDMA (7.5 mg/kg, i.p.) was reduced in rats treated previously with the neurotoxic regimen of MDMA when compared with that in control animals. In addition, the magnitude of the 5-HT behavioral syndrome, as well as the hyperthermic response, produced by MDMA was markedly diminished in rats that had previously received the neurotoxic regimen of MDMA. CONCLUSIONS: It is concluded that the long-term depletion of brain 5-HT produced by MDMA is accompanied by impairments in 5-HT function, as evidenced by the deficits in the neurochemical, thermal and behavioral responses to subsequent MDMA administration

MH  - Animal

MH  - Behavior,Animal

MH  - drug effects

MH  - Body Temperature

MH  - Brain Chemistry

MH  - Dopamine

MH  - metabolism

MH  - Dose-Response Relationship,Drug

MH  - Extracellular Space

MH  - Hallucinogens

MH  - administration & dosage

MH  - toxicity

MH  - Injections,Intraperitoneal

MH  - Male

MH  - Microdialysis

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Neurotoxicity Syndromes

MH  - psychology

MH  - Neurotoxins

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Serotonin Syndrome

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 20065491LA - EngRN - 0 (Hallucinogens)RN - 0 (Neurotoxins)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)PT - JOURNAL ARTICLEID - DA07427/DA/NIDADA - 20000124IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 200003

UR  - PM:0010591870

SO  - Psychopharmacology (Berl) 1999 Nov ;147(1):66-72

 

55

UI  - 8

AU  - Virden TB

AU  - Baker LE

AD  - Department of Psychology, Western Michigan University, Kalamazoo 49008, USA. tvirden@imap4.asu.edu

TI  - Disruption of the discriminative stimulus effects of S(+)-3,4- methylenedioxymethamphetamine (MDMA) by (+/-)-MDMA neurotoxicity: protection by fluoxetine

AB  - This study utilized drug discrimination procedures to assess the functional consequences of (+/-)-3,4-methylenedioxymethamphetamine (MDMA)-induced serotonin depletion, and to determine whether concomitant injections of fluoxetine averted these effects. Twelve male Sprague-Dawley rats were trained to discriminate S(+)-MDMA (1.5 mg/kg, s.c.) from saline in a two-lever, water-reinforced operant procedure. After dose generalization tests were completed, training was suspended, and subjects were administered saline injections twice daily for four days. Ten days later, tests were conducted with S(+)-MDMA (1.5 mg/kg) and saline, to ascertain that discriminative stimulus control was maintained in the absence of training over a two-week period. All subjects received two additional weeks of training. Subsequently, (+/-)- MDMA (20 mg/kg, s.c.) was administered twice daily for four days, concomitantly with either 5.0 mg/kg fluoxetine (FLX) or saline (SAL) injections, and stimulus generalization tests with S(+)-MDMA and SAL were conducted after ten days. In the rats administered (+/-)-MDMA + SAL injections, S(+)-MDMA-appropriate responding dropped from 99.24% to 44.99% during S(+)-MDMA generalization tests, and rose from 2.78% to 22.14% during SAL generalization tests. This disruption did not occur, however, in rats administered the combination of (+/-)-MDMA and FLX injections. Subsequent training reestablished discriminative stimulus control by S(+)-MDMA in the (+/-)-MDMA + SAL-treated rats. Postmortem neurochemical assays indicated that 5-HT levels were significantly reduced in the prefrontal cortices of rats given (+/-)-MDMA + SAL, compared to both drug-naive control rats and (+/-)-MDMA + FLX-treated rats. 5-HIAA levels were significantly lower in the prefrontal cortices of both (+/-)-MDMA + SAL-treated rats and (+/-)-MDMA + FLX-treated rats, relative to control. These results support previous findings that fluoxetine protects against (+/-)-MDMA-induced 5-HT depletion. Moreover, this study demonstrated that drug discrimination is a sensitive assay in which to examine behavioral correlates of (+/-)-MDMA- induced serotonergic deficits, and the protection against these deficits by fluoxetine

MH  - Animal

MH  - Brain Chemistry

MH  - drug effects

MH  - Discrimination (Psychology)

MH  - Dose-Response Relationship,Drug

MH  - Fluoxetine

MH  - therapeutic use

MH  - Generalization,Stimulus

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - administration & dosage

MH  - pharmacology

MH  - toxicity

MH  - Nervous System Diseases

MH  - chemically induced

MH  - pathology

MH  - prevention & control

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - metabolism

MH  - Serotonin Agents

MH  - Serotonin Uptake Inhibitors

RP  - NOT IN FILE

NT  - UI - 20241744LA - EngRN - 0 (Serotonin Agents)RN - 0 (Serotonin Uptake Inhibitors)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54910-89-3 (Fluoxetine)PT - JOURNAL ARTICLEDA - 20000518IS - 0955-8810SB - MCY - ENGLANDJC - CM8AA - AuthorEM - 200007

UR  - PM:0010780832

SO  - Behav Pharmacol 1999 Mar ;10(2):195-204

 

56

UI  - 42

AU  - Vollenweider FX

AU  - Remensberger S

AU  - Hell D

AU  - Geyer MA

AD  - Psychiatric University Hospital Zurich, Research Department, Switzerland. vollen@bli.unizh.ch

TI  - Opposite effects of 3,4-methylenedioxymethamphetamine (MDMA) on sensorimotor gating in rats versus healthy humans

AB  - RATIONALE: Prepulse inhibition of acoustic startle refers to the reduction in the startle response when the startling stimulus is preceded by a weak prepulse stimulus. This phenomenon provides an operational measure of sensorimotor gating that has been found to be reduced in patients with schizophrenia and rats treated with serotonin agonists or serotonin releasers. OBJECTIVE: In this study, we compared the effects of a serotonin releaser, MDMA, on prepulse inhibition in laboratory rats and healthy human volunteers. In particular, we investigated whether MDMA disrupts PPI in humans as observed in animal studies. METHODS: Rats were tested after placebo and MDMA in a counterbalanced order at an interval of 1 week, with separate groups of rats being used for each dose of MDMA (1.7, 5.4 and 17.0 mg/kg). On each test day, rats were first tested after no injections and retested 2 h later, 10 min after a subcutaneous injection of placebo or MDMA. For the human study, a placebo-controlled within-subject design and double-blind procedures were used. Subjects were examined twice at a 2 to 4 week interval after either placebo or drug administration (order being counterbalanced). On each test day, subjects underwent baseline testing including psychological and PPI measures. Ninety minutes later, subjects received placebo or MDMA (1.7 mg/kg PO) and were retested after 75 min during the peak of behavioral effects of MDMA. RESULTS: As expected, MDMA decreased prepulse inhibition in a dose-related fashion in rats. In contrast, a typical recreational dose of MDMA (1.7 mg/kg, orally) increased prepulse inhibition in subjects experiencing robust psychological effects. CONCLUSIONS: This surprising disparity between the effects of the drug in rats and humans may reflect a species- specific difference in the mechanism of action of MDMA or in the behavioral expression of a similar pharmacological effect, or both

MH  - Acoustic Stimulation

MH  - Adult

MH  - Affect

MH  - drug effects

MH  - Analysis of Variance

MH  - Animal

MH  - Comparative Study

MH  - Dose-Response Relationship,Drug

MH  - Double-Blind Method

MH  - Habituation (Psychophysiology)

MH  - Human

MH  - Middle Age

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - administration & dosage

MH  - pharmacology

MH  - Psychometrics

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin Agents

MH  - Startle Reaction

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 99293973LA - EngRN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - CLINICAL TRIALPT - CONTROLLED CLINICAL TRIALPT - JOURNAL ARTICLEID - DA02925/DA/NIDAID - MH01228/MH/NIMHDA - 19990805IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199910

UR  - PM:0010367553

SO  - Psychopharmacology (Berl) 1999 Apr ;143(4):365-372

 

57

UI  - 33

AU  - Vollenweider FX

AU  - Gamma A

AU  - Liechti M

AU  - Huber T

TI  - Is a single dose of MDMA harmless? [letter]

MH  - Animal

MH  - Clinical Trials

MH  - standards

MH  - Ethics,Medical

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Hydroxyindoleacetic Acid

MH  - metabolism

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Nerve Degeneration

MH  - chemically induced

MH  - Serotonin

RP  - NOT IN FILE

NT  - UI - 99411458LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - LETTERDA - 19991008IS - 0893-133XSB - MCY - UNITED STATESJC - ADQEM - 199912

UR  - PM:0010481844

SO  - Neuropsychopharmacology 1999 Oct ;21(4):598-600

 

58

UI  - 26

AU  - Walker TM

AU  - Davenport-Jones JE

AU  - Fox RM

AU  - Atterwill CK

AD  - Department of Strategic Toxicological Sciences, GlaxoWellcome, Ware, Herts, UK

TI  - The neurotoxic effects of methylenedioxymethamphetamine (MDMA) and its metabolites on rat brain spheroids in culture

AB  - Rat whole-brain spheroids were used to assess the intrinsic neurotoxicity of methylenedioxy-methamphetamine (MDMA, Ecstasy) and two of its metabolites, dihydroxymethamphetamine (DHMA) and 6-hydroxy-MDMA (6-OH MDMA). Exposure of brain spheroids to MDMA or the metabolite 6-OH MDMA (up to 500 micromol/L) for 5 days in culture did not alter intracellular levels of glutathione (GSH), glial fibrillary acidic protein (GFAP) or serotonin (5-HT). In contrast, exposure to the metabolite DHMA, which can deplete intracellular thiols, significantly increased GSH levels (up to 170% of control) following exposure to 50 and 100 micromol/L DHMA. There was also a significant reduction in the levels of glial fibrillary acidic protein (GFAP) and GSH by DHMA at the highest concentration tested (500 micromol/L) but there was no effect on 5HT. This may constitute a sublethal neurotoxic compensatory response to DHMA in an attempt to replenish depleted intraneural GSH levels following metabolite exposure. Rat whole-brain spheroids may thus be a useful in vitro model to delineate mechanisms and effects of this class of neurotoxin

MH  - Animal

MH  - Biological Markers

MH  - Brain

MH  - cytology

MH  - drug effects

MH  - enzymology

MH  - metabolism

MH  - Brain Diseases

MH  - chemically induced

MH  - Cytosol

MH  - Deoxyepinephrine

MH  - analogs & derivatives

MH  - toxicity

MH  - Dose-Response Relationship,Drug

MH  - Fetus

MH  - Glial Fibrillary Acidic Protein

MH  - Glutathione

MH  - Lactate Dehydrogenase

MH  - secretion

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Serotonin

MH  - Serotonin Agents

MH  - Spheroids

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 20046491LA - EngRN - EC 1.1.1.27 (Lactate Dehydrogenase)RN - 0 (Biological Markers)RN - 0 (Glial Fibrillary Acidic Protein)RN - 0 (Serotonin Agents)RN - 136706-34-8 (6-hydroxy-N-methyl-3,4-methylenedioxyamphetamine)RN - 15398-87-5 (alpha-methylepinine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 501-15-5 (Deoxyepinephrine)RN - 70-18-8 (Glutathione)PT - JOURNAL ARTICLEDA - 19991229IS - 0742-2091SB - MCY - NETHERLANDSJC - CBTAA - AuthorEM - 200003

UR  - PM:0010580546

SO  - Cell Biol Toxicol 1999 Jun ;15(3):137-142

 

59

UI  - 53

AU  - Walubo A

AU  - Seger D

AD  - Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA

TI  - Fatal multi-organ failure after suicidal overdose with MDMA, 'ecstasy': case report and review of the literature

AB  - A 53-year-old prisoner died of multiorgan failure after a suicidal overdose with 3,4-methylenedeoxymethamphetamine (MDMA, 'Ecstasy'). Twelve hours after ingestion of MDMA, the patient became severely hyperthermic (107.2 degrees F) with evidence of rhabdomyolysis. He subsequently developed acute respiratory distress syndrome (ARDS), disseminated intravascular coagulopathy (DIC) and acute renal failure. At autopsy, plasma concentration of MDMA was 3.05 mg/L. This case shows that MDMA is still abused in our community and clinicians should know the symptoms of MDMA intoxication. In particular, MDMA should be considered when patients have symptoms or signs of increased sympathetic activity. The pathophysiology and treatment of MDMA-induced hyperthermia are discussed

MH  - Case Report

MH  - Disseminated Intravascular Coagulation

MH  - chemically induced

MH  - Fatal Outcome

MH  - Fever

MH  - Human

MH  - Kidney Failure

MH  - Male

MH  - Middle Age

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - blood

MH  - poisoning

MH  - Respiratory Distress Syndrome,Adult

MH  - Rhabdomyolysis

MH  - Suicide

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 99199798LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19990621IS - 0960-3271SB - MCY - ENGLANDJC - AQLAA - AuthorEM - 199908

UR  - PM:0010100025

SO  - Hum Exp Toxicol 1999 Feb ;18(2):119-125

 

60

UI  - 50

AU  - Zahn KA

AU  - Li RL

AU  - Purssell RA

AD  - Division of Emergency Medicine, University of British Columbia, Vancouver, Canada

TI  - Cardiovascular toxicity after ingestion of "herbal ecstacy" [see comments]

AB  - "Herbal Ecstacy" (sic) is an alternative drug of abuse usually containing both ephedrine and caffeine. Our literature search did not reveal any other reported cases of cardiovascular toxicity related to herbal "drugs of abuse." A case of cardiovascular toxicity following the ingestion of herbal ecstacy is presented. A 21-year-old male presented to the emergency department with an initial blood pressure of 220/110 mmHg and ventricular dysrhythmias after ingesting four capsules of herbal ecstacy. He was treated with lidocaine and sodium nitroprusside, and his symptoms resolved in 9 h. The pathophysiology and clinical course of ephedrine toxicity are discussed. Emergency physicians should consider ephedrine preparations in the differential diagnosis of patients presenting with a sympathomimetic toxidrome. Drugs of abuse containing "herbal" products can produce serious morbidity and mortality

MH  - Adult

MH  - Arrhythmia

MH  - chemically induced

MH  - Blood Pressure

MH  - drug effects

MH  - Cardiovascular System

MH  - Case Report

MH  - Central Nervous System Stimulants

MH  - adverse effects

MH  - Emergencies

MH  - Ephedrine

MH  - Human

MH  - Hypertension

MH  - Male

MH  - Street Drugs

MH  - Substance-Related Disorders

RP  - NOT IN FILE

NT  - UI - 99209864LA - EngRN - 0 (Central Nervous System Stimulants)RN - 0 (Street Drugs)RN - 299-42-3 (Ephedrine)PT - JOURNAL ARTICLEDA - 19990520IS - 0736-4679SB - MCY - UNITED STATESJC - IBOAA - AuthorEM - 199907RO - M:LC1

UR  - PM:0010195489

SO  - J Emerg Med 1999 Mar ;17(2):289-291

 

61

UI  - 78

AU  - Aguirre N

AU  - Ballaz S

AU  - Lasheras B

AU  - Del Rio J

AD  - Department of Pharmacology, University of Navarra Medical School, Pamplona, Spain

TI  - MDMA ('Ecstasy') enhances 5-HT1A receptor density and 8-OH-DPAT-induced hypothermia: blockade by drugs preventing 5-hydroxytryptamine depletion

AB  - One week after a single administration of 3,4- methylenedioxymethamphetamine (MDMA HCI, 30 mg/kg i.p.), 5-HT1A receptor density was significantly increased by approximately 25-30% in the frontal cortex and hypothalamus of rats. The increased density correlated with the potentiation of the hypothermic response to the 5- HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH- DPAT, 1 mg/kg s.c.). Hypothalamic 5-HT7 receptors, which also bind 8-OH- DPAT, were not changed, however, by MDMA. Fluoxetine (5 mg/kg s.c.), ketanserin (5 mg/kg s.c.) or haloperidol (2 mg/kg i.p.), given 15 min prior to MDMA, prevented the depletion of 5-hydroxytryptamine (5-HT) induced by MDMA and also blocked the effects of this neurotoxin on 5- HT1A receptor density and on 8-OH-DPAT-induced hypothermia. The protection afforded by drugs against 5-HT loss did not correlate, however, with the antagonism of the acute hyperthermic effect of MDMA. The present results indicate that drugs able to prevent or to attenuate MDMA-induced 5-HT loss also prevent the changes in 5-HT1A receptor density as well as the enhanced hypothermic response to the 5-HT1A receptor agonist 8-OH-DPAT in MDMA-treated rats

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - Hydroxyindoleacetic Acid

MH  - metabolism

MH  - Hypothalamus

MH  - Hypothermia

MH  - chemically induced

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - antagonists & inhibitors

MH  - pharmacology

MH  - Prefrontal Cortex

MH  - Rats

MH  - Rats,Wistar

MH  - Receptors,Serotonin

MH  - Serotonin Agents

MH  - Serotonin Agonists

MH  - Serotonin Uptake Inhibitors

MH  - Support,Non-U.S.Gov't

MH  - 8-Hydroxy-2-(di-n-propylamino)tetralin

RP  - NOT IN FILE

NT  - UI - 98314466LA - EngRN - 0 (Receptors, Serotonin)RN - 0 (Serotonin Agents)RN - 0 (Serotonin Agonists)RN - 0 (Serotonin Uptake Inhibitors)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 78950-78-4 (8-Hydroxy-2-(di-n-propylamino)tetralin)PT - JOURNAL ARTICLEDA - 19980916IS - 0014-2999SB - MCY - NETHERLANDSJC - EN6AA - AuthorEM - 199811

UR  - PM:0009652358

SO  - Eur J Pharmacol 1998 Apr 10 ;346(2-3):181-188

 

62

UI  - 66

AU  - Bango J

AU  - Fadon P

AU  - Mata F

AU  - Rubio G

AU  - Santo-Domingo J

AD  - Servicio de Psiquiatria, Hospital Universitario La Paz, Madrid

TI  - [Psychiatric disorders and consumption of ecstasy drug (MDMA): review of published case reports]

AB  - BACKGROUND: Ecstasy use have raised in recent years and it have been related to psychopathological symptoms. The comsumption pattern associated with psychiatric complications is unknown. METHOD: Thirty- six case reports about psychiatric complications due to ecstasy and published from 1985 to 1997 were studied. RESULTS: The disorders with higher prevalence were psychosis (n = 21), panic attacks (n = 12) and depressive symptoms (n = 3). Seventy two per cent were substance abusers. Urinary drugs screening were present in 28%, only in two subjects might detect amphetamine. Men had higher MDMA doses compsumption and higher prevalence of background psychiatric disorders than women. Subjects with psychotic symptomatology had more psychiatric background, higher doses of MDMA comsumption and for a long time than individuals with depressive or panic attacks symptomatology. CONCLUSIONS: The review of the case reports of psychiatric complications related to ecstasy use do not allow to conclude that ecstasy use was the main responsible factor for psychiatric symptoms. They could be related to an individual vulnerability and or to lasting of comsumption

MH  - Adolescence

MH  - Adult

MH  - English Abstract

MH  - Female

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Male

MH  - Mental Disorders

MH  - chemically induced

MH  - psychology

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Retrospective Studies

MH  - Substance-Related Disorders

RP  - NOT IN FILE

NT  - UI - 99024992LA - SpaRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW LITERATUREDA - 19990225IS - 0300-5062CY - SPAINJC - 2AMAA - AuthorEM - 199904

UR  - PM:0009807860

SO  - Actas Luso Esp Neurol Psiquiatr Cienc Afines 1998 Jul ;26(4):260-263

 

63

UI  - 96

AU  - Bilsky EJ

AU  - Montegut MJ

AU  - Nichols ML

AU  - Reid LD

AD  - Department of Biological Sciences, University of Northern Colorado, Greeley 80639, USA. ejbilsk@bentley.univnorthco.edu

TI  - CGS 10746B, a novel dopamine release inhibitor, blocks the establishment of cocaine and MDMA conditioned place preferences

AB  - Cocaine and methylenedioxymethamphetamine (MDMA), two drugs self- administered by humans and laboratory animals, have previously been shown to produce conditioned place preferences (CPPs) among rats, an index of drug-reward relevant events. Both of these agents increase functional levels of dopamine that may be critical to their rewarding properties. Here, the effects of doses of CGS 10746B, an agent reported to attenuate the release of dopamine without occupying dopamine receptors, are assessed on cocaine and MDMA's ability to produce a CPP. CGS 10746B dose dependently blocked the establishment of a MDMA CPP. A 30 mg/kg dose of CGS 10746B, which completely blocked the MDMA CPP, also blocked the establishment of a cocaine CPP. Release of dopamine appears critical to the ability of these agents to establish a CPP

MH  - Analysis of Variance

MH  - Animal

MH  - Choice Behavior

MH  - drug effects

MH  - Cocaine

MH  - antagonists & inhibitors

MH  - Conditioning,Operant

MH  - Cues

MH  - Dopamine

MH  - metabolism

MH  - Dopamine Agents

MH  - pharmacology

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Support,U.S.Gov't,P.H.S.

MH  - Thiazepines

RP  - NOT IN FILE

NT  - UI - 98103795LA - EngRN - 0 (Dopamine Agents)RN - 0 (Thiazepines)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-36-2 (Cocaine)RN - 51-61-6 (Dopamine)RN - 81382-52-7 (CGS 10746B)PT - JOURNAL ARTICLEID - DA 04440/DA/NIDAID - DA 08937/DA/NIDADA - 19980309IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199805

UR  - PM:0009443558

SO  - Pharmacol Biochem Behav 1998 Jan ;59(1):215-220

 

64

UI  - 62

AU  - Bolla KI

AU  - McCann UD

AU  - Ricaurte GA

AD  - Department of Neurology, Johns Hopkins Medical Institutions, Baltimore, MD, USA

TI  - Memory impairment in abstinent MDMA ("Ecstasy") users [see comments]

AB  - BACKGROUND: Methylenedioxymethamphetamine (MDMA, or "Ecstasy") is a popular recreational drug of abuse that is known to damage brain serotonergic neurons in animals and possibly humans. Few functional consequences of MDMA-induced serotonin (5-HT) neurotoxicity have been identified, either in animals or humans. This study sought to determine whether individuals with a history of extensive MDMA use showed evidence of memory impairment, because brain serotonin has been implicated in mnemonic function. METHOD: The authors compared 24 abstinent MDMA users and 24 control subjects on several standardized tests of memory, after matching subjects for age, gender, educational level, and vocabulary score (a surrogate of verbal intelligence). The authors also explored correlations between changes in memory function and decrements in CSF 5-hydroxyindoleacetic acid (5-HIAA), which serves as a marker of central 5-HT neural function. RESULTS: Greater use of MDMA (total milligrams per month) was associated with greater impairment in immediate verbal memory (p < 0.02) and delayed visual memory (p < 0.06). Furthermore, lower vocabulary scores were associated with stronger dose-related effects, with men having greater dose- related deficits than women. Lastly, lower concentrations of CSF 5-HIAA were associated with poorer memory performance. CONCLUSION: Abstinent MDMA users have impairment in verbal and visual memory. The extent of memory impairment correlates with the degree of MDMA exposure and the reduction in brain 5-HT, as indexed by CSF 5-HIAA

MH  - Adult

MH  - Female

MH  - Human

MH  - Hydroxyindoleacetic Acid

MH  - cerebrospinal fluid

MH  - Male

MH  - Memory

MH  - drug effects

MH  - Middle Age

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - administration & dosage

MH  - toxicity

MH  - Pattern Recognition,Visual

MH  - Regression Analysis

MH  - Serotonin

MH  - Serotonin Agents

MH  - Street Drugs

MH  - Support,U.S.Gov't,P.H.S.

MH  - Verbal Learning

RP  - NOT IN FILE

NT  - UI - 99071140LA - EngRN - 0 (Serotonin Agents)RN - 0 (Street Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - JOURNAL ARTICLEID - R01 DA06275/DA/NIDAID - DA05707/DA/NIDAID - DA05938/DA/NIDAID - +DA - 19981230IS - 0028-3878SB - ASB - MCY - UNITED STATESJC - NZ0AA - AuthorEM - 199903

UR  - PM:0009855498

SO  - Neurology 1998 Dec ;51(6):1532-1537

 

65

UI  - 84

AU  - Brody S

AU  - Krause C

AU  - Veit R

AU  - Rau H

AD  - Institute of Medical Psychology and Behavioral Neurobiology, Eberhard- Karls University of Tubingen, Germany. stuart.brody@uni-tuebingen.de

TI  - Cardiovascular autonomic dysregulation in users of MDMA ("Ecstasy")

AB  - The present study examined resting heart rate variability (HRV; an index of parasympathetic tone) and heart rate response to the Valsalva maneuver (Valsalva ratio; an index of overall autonomic responsiveness) in 12 repeat users of 3.4-methylenedioxymethamphetamine (MDMA, "Ecstasy"), and a matched comparison group of presumed nonusers. HRV and Valsalva ratio were smaller in users than in controls. Three out of 12 MDMA users but no controls had Valsalva ratios below 1.50, the cut- off for autonomic dysfunction. In several users, there was a total absence of post-Valsalva release bradycardia. All MDMA users were polydrug users. Parasympathetic cardiovascular tone appears impaired in repeat MDMA users, although the ubiquitous problems in such epidemiologic designs (including lack of testing before the first use of the drug and confounding with use of other drugs) preclude definitive causal interpretations

MH  - Adolescence

MH  - Adult

MH  - Autonomic Nervous System

MH  - drug effects

MH  - Blood Pressure

MH  - Comparative Study

MH  - Female

MH  - Hallucinogens

MH  - adverse effects

MH  - Heart Rate

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 98261212LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19980807IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199810

UR  - PM:0009600585

SO  - Psychopharmacology (Berl) 1998 Apr ;136(4):390-393

 

66

UI  - 79

AU  - Colado MI

AU  - Granados R

AU  - O'Shea E

AU  - Esteban B

AU  - Green AR

AD  - Departamento de Farmacologia, Facultad de Medicina, Universidad Complutense, Madrid, Spain

TI  - Role of hyperthermia in the protective action of clomethiazole against MDMA ('ecstasy')-induced neurodegeneration, comparison with the novel NMDA channel blocker AR-R15896AR

AB  - 1. The immediate effect of administration of 3,4- methylenedioxymethamphetamine (MDMA or 'ecstasy') on rectal temperature and the effect of putative neuroprotective agents on this change has been examined in rats. The influence of the temperature changes on the long term MDMA-induced neurodegeneration of cerebral 5- hydroxytryptamine (5-HT) nerve terminals was also examined. 2. The novel low affinity N-methyl-D-aspartate (NMDA) receptor channel blocker AR-R15896AR (20 mg kg(-1), i.p.) given 5 min before and 55 min after MDMA (15 mg kg(-1), i.p.) did not prevent the MDMA-induced hyperthermia and did not alter either the MDMA-induced neurodegenerative loss of 5- HT and 5-hydroxyindoleacetic acid (5-HIAA) in cortex, striatum and hippocampus or loss of [3H]-paroxetine binding in cortex 7 days later. 3. The neuroprotective agent clomethiazole (50 mg kg(-1), i.p.) given 5 min before and 55 min after MDMA (15 mg kg(-1)) abolished the MDMA- induced hyperthermic response and markedly attenuated the loss of 5-HT, 5-HIAA and [3H]-paroxetine binding in the brain regions examined 7 days later. 4. When rats treated with MDMA plus clomethiazole were kept at high ambient temperature for 5 h post-MDMA, thereby keeping their body temperature elevated to near that seen in rats given MDMA alone, the MDMA-induced loss of 5-HT, 5-HIAA and [3H]-paroxetine was still attenuated. However, the protection (39%) afforded by the clomethiazole administration was less than seen in rats kept at normal ambient temperature (75%). 5. These data support the proposals of others that NMDA receptor antagonists are neuroprotective against MDMA-induced degeneration only if they induce hypothermia and further suggest that increased glutamate activity may not be involved in the neurotoxic action of MDMA. 6. These data further demonstrate that a proportion of the neuroprotective action of clomethiazole is due to an effect on body temperature but that, in addition, the compound protects against MDMA- induced damage by an unrelated mechanism

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - physiology

MH  - Brain Chemistry

MH  - Chlormethiazole

MH  - pharmacology

MH  - Comparative Study

MH  - Excitatory Amino Acid Antagonists

MH  - Fever

MH  - physiopathology

MH  - Hydroxyindoleacetic Acid

MH  - metabolism

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - antagonists & inhibitors

MH  - toxicity

MH  - Nerve Degeneration

MH  - chemically induced

MH  - prevention & control

MH  - Neuroprotective Agents

MH  - Paroxetine

MH  - pharmacokinetics

MH  - Pyridines

MH  - Rats

MH  - Receptors,N-Methyl-D-Aspartate

MH  - Serotonin

MH  - Serotonin Uptake Inhibitors

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 98309686LA - EngRN - 0 (Excitatory Amino Acid Antagonists)RN - 0 (FPL 15896AR)RN - 0 (Neuroprotective Agents)RN - 0 (Pyridines)RN - 0 (Receptors, N-Methyl-D-Aspartate)RN - 0 (Serotonin Uptake Inhibitors)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 533-45-9 (Chlormethiazole)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 61869-08-7 (Paroxetine)PT - JOURNAL ARTICLEDA - 19980916IS - 0007-1188SB - MCY - ENGLANDJC - B00AA - AuthorEM - 199811

UR  - PM:0009647471

SO  - Br J Pharmacol 1998 Jun ;124(3):479-484

 

67

UI  - 92

AU  - Connor TJ

AU  - McNamara MG

AU  - Finn D

AU  - Currid A

AU  - O'Malley M

AU  - Redmond AM

AU  - Kelly JP

AU  - Leonard BE

AD  - Department of Pharmacology, University College Galway, Ireland

TI  - Acute 3,4-methylenedioxymethamphetamine(MDMA) administration produces a rapid and sustained suppression of immune function in the rat

AB  - (+)-3,4-Methylenedioxymethamphetamine (MDMA;'Ecstasy') is a ring substituted phenylisopropylamine that is structurally related to both amphetamines and hallucinogens. The unique behavioural activating properties of MDMA have led to its widespread abuse. MDMA induces many neurochemical, behavioural and endocrine alterations which closely resemble those elicited by exposure to acute stress, suggesting that MDMA could be regarded as a 'chemical stressor'. In addition to the neurochemical, behavioural and endocrine effects of stressor exposure, it has been reported that stress produces alterations in immune function. However, to date the effects of MDMA on immune function have been restricted to in vitro investigations. In this study we report, for the first time, that acute in vivo administration of MDMA (20 mg/kg, i.p.) produced a rapid (within 30 min) suppression of Con A- induced lymphocyte proliferation and a profound reduction in the total leucocyte count in rats that persisted for at least 6 h following injection. These alterations in immune function were accompanied by a significant increase in plasma corticosterone concentrations 30 min post MDMA administration which had returned to baseline values within 6 h of drug administration. In addition, there was a significant depletion in cortical 5-HT concentrations both 30 min and 6 h after MDMA administration. The results of this study provide evidence that in addition to the well established toxic effects of MDMA on the central serotonergic system, a single administration of this widely abused drug induces a rapid and sustained suppression of immune function

MH  - Animal

MH  - Cerebral Cortex

MH  - drug effects

MH  - metabolism

MH  - Concanavalin A

MH  - Corticosterone

MH  - blood

MH  - Female

MH  - Hallucinogens

MH  - administration & dosage

MH  - toxicity

MH  - Hydroxyindoleacetic Acid

MH  - analysis

MH  - Immunity,Cellular

MH  - Leukocyte Count

MH  - Lymphocyte Transformation

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Serotonin Agents

MH  - T-Lymphocytes

MH  - immunology

MH  - Time Factors

RP  - NOT IN FILE

NT  - UI - 98165670LA - EngRN - 0 (Hallucinogens)RN - 0 (Serotonin Agents)RN - 11028-71-0 (Concanavalin A)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-22-6 (Corticosterone)RN - 50-67-9 (Serotonin)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - JOURNAL ARTICLEDA - 19980511IS - 0162-3109SB - MCY - NETHERLANDSJC - GY3AA - AuthorEM - 199807

UR  - PM:0009506825

SO  - Immunopharmacology 1998 Jan ;38(3):253-260

 

68

UI  - 76

AU  - Dafters RI

AU  - Lynch E

AD  - Psychology Department, Glasgow University, UK

TI  - Persistent loss of thermoregulation in the rat induced by 3,4- methylenedioxymethamphetamine (MDMA or "Ecstasy") but not by fenfluramine

AB  - Using radio-biotelemetry, the timecourse of recovery and sensitivity to ambient temperature (Ta) of the thermogenic response of methylenedioxymethamphetamine (MDMA or "Ecstasy") was examined. Ambient temperatures of 17 and 22 degrees C produced very different response profiles, with the lower temperature producing a hypothermic response to 10 and 15 mg/kg doses of MDMA, and the higher temperature producing a profound hyperthermia to the same doses. Although the peak responses to the drug had subsided within 5 h of administration, residual effects, in the form of an elevation of body temperature during the "low" phase of the diurnal cycle, were present for a further 48 h. Long- lasting disruption of the thermoregulatory system following a short series of MDMA administrations (10 mg/kg once per day for 4 days) was shown by exposing the rats in the undrugged state to a thermoregulatory challenge, consisting of 60-min exposure to a Ta of 30 degrees C, at 1 week before, and at 4 weeks and 14 weeks after the drug administration. MDMA-treated rats showed a prolonged hyperthermic response to the challenge at both post-drug intervals compared with fenfluramine- treated rats and saline-treated controls. Thus, the results indicate both that MDMA's thermogenic effects are more sensitive to Ta than previously demonstrated, and that the serotonergic neurotoxicity of the drug may produce long-lasting changes in thermoregulatory mechanisms

MH  - Amphetamine

MH  - pharmacology

MH  - Animal

MH  - Body Temperature Regulation

MH  - drug effects

MH  - Dopamine Agents

MH  - Female

MH  - Fenfluramine

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Rats,Wistar

MH  - Serotonin Agents

RP  - NOT IN FILE

NT  - UI - 98382417LA - EngRN - 0 (Dopamine Agents)RN - 0 (Serotonin Agents)RN - 300-62-9 (Amphetamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 458-24-2 (Fenfluramine)PT - JOURNAL ARTICLEDA - 19981026IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199901

UR  - PM:0009718291

SO  - Psychopharmacology (Berl) 1998 Jul ;138(2):207-212

 

69

UI  - 77

AU  - Frederick DL

AU  - Ali SF

AU  - Gillam MP

AU  - Gossett J

AU  - Slikker W

AU  - Paule MG

AD  - Division of Neurotoxicology, National Center for Toxicological Research, Jefferson Arkansas 72079, USA. df50029@GlaxoWellcome.com

TI  - Acute effects of dexfenfluramine (d-FEN) and methylenedioxymethamphetamine (MDMA) before and after short-course, high-dose treatment

AB  - The acute behavioral effects of methylenedioxymethamphetamine (MDMA) and dexfenfluramine (d-FEN) were assessed in six rhesus monkeys using performance in the National Center for Toxicological Research (NCTR) Operant Test Battery (OTB); three additional animals served as controls for neurochemical endpoints. The OTB consists of five food-reinforced tasks designed to model aspects of learning, short-term memory and attention, time estimation, motivation, and color and position discrimination. Shortly after the acute effects of each drug were determined, three of the monkeys received a short-course, high-dose exposure (2x /day x 4 days, intramuscular (i.m.) injections) of MDMA (10 mg/kg), while three monkeys were exposed to an identical regimen of d-FEN (5 mg/kg). Approximately one month later, the acute effects of each drug were again determined. In monkeys exposed to high-dose d-FEN, the sensitivities of the OTB tasks to acute disruption by either MDMA or d-FEN were essentially unchanged. Conversely, monkeys treated with high-dose MDMA were less sensitive to the acute behavioral effects of both drugs, although such an effect was seen more frequently for d-FEN and was OTB task specific. Thus a residual behavioral tolerance to the acute behavioral effects of MDMA and d-FEN was noted after high-dose MDMA exposure, but not after high-dose d-FEN exposure. These findings are surprising, as similar neurochemical effects (i.e., significant decreases of ca. 50% in serotonin in frontal cortex and hippocampus) were observed in all monkeys approximately six months after short- course, high-dose MDMA or d-FEN treatment

MH  - Animal

MH  - Behavior,Animal

MH  - drug effects

MH  - Brain

MH  - metabolism

MH  - Dose-Response Relationship,Drug

MH  - Drug Administration Schedule

MH  - Drug Tolerance

MH  - Fenfluramine

MH  - administration & dosage

MH  - pharmacology

MH  - Macaca mulatta

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Neuropsychological Tests

MH  - Serotonin

MH  - Time Factors

RP  - NOT IN FILE

NT  - UI - 98333273LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 458-24-2 (Fenfluramine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEDA - 19980813IS - 0077-8923SB - MSB - XCY - UNITED STATESJC - 5NMAA - AuthorEM - 199810

UR  - PM:0009668676

SO  - Ann N Y Acad Sci 1998 May 30 ;844():183-190

 

70

UI  - 61

AU  - Greer GR

AU  - Tolbert R

AD  - Heffter Research Institute, Santa Fe, New Mexico, USA

TI  - A method of conducting therapeutic sessions with MDMA

AB  - A method for preparing clients and conducting therapeutic sessions with 3,4-methylenedioxymethamphetamine (MDMA) is described, with emphasis on the need for careful attention to the mental set of therapists and clients and the setting of the session. The therapists' belief was that MDMA inhibited the fear response to a perceived emotional threat, allowing the client to place the emotional sequelae of past experiences into a more realistic perspective in their current emotional lives and relationships. Clients were carefully screened and prepared until they had a clear purpose for the session, including a willingness to experience and to learn from anything that might happen. Sympathomimetic effects of MDMA determined the medical contraindications, and clients with histories of serious functional psychiatric impairments were excluded. Total doses of 75-150 mg, plus 50 mg if requested later, were administered, followed by clients lying down and listening to music with eyeshades and headphones during the peak MDMA effect. Screening and follow-up questionnaires were utilized. Two case histories are presented: a man achieving relief of pain from multiple myeloma, and a woman finding relief from problems as the daughter of Holocaust survivors. Use of consciousness-altering drugs in other contexts is discussed

MH  - Adult

MH  - Aged

MH  - Bone Neoplasms

MH  - complications

MH  - Case Report

MH  - Depressive Disorder

MH  - drug therapy

MH  - psychology

MH  - Female

MH  - Hallucinogens

MH  - therapeutic use

MH  - Human

MH  - Male

MH  - Multiple Myeloma

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Pain,Intractable

MH  - therapy

MH  - Psychotherapy

MH  - methods

RP  - NOT IN FILE

NT  - UI - 99122231LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19990329IS - 0279-1072SB - MCY - UNITED STATESJC - JLPAA - AuthorEM - 199906

UR  - PM:0009924843

SO  - J Psychoactive Drugs 1998 Oct ;30(4):371-379

 

71

UI  - 63

AU  - Henry JA

AU  - Hill IR

TI  - Fatal interaction between ritonavir and MDMA [letter] [see comments]

MH  - Acquired Immunodeficiency Syndrome

MH  - drug therapy

MH  - Adult

MH  - Anti-HIV Agents

MH  - poisoning

MH  - Case Report

MH  - Drug Interactions

MH  - Drug Therapy,Combination

MH  - Fatal Outcome

MH  - Hallucinogens

MH  - Heart Arrest

MH  - chemically induced

MH  - Human

MH  - Liver Diseases,Alcoholic

MH  - complications

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Ritonavir

RP  - NOT IN FILE

NT  - UI - 99063100LA - EngRN - 0 (Anti-HIV Agents)RN - 0 (Hallucinogens)RN - 0 (Ritonavir)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - LETTERDA - 19981222IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199902RO - M:LC1

UR  - PM:0009848354

SO  - Lancet 1998 Nov 28 ;352(9142):1751-1752

 

72

UI  - 80

AU  - Henry JA

AU  - Fallon JK

AU  - Kicman AT

AU  - Hutt AJ

AU  - Cowan DA

AU  - Forsling M

TI  - Low-dose MDMA ("ecstasy") induces vasopressin secretion [letter]

MH  - Adult

MH  - Argipressin

MH  - blood

MH  - secretion

MH  - Comparative Study

MH  - Hallucinogens

MH  - pharmacology

MH  - Human

MH  - Hyponatremia

MH  - chemically induced

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 98297877LA - EngRN - 0 (Hallucinogens)RN - 113-79-1 (Argipressin)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - CLINICAL TRIALPT - CONTROLLED CLINICAL TRIALPT - LETTERDA - 19980710IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199809

UR  - PM:0009635954

SO  - Lancet 1998 Jun 13 ;351(9118):1784

 

73

UI  - 89

AU  - Kalivas PW

AU  - Duffy P

AU  - White SR

AD  - Alcohol and Drug Abuse Program, Washington State University, Pullman 99164-6520, USA

TI  - MDMA elicits behavioral and neurochemical sensitization in rats

AB  - Rats were treated with repeated injections of saline or one of two doses of (+/-)3,4-methylenedioxymethamphetamine (MDMA; 5 or 20 mg/kg, s.c.). Rats pretreated with either of the two repeated MDMA treatment regimens demonstrated an augmented increase in motor activity to an injection of MDMA made 12 days after the last repeated injection compared with either the first MDMA injection or MDMA given to animals pretreated with repeated saline. Furthermore, animals pretreated with the highest dose of repeated MDMA revealed a greater behavioral response to cocaine (15 mg/kg, i.p.). Microdialysis was conducted in the nucleus accumbens and the capacity of MDMA (5 mg/kg, s.c.) to elevate extracellular dopamine content was augmented in rats pretreated with repeated MDMA compared with the animals pretreated with repeated saline. These data reveal repeated MDMA administration produces behavioral sensitization and enhanced dopamine transmission in the nucleus accumbens of rats

MH  - Animal

MH  - Behavior,Animal

MH  - drug effects

MH  - Biogenic Monoamines

MH  - metabolism

MH  - Brain Chemistry

MH  - Chromatography,High Pressure Liquid

MH  - Cocaine

MH  - pharmacology

MH  - Dopamine

MH  - Dopamine Uptake Inhibitors

MH  - Electrochemistry

MH  - Hallucinogens

MH  - Male

MH  - Microdialysis

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Nucleus Accumbens

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Support,U.S.Gov't,P.H.S.

MH  - Time Factors

RP  - NOT IN FILE

NT  - UI - 98233146LA - EngRN - 0 (Biogenic Monoamines)RN - 0 (Dopamine Uptake Inhibitors)RN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-36-2 (Cocaine)RN - 51-61-6 (Dopamine)PT - JOURNAL ARTICLEID - DA-08116/DA/NIDAID - DA-03906/DA/NIDAID - MH-40817/MH/NIMHID - +DA - 19980623IS - 0893-133XSB - MCY - UNITED STATESJC - ADQAA - AuthorEM - 199808

UR  - PM:0009571655

SO  - Neuropsychopharmacology 1998 Jun ;18(6):469-479

 

74

UI  - 73

AU  - Kramer HK

AU  - Poblete JC

AU  - Azmitia EC

AD  - Department of Psychiatry, New York University Medical Center, Millhauser Labs, New York 10016, USA

TI  - Characterization of the translocation of protein kinase C (PKC) by 3,4- methylenedioxymethamphetamine (MDMA/ecstasy) in synaptosomes: evidence for a presynaptic localization involving the serotonin transporter (SERT)

AB  - 3, 4-methylenedioxymethamphetamine (MDMA or Ecstasy) is a substituted amphetamine whose acute and long-term effects on the serotonin system are dependent on an interaction with the 5-HT uptake transporter (SERT). Although much of the work dedicated to the study of this compound has focused on its ability to release monoamines, this drug has many important metabolic consequences on neurons and glial cells. The identification of these physiological responses will help to bridge the gap that exists in the information between the acute and neurotoxic effects of amphetamines. Substituted amphetamines have the ability to produce a long-term translocation of protein kinase C (PKC) in vivo, and this action may be crucial to the development of serotonergic neurotoxicity. Our earlier results suggested that PKC activation occurred through pre- and postsynaptic mechanisms. Because the primary site of action of these drugs is the 5-HT transporter, we now expand on our previous results and attempt to characterize MDMA's ability to translocate PKC within cortical 5-HT nerve terminals. In synaptosomes, MDMA produced a concentration-dependent increase in membrane-bound PKC (as measured by 3H-phorbol 12, 13 dibutyrate, 3H-PDBu) bindings sites. This response was abolished by cotreatment with the specific serotonin reuptake inhibitor (SSRI), fluoxetine, but not by the 5-HT2A/2C antagonist, ketanserin. In contrast, full agonists to 5-HT1A and 5-HT2 receptors did not produce significant PKC translocation. MDMA-mediated PKC translocation also requires the presence of extracellular calcium ions. Using assay conditions where extracellular calcium was absent prevented in vitro activation of PKC by MDMA. Prolonged PKC translocation has been hypothesized to contribute to the calcium- dependent neurotoxicity produced by substituted amphetamines. In addition, many physiological processes within 5-HT nerve terminals, including 5-HT reuptake and vesicular serotonin release, are susceptible to modification by PKC-dependent protein phosphorylation. Our results suggest that prolonged activation of PKC within the 5-HT nerve terminal may contribute to lasting changes in the homeostatic function of 5-HT neurons, leading to the degeneration of specific cellular elements after repeated MDMA exposure

MH  - p-Chloroamphetamine

MH  - pharmacology

MH  - Animal

MH  - Calcium

MH  - Cerebral Cortex

MH  - drug effects

MH  - metabolism

MH  - Comparative Study

MH  - Female

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Protein Kinase C

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin Agents

MH  - Synaptosomes

RP  - NOT IN FILE

NT  - UI - 98384702LA - EngRN - EC 2.7.1.- (Protein Kinase C)RN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 64-12-0 (p-Chloroamphetamine)RN - 7440-70-2 (Calcium)PT - JOURNAL ARTICLEDA - 19981125IS - 0893-133XSB - MCY - UNITED STATESJC - ADQAA - AuthorEM - 199901

UR  - PM:0009718590

SO  - Neuropsychopharmacology 1998 Oct ;19(4):265-277

 

75

UI  - 81

AU  - Malberg JE

AU  - Seiden LS

AD  - University of Chicago, Department of Pharmacological and Physiological Sciences, Chicago, Illinois 60637, USA

TI  - Small changes in ambient temperature cause large changes in 3,4- methylenedioxymethamphetamine (MDMA)-induced serotonin neurotoxicity and core body temperature in the rat

AB  - The amphetamine derivative 3,4-methylenedioxymethamphetamine (MDMA) is a drug of abuse and has been shown to be neurotoxic to 5-HT terminals in many species. MDMA-engendered neurotoxicity has been shown to be affected by both ambient temperature and core body temperature. We now report that small (2 degreesC) changes in ambient temperature produce changes in core temperature in MDMA-treated rats, but the same changes in ambient temperature do not affect core temperature of saline-treated animals. Furthermore, increases in core temperature of MDMA-treated animals increase neurotoxicity. Rats were given MDMA (20 or 40 mg/kg) or saline and placed in an ambient temperature of 20, 22, 24, 26, 28, or 30 degreesC using a novel temperature measurement apparatus that controls ambient temperature +/-0.5 degrees C. Two weeks after MDMA treatment, the rats were killed, and regional 5-HT and 5-hydroxyindole acetic acid levels were analyzed as a measure of neurotoxicity. Rats treated with MDMA at 20 and 22 degrees C showed a hypothermic core temperature response. Treatment with MDMA at 28 and 30 degreesC produced a hyperthermic response. At ambient temperatures of 20-24 degrees C, neurotoxicity was not observed in the frontal cortex, somatosensory cortex, hippocampus, or striatum. At ambient temperatures of 26-30 degrees C, neurotoxicity was seen and correlated with core temperature in all regions examined. These data indicate that ambient temperature has a significant affect on MDMA neurotoxicity, core temperature, and thermoregulation in rats. This finding has implications on both the temperature dependence of the mechanism of MDMA neurotoxicity and human use because fatal hyperthermia is associated with MDMA use in humans

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - Body Temperature Regulation

MH  - Brain Chemistry

MH  - Corpus Striatum

MH  - chemistry

MH  - Dopamine

MH  - analysis

MH  - Fever

MH  - metabolism

MH  - mortality

MH  - Frontal Lobe

MH  - Hippocampus

MH  - Homovanillic Acid

MH  - Hydroxyindoleacetic Acid

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - toxicity

MH  - Neurotoxins

MH  - pharmacology

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Serotonin Agents

MH  - Sodium Chloride

MH  - Somatosensory Cortex

MH  - Support,U.S.Gov't,P.H.S.

MH  - Temperature

MH  - 3,4-Dihydroxyphenylacetic Acid

RP  - NOT IN FILE

NT  - UI - 98299899LA - EngRN - 0 (Neurotoxins)RN - 0 (Serotonin Agents)RN - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)RN - 306-08-1 (Homovanillic Acid)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 7647-14-5 (Sodium Chloride)PT - JOURNAL ARTICLEID - DA00085/DA/NIDAID - MH-105-62/MH/NIMHDA - 19980702IS - 0270-6474SB - MCY - UNITED STATESJC - JDFAA - AuthorEM - 199809

UR  - PM:0009634574

SO  - J Neurosci 1998 Jul 1 ;18(13):5086-5094

 

76

UI  - 65

AU  - McCann UD

AU  - Szabo Z

AU  - Scheffel U

AU  - Dannals RF

AU  - Ricaurte GA

AD  - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, Maryland, USA

TI  - Positron emission tomographic evidence of toxic effect of MDMA ("Ecstasy") on brain serotonin neurons in human beings [see comments]

AB  - BACKGROUND: (+/-)3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy") is a popular recreational drug that selectively damages brain serotonin (5- HT) neurons in animals at doses that closely approach those used by humans. We investigated the status of brain 5-HT neurons in MDMA users. METHODS: We enrolled 14 previous users of MDMA who were currently abstaining from use and 15 controls who had never used MDMA. We used positron emission tomography (PET) with the radioligand carbon-11- labelled McN-5652, which selectively labels the 5-HT transporter. We analysed whether there were differences in 5-HT transporter binding between abstinent MDMA users and participants in the control group. Blood and urine samples were taken and tested to check for abstinence. FINDINGS: MDMA users showed decreased global and regional brain 5-HT transporter binding compared with controls. Decreases in 5-HT transporter binding positively correlated with the extent of previous MDMA use. INTERPRETATION: Quantitative PET studies with a ligand selective for 5-HT transporters can be used to assess the status of 5- HT neurons in the living human brain. We show direct evidence of a decrease in a structural component of brain 5-HT neurons in human MDMA users

MH  - Adult

MH  - Brain

MH  - drug effects

MH  - Comparative Study

MH  - Female

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - Neurons

MH  - metabolism

MH  - Serotonin

MH  - Serotonin Agents

MH  - Support,U.S.Gov't,P.H.S.

MH  - Tomography,Emission-Computed

RP  - NOT IN FILE

NT  - UI - 99023143LA - EngRN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - CLINICAL TRIALPT - CONTROLLED CLINICAL TRIALPT - JOURNAL ARTICLEID - DA05938/DA/NIDAID - DA06275/DA/NIDAID - DA10217/DA/NIDAID - +DA - 19981120IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SAA - AuthorEM - 199901RO - M:LC1RO - M:LC2

UR  - PM:0009807990

SO  - Lancet 1998 Oct 31 ;352(9138):1433-1437

 

77

UI  - 74

AU  - Morgan MJ

AD  - Department of Psychology, University of Wales, Swansea, S. Wales, UK

TI  - Recreational use of "ecstasy" (MDMA) is associated with elevated impulsivity

AB  - Recent preclinical evidence suggests that repeated exposure to 3, 4- methylenedioxy-methamphetamine (MDMA; "ecstasy") produces long-term reductions in serotonin (5-HT) levels. 5-HT has been implicated in the regulation of mood, anxiety, aggression, impulsivity, and cognition. Accordingly, in the first of two separate studies, these variables were investigated in three groups: (1) MDMA group--recreational ecstasy users (who also used other illicit substances); (2) polydrug controls-- who had never taken ecstasy, but otherwise had drug histories and personal characteristics similar to the ecstasy users; and (3) nondrug controls--who had never used illicit drugs, but had similar personal characteristics. All participants completed mood (Likert) scales, personality questionnaires (which included the impulsiveness, venturesomeness and empathy questionnaire-IVE), spatial span and "Tower of London" (TOL) tests, and a behavioural measure of impulsivity, the matching familiar figures test (MFF20). There were no group differences in mood, anxiety, anger/hostility, and cognitive performance, but the MDMA group committed significantly more errors in the MFF20. Subsequently, a larger sample of participants were administered mood (the General Health Questionnaire or GHQ) and personality (IVE) questionnaires before the administration of a TOL test, followed by the MFF20, and a second TOL test. Although there were no group differences in TOL performance, ecstasy users were again found to commit more errors in the MFF20 than polydrug users. Furthermore, the GHQ and IVE scores of the ecstasy users in the second study indicated, respectively, that they were more psychologically disturbed and impulsive than nondrug controls. The combined data from the two studies indicated that ecstasy users exhibited elevated impulsivity on both self-report and behavioral measures and that those who had taken the most ecstasy had the most elevated trait impulsiveness scores. These findings are consistent with previous evidence that elevated levels of impulsivity in humans are associated with reduced levels of serotonergic function

MH  - Adult

MH  - Affect

MH  - drug effects

MH  - Cognition

MH  - Comparative Study

MH  - Female

MH  - Hallucinogens

MH  - pharmacology

MH  - Human

MH  - Impulsive Behavior

MH  - chemically induced

MH  - psychology

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Questionnaires

MH  - Substance-Related Disorders

RP  - NOT IN FILE

NT  - UI - 98384701LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - CLINICAL TRIALPT - JOURNAL ARTICLEDA - 19981125IS - 0893-133XSB - MCY - UNITED STATESJC - ADQAA - AuthorEM - 199901

UR  - PM:0009718589

SO  - Neuropsychopharmacology 1998 Oct ;19(4):252-264

 

78

UI  - 90

AU  - Morimoto BH

AU  - Lovell S

AU  - Kahr B

AD  - AMUR Pharmaceuticals, San Carlos, CA 94070, USA. morimoto@amur.com

TI  - Ecstasy: 3,4-methylenedioxymethamphetamine (MDMA)

AB  - The crystal structure of 3,4-methylenedioxymethamphetamine [systematic name: N-methyl-1-[3,4-(methylenedioxy) phenyl]-2-aminopropane] hydrochloride, C11H15NO2.HCl, also known as 'ecstasy' or MDMA, has been determined by X-ray diffraction

MH  - Crystallization

MH  - Crystallography,X-Ray

MH  - Hallucinogens

MH  - chemistry

MH  - Hydrogen Bonding

MH  - Models,Molecular

MH  - Molecular Structure

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 98201023LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19980424IS - 0108-2701SB - MCY - DENMARKJC - AI5AA - AuthorEM - 199807

UR  - PM:0009540200

SO  - Acta Crystallogr C 1998 Feb 15 ;54 ( Pt 2)():229-231

 

79

UI  - 64

AU  - Muck-Seler D

AU  - Takahashi S

AU  - Diksic M

AD  - Cone Laboratory for Neurosurgical Research, Department of Neurology and Neurosurgery, and Montreal Neurological Institute, McGill University, 3801 University St., Montreal, Quebec, Canada

TI  - The effect of MDMA (3,4-methylenedioxymethamphetamine) on the 5-HT synthesis rate in the rat brain: an autoradiographic study

AB  - The effect of MDMA (3,4-methylenedioxymethamphetamine), a psychotropic amphetamine derivative, treatment on the rate of serotonin (5- hydroxytryptamine; 5-HT) synthesis in the rat brain was studied by autoradiography using alpha-[14C]-methyl-l-tryptophan method. Three different treatment protocols were compared to the control (saline) treated rats: (1) rats treated twice with 10 mg/kg every 12 h (20 mg/kg total) and injected tracer for the synthesis measurements 15 h later; (2) rats treated with four injections of 5 mg/kg every 12 h (20 mg/kg total) and injected tracer for the synthesis measurement 17 h after the last dose; and (3) rats given eight injections of 5 mg/kg every 12 h for four days (40 mg/kg) and used in the synthesis study 14 days after the last dose. Results showed a significant decrease in the rate of synthesis in the majority of cerebral structures examined in the 10 mg/kg group. In contrast the group receiving the same total amount (20 mg/kg) of MDMA but over two days (4x5 mg/kg) showed a significant increase in 5-HT synthesis in comparison to controls. The 5-HT synthesis rates measured 14 days after the last dose (four days, 8x5 mg/kg) were significantly reduced. The findings suggest that MDMA can produce either an increase or a decrease in the 5-HT synthesis a short time after a total dose of 20 mg/kg depending on the dose fractionation. However, 14 days after total dose of 40 mg/kg given over four days the synthesis rate was significantly reduced in many brain structures. The latter suggests a possible effect of the MDMA neurotoxicity on the serotonergic neurons, in addition to a possible influence on 5-HT synthesis via a feedback mechanism. Copyright 1998 Elsevier Science B.V

MH  - Algorithms

MH  - Animal

MH  - Autoradiography

MH  - Brain

MH  - anatomy & histology

MH  - Brain Chemistry

MH  - drug effects

MH  - Kinetics

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Rats,Wistar

MH  - Serotonin

MH  - biosynthesis

MH  - Serotonin Agents

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

MH  - Tryptophan

MH  - blood

MH  - metabolism

RP  - NOT IN FILE

NT  - UI - 99032894LA - EngRN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 73-22-3 (Tryptophan)PT - JOURNAL ARTICLEID - RO1-NS-29629/NS/NINDSDA - 19990129IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199904

UR  - PM:0009813249

SO  - Brain Res 1998 Nov 9 ;810(1-2):76-86

 

80

UI  - 70

AU  - O'Shea E

AU  - Granados R

AU  - Esteban B

AU  - Colado MI

AU  - Green AR

AD  - Departamento de farmacologia, Facultad de Medicina, Universidad Complutense, Madrid, Spain

TI  - The relationship between the degree of neurodegeneration of rat brain 5- HT nerve terminals and the dose and frequency of administration of MDMA ('ecstasy')

AB  - The effect of varying the dose and frequency of administration of 3,4- methylenedioxymethamphetamine (MDMA or 'ecstasy') on both the acute hyperthermic response and the long term neurodegeneration of 5- hydroxytryptamine (5-HT) nerve terminals in the brain has been studied in Dark Agouti rats. A single injection (4-15 mg/kg i.p.) of MDMA produced immediate dose-related hyperthermia and a dose-related decrease in 5-HT, 5-hydroxyindoleacetic acid (5-HIAA) and [3H]paroxetine binding in regions of the brain 7 days later, with a dose of 4 mg/kg having no degenerative effect. This dose was also without effect when given once daily for 4 days, but produced a marked loss of [3H]paroxetine binding and indole concentration ( approximately 55%) when given twice daily for 4 days. When a dose of 4 mg/kg was given twice weekly for 8 weeks it had no effect on these serotoninergic markers, despite a clear anorectic effect of the drug being seen. These data demonstrate that MDMA-induced neurodegeneration is related to both the dose and frequency of administration and indicate that damage to 5- HT neurones can occur in the absence of a hyperthermic response to the drug. We suggest that damage occurs when endogenous free radical scavenging mechanisms become overwhelmed or exhausted

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - Brain

MH  - metabolism

MH  - pathology

MH  - Cerebral Cortex

MH  - Corpus Striatum

MH  - Dose-Response Relationship,Drug

MH  - Drug Administration Schedule

MH  - Hippocampus

MH  - Hydroxyindoleacetic Acid

MH  - Injections,Intraperitoneal

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - toxicity

MH  - Nerve Degeneration

MH  - chemically induced

MH  - Nerve Endings

MH  - Paroxetine

MH  - pharmacokinetics

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Serotonin

MH  - Serotonin Agents

MH  - Support,Non-U.S.Gov't

MH  - Tissue Distribution

RP  - NOT IN FILE

NT  - UI - 98447282LA - EngRN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 61869-08-7 (Paroxetine)PT - JOURNAL ARTICLEDA - 19990107IS - 0028-3908SB - MCY - ENGLANDJC - NZBAA - AuthorEM - 199903

UR  - PM:0009776387

SO  - Neuropharmacology 1998 Jul ;37(7):919-926

 

81

UI  - 83

AU  - Obradovic T

AU  - Imel KM

AU  - White SR

AD  - Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman, WA 99164, USA

TI  - Repeated exposure to methylenedioxymethamphetamine (MDMA) alters nucleus accumbens neuronal responses to dopamine and serotonin

AB  - The purpose of this experiment was to investigate the effects of repeated exposure to methylenedioxymethamphetamine (MDMA) on responses of neurons in the nucleus accumbens of anesthetized rats to microiontophoretically-applied dopamine and serotonin. In tests conducted 1-4 days or 9-15 days following the last injection of MDMA (20 mg/kg, s.c., twice daily for 4 days), the inhibitory effects of both dopamine and serotonin on glutamate-evoked firing of nucleus accumbens cells were significantly attenuated compared to effects in control rats that were pretreated with saline injections. The inhibitory effect of the D1 receptor agonist SKF38393 was also significantly attenuated in the MDMA-pretreated rats. In contrast, the amount of inhibition of glutamate-evoked firing produced by application of GABA did not significantly differ between the MDMA-pretreated and the saline-pretreated rats. The neurotoxicity of the MDMA treatment regimen was confirmed by demonstrating that 3H-paroxetine binding was significantly decreased in the medial prefrontal cortex and the nucleus accumbens of the MDMA-pretreated rats. The mechanisms that produce the attenuated inhibitory responses to dopamine and serotonin following repeated injections of MDMA are not known. However, the results of these experiments indicate that repeated MDMA administration induces long-lasting changes in dopaminergic as well as serotonergic neurotransmission in the nucleus accumbens. Copyright 1998 Elsevier Science B.V

MH  - Animal

MH  - Dopamine

MH  - pharmacology

MH  - Drug Administration Schedule

MH  - Evoked Potentials

MH  - drug effects

MH  - Glutamic Acid

MH  - Gaba

MH  - Injections,Subcutaneous

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - administration & dosage

MH  - Neurons

MH  - physiology

MH  - Nucleus Accumbens

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Receptors,Dopamine D1

MH  - agonists

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

MH  - Sk&F-38393

MH  - Time Factors

RP  - NOT IN FILE

NT  - UI - 98195323LA - EngRN - 0 (Receptors, Dopamine D1)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 56-12-2 (GABA)RN - 56-86-0 (Glutamic Acid)RN - 67287-49-4 (SK&F-38393)PT - JOURNAL ARTICLEID - DA08116/DA/NIDADA - 19980529IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199808

UR  - PM:0009526029

SO  - Brain Res 1998 Feb 23 ;785(1):1-9

 

82

UI  - 87

AU  - Parrott AC

AD  - Faculty of Science and Health, Department of Psychology, University of East London, UK. andy2@uel.ac.uk

TI  - The psychobiology of MDMA or 'ecstasy': symposium arranged by the Psychobiology Section, at the Annual Conference of the British Psychological Society, Heriot-Watt University, Edinburgh, April 1997

MH  - Animal

MH  - Cognition

MH  - drug effects

MH  - Emotions

MH  - Female

MH  - Hallucinogens

MH  - pharmacology

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Neurons

MH  - physiology

MH  - Street Drugs

RP  - NOT IN FILE

NT  - UI - 98244365LA - EngRN - 0 (Hallucinogens)RN - 0 (Street Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - CONGRESSESDA - 19980623IS - 0269-8811SB - MCY - UNITED STATESJC - CPHEM - 199808

UR  - PM:0009584974

SO  - J Psychopharmacol 1998  ;12(1):97-102

 

83

UI  - 88

AU  - Parrott AC

AU  - Lees A

AU  - Garnham NJ

AU  - Jones M

AU  - Wesnes K

AD  - Department of Psychology, University of East London, UK. andy2@uel.ac.uk

TI  - Cognitive performance in recreational users of MDMA of 'ecstasy': evidence for memory deficits

AB  - Cognitive task performance was assessed in three groups of young people: 10 regular users of 3,4-methylenedioxymethamphetamine (MDMA) who had taken 'ecstasy' 10 times or more; 10 novice MDMA users who had taken 'ecstasy' one to nine times; and 10 control subjects who had never taken MDMA. A computerized battery of cognitive tasks (Cognitive Drug Research system) was undertaken on a day when subjects were drug free. Performance on the response speed and vigilance measures (simple reaction time, choice reaction time, number vigilance), was similar across the three subgroups. However on immediate word recall and delayed word recall, both groups of MDMA users recalled significantly less words than controls. Animal research has shown that MDMA can lead to serotonergic neurodegeneration, particularly in the hippocampus and frontal cortex. Although the design of this study was far from ideal, these data are consistent with other findings of memory decrements in recreational MDMA users, possibly caused by serotonergic neurotoxicity

MH  - Adolescence

MH  - Adult

MH  - Analysis of Variance

MH  - Cognition

MH  - drug effects

MH  - Female

MH  - Hallucinogens

MH  - pharmacology

MH  - Human

MH  - Male

MH  - Memory

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Reaction Time

MH  - Street Drugs

RP  - NOT IN FILE

NT  - UI - 98244362LA - EngRN - 0 (Hallucinogens)RN - 0 (Street Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19980623IS - 0269-8811SB - MCY - UNITED STATESJC - CPHAA - AuthorEM - 199808

UR  - PM:0009584971

SO  - J Psychopharmacol 1998  ;12(1):79-83

 

84

UI  - 69

AU  - Parrott AC

AU  - Lasky J

AD  - Department of Psychology, University of East London, UK. andy2@uel.ac.uk

TI  - Ecstasy (MDMA) effects upon mood and cognition: before, during and after a Saturday night dance

AB  - Three groups of young people (aged 19-30 years) were compared: 15 regular ecstasy users who had taken MDMA (3,4- methylenedioxymethamphetamine) on ten or more occasions; 15 novice ecstasy users who had taken MDMA on fewer than ten previous occasions; and 15 controls who had never taken MDMA. Each subject completed a cognitive test and mood scale battery four times: an initial drug-free baseline, at a Saturday night dance/club (on-drug), then 2 days later, and 7 days later. On the Saturday night, regular ecstasy users took an average of 1.80 MDMA tablets, novice users took 1.45 MDMA tablets, while controls mostly drank alcohol. The consumption of cannabis and cocaine at the club was similar across groups. All three groups reported positive moods at the dance club (on-drug), although there were borderline trends (P < 0.10) for less sadness/depression in the MDMA subgroups. However 2 days afterwards, the ecstasy users felt significantly more depressed, abnormal, unsociable, unpleasant, and less good tempered, than the controls. Cognitive performance on both tasks (verbal recall, visual scanning) was significantly reduced on- MDMA. Memory recall was also significantly impaired in drug-free MDMA users, with regular ecstasy users displaying the worst memory scores at every test session. This agrees with previous findings of memory impairments in drug-free ecstasy users. Animal data have shown that MDMA can generate long-term serotonergic neurodegeneration in various brain areas, including the hippocampus. The cognitive deficits in drug- free recreational ecstasy users, suggest that MDMA may also be neurotoxic in humans

MH  - Adult

MH  - Affect

MH  - drug effects

MH  - Analysis of Variance

MH  - Cognition

MH  - Dancing

MH  - Female

MH  - Hallucinogens

MH  - adverse effects

MH  - pharmacology

MH  - Human

MH  - Male

MH  - Memory

MH  - Memory Disorders

MH  - chemically induced

MH  - N-Methyl-3,4-methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 98455404LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19981228IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199903

UR  - PM:0009784083

SO  - Psychopharmacology (Berl) 1998 Oct ;139(3):261-268

 

85

UI  - 71

AU  - Sabol KE

AU  - Seiden LS

AD  - University of Mississippi, Department of Psychology, 301 Peabody Bldg., University, MS 38677, USA

TI  - Reserpine attenuates D-amphetamine and MDMA-induced transmitter release in vivo: a consideration of dose, core temperature and dopamine synthesis

AB  - Amphetamine releases dopamine through a transporter-mediated mechanism. The purpose of this report was to further our understanding of the intracellular pool from which amphetamine releases dopamine: the cytoplasmic pool, the vesicular pool, or both. Rats were treated with D- amphetamine (AMPH) (1.0 or 10.0 mg/kg) or an amphetamine analog, methylenedioxymethamphetamine (MDMA) (2.0, 5.0, or 10.0 mg/kg). Pre- treatment with 10.0 mg/kg reserpine (18 h prior to AMPH or MDMA) attenuated dopamine release for high and low AMPH doses; however the low-dose effect showed borderline significance. Pre-treatment with 10.0 mg/kg reserpine attenuated dopamine and serotonin release induced by MDMA. The dopamine effect was seen at all three MDMA doses; the effect on serotonin was only measured at the 10.0 mg/kg dose. Reserpine pre- treatment caused reductions in core body temperature; heating the rats to normal body temperature for 3 h prior to AMPH or MDMA, and during the 4 h post-treatment period partially reversed the reserpine-induced attenuation of dopamine release. However, the intermediate level of dopamine release for the reserpinized-heated animals was not significantly different from either the reserpine group (not heated) or the AMPH or MDMA alone groups. In a separate group of rats, the effects of reserpine and reserpine+heat on dopamine synthesis were measured. DOPA accumulation after treatment with the aromatic acid decarboxylase inhibitor NSD-1015 (100 mg/kg, 30 min before sacrifice), was greater in rats treated with reserpine compared to controls; heating the reserpinized rats did not significantly alter the amount of DOPA accumulation; however there was a trend towards further increase. These results suggest that D-amphetamine releases dopamine that is stored in both vesicles and the cytoplasm. Cooling may contribute to the attenuation of AMPH or MDMA-induced dopamine release observed after reserpine; however, AMPH or MDMA dependence upon vesicular stores most likely explains the diminished release after reserpine. The attenuation of AMPH or MDMA-induced transmitter release by reserpine is thought to be counteracted by a reserpine-induced replenishment of stores. Therefore, all doses of D-amphetamine may use vesicular stores; the degree to which new synthesis counteracts the vesicular depletion may be the variable which differentiates low from high doses of D- amphetamine. Copyright 1998 Elsevier Science B.V

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - physiology

MH  - Dextroamphetamine

MH  - pharmacology

MH  - Dopamine

MH  - biosynthesis

MH  - Dopamine Agents

MH  - Dose-Response Relationship,Drug

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Neurotransmitters

MH  - metabolism

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Reserpine

MH  - Serotonin Agents

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 98413063LA - EngRN - 0 (Dopamine Agents)RN - 0 (Neurotransmitters)RN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-55-5 (Reserpine)RN - 51-61-6 (Dopamine)RN - 51-64-9 (Dextroamphetamine)PT - JOURNAL ARTICLEID - DA00085/DA/NIDADA - 19981120IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199901

UR  - PM:0009739110

SO  - Brain Res 1998 Sep 21 ;806(1):69-78

 

86

UI  - 93

AU  - Schechter MD

AD  - Department of Pharmacology, Northeastern Ohio Universities College of Medicine, Rootstown 44272-0095, USA

TI  - MDMA-like stimulus effects of hallucinogens in male Fawn-Hooded rats

AB  - A two-lever, food-motivated, operant technique was employed to train the purportedly serotonergically dysfunctional Fawn-Hooded (FH) rat to discriminate 1.5 mg/kg MDMA. Once all 10 male subjects learned the MDMA- vehicle discrimination at criterion performance level, doses different than the training dose were used to generate a dose-response discrimination gradient. The ED50 value of MDMA was shown to be 0.136 mg/kg, not significantly different from that of previously trained Sprague-Dawley male rats. Thus, the Fawn-Hooded rat appears to not differ in its sensitivity to lower doses of MDMA. Testing for MDMA-like stimulus generalizations with other drugs indicated that the MDMA derivative MDE produced generalization at a dose of 2.25 mg/kg and allowed for an ED50 value of 0.496 mg/kg. Like MDE, the testing of alpha-ethyltryptamine was shown to produce MDMA-like responding. Lastly, a dose of 0.12 mg/kg LSD produced 90% MDMA-lever selection. In contrast to MDMA generalizations to these three drugs, testing of cocaine at doses of 2.5-10 mg/kg and mescaline at 8-14 mg/kg did not produce MDMA-like discriminative effects. The results of this testing in the presumably serotonergically dysfunctional Fawn-Hooded rat would indicate that this line not only can discriminate MDMA as well as heterogenous-bred lines, but also shows the same discriminative generalizations and nongeneralizations from MDMA to serotonergic and dopaminergic agents

MH  - Animal

MH  - Central Nervous System Stimulants

MH  - pharmacology

MH  - Conditioning,Operant

MH  - drug effects

MH  - Cues

MH  - Discrimination (Psychology)

MH  - Dopamine Agents

MH  - Dose-Response Relationship,Drug

MH  - Generalization,Stimulus

MH  - Hallucinogens

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - genetics

MH  - physiology

MH  - Serotonin Agents

RP  - NOT IN FILE

NT  - UI - 98135835LA - EngRN - 0 (Central Nervous System Stimulants)RN - 0 (Dopamine Agents)RN - 0 (Hallucinogens)RN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEDA - 19980331IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199806

UR  - PM:0009476968

SO  - Pharmacol Biochem Behav 1998 Feb ;59(2):265-270

 

87

UI  - 85

AU  - Schechter MD

AD  - Department of Pharmacology, Northeastern Ohio Universities College of Medicine, Rootstown 44272-0095, USA. mds@neou-com.edu

TI  - 'Candyflipping': synergistic discriminative effect of LSD and MDMA

AB  - The co-administration of D-lysergic acid diethylamide (LSD; 'Acid') and 3,4-methylenedioxymethamphetamine (MDMA; 'Ecstasy'; 'XTC'), has reached a prevalence that has allowed for the street terminology 'candyflipping' to describe the combination. Internet sites indicate a significant enhancement of central effects with their simultaneous use. In this preliminary observation, male Fawn-Hooded rats were trained to discriminate 1.5 mg/kg MDMA and were, subsequently, tested with doses of MDMA (0.15 mg/kg) or LSD (0.04 mg/kg) that each produced a saline- like response. Co-administration of these doses of MDMA and LSD synergized to produce a maximal MDMA-like response. The possible mechanism for synergistic action upon central serotonergic neurons is discussed to explain the observed effect

MH  - Animal

MH  - Behavior,Animal

MH  - drug effects

MH  - Discrimination Learning

MH  - Drug Synergism

MH  - Hallucinogens

MH  - administration & dosage

MH  - pharmacology

MH  - Lysergic Acid Diethylamide

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Serotonin Agents

RP  - NOT IN FILE

NT  - UI - 98202230LA - EngRN - 0 (Hallucinogens)RN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-37-3 (Lysergic Acid Diethylamide)PT - JOURNAL ARTICLEDA - 19980521IS - 0014-2999SB - MCY - NETHERLANDSJC - EN6AA - AuthorEM - 199807

UR  - PM:0009543229

SO  - Eur J Pharmacol 1998 Jan 12 ;341(2-3):131-134

 

88

UI  - 86

AU  - Scheffel U

AU  - Szabo Z

AU  - Mathews WB

AU  - Finley PA

AU  - Dannals RF

AU  - Ravert HT

AU  - Szabo K

AU  - Yuan J

AU  - Ricaurte GA

AD  - Department of Radiology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA

TI  - In vivo detection of short- and long-term MDMA neurotoxicity--a positron emission tomography study in the living baboon brain

AB  - The present study evaluated short- and long-term effects of MDMA (3,4- methylenedioxymethamphetamine) in the baboon brain using PET and [11C](+)McN 5652, a potent 5-HT transporter ligand, as well as [11C]RTI- 55, a cocaine derivative which labels both 5-HT and dopamine transporters. Following baseline PET scans with [11C](+)McN5652, [11C](- )McN5652 (the inactive enantiomer of the active enantiomer [11C](+)McN5652) and [11C]RTI-55, a baboon was treated with MDMA (5 mg/kg, s.c., twice daily for four consecutive days). PET studies at 13, 19, and 40 days post-MDMA revealed decreases in mean radioactivity levels in all brain regions when using [11C](+)McN 5652, but not with [11C](-)McN5652 or [11C]RTI-55. Reductions in specific [11C](+)McN5652 binding (calculated as the difference in radioactivity concentrations between (+) and (-)[11C]McN5652) ranged from 44% in the pons to 89% in the occipital cortex. PET studies at 9 and 13 months showed regional differences in the apparent recovery of 5-HT transporters, with increases in some brain regions (e.g., hypothalamus) and persistent decreases in others (e.g., neocortex). Data obtained from PET studies correlated well with regional 5-HT axonal marker concentrations in the CNS measured after sacrifice of the animal. The results of these studies indicate that PET imaging of the living nonhuman primate brain with [11C](+)McN5652 can detect changes in regional 5-HT transporter density secondary to MDMA-induced neurotoxicity. Using PET, it should also be feasible to use [11C](+)McN5652 to determine whether human MDMA users are also susceptible to MDMA's neurotoxic effects

MH  - Animal

MH  - Autoradiography

MH  - Brain

MH  - radionuclide imaging

MH  - Brain Chemistry

MH  - drug effects

MH  - Brain Diseases

MH  - chemically induced

MH  - Carbon Isotopes

MH  - Carrier Proteins

MH  - metabolism

MH  - Cocaine

MH  - analogs & derivatives

MH  - diagnostic use

MH  - Iodine Radioisotopes

MH  - Isoquinolines

MH  - Male

MH  - Membrane Glycoproteins

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - toxicity

MH  - Papio

MH  - Radioligand Assay

MH  - Serotonin Agents

MH  - Serotonin Antagonists

MH  - Support,U.S.Gov't,P.H.S.

MH  - Tomography,Emission-Computed

RP  - NOT IN FILE

NT  - UI - 98253940LA - EngRN - 0 (serotonin transporter)RN - 0 (Carbon Isotopes)RN - 0 (Carrier Proteins)RN - 0 (Iodine Radioisotopes)RN - 0 (Isoquinolines)RN - 0 (Membrane Glycoproteins)RN - 0 (Serotonin Agents)RN - 0 (Serotonin Antagonists)RN - 133647-95-7 (RTI 55)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-36-2 (Cocaine)RN - 96795-90-3 (McN 5652)PT - JOURNAL ARTICLEID - DA 06309/DA/NIDAID - DA 10217/DA/NIDAID - DA 06275/DA/NIDADA - 19980701IS - 0887-4476SB - MCY - UNITED STATESJC - VFLAA - AuthorEM - 199809

UR  - PM:0009593108

SO  - Synapse 1998 Jun ;29(2):183-192

 

89

UI  - 68

AU  - Schifano F

AU  - Di Furia L

AU  - Forza G

AU  - Minicuci N

AU  - Bricolo R

AD  - Addiction Treatment Unit No. 1 (SerT 1), Padova, Italy. schifano@ux1.unipd.it

TI  - MDMA ('ecstasy') consumption in the context of polydrug abuse: a report on 150 patients

AB  - The present study examined the characteristics and the possible psychopathological consequences of ecstasy (MDMA, 3,4- methylenedioxymethamphetamine) use. One hundred and fifty consecutive patients, presenting to the Padova (Italy) Addiction Treatment Unit and who had taken ecstasy on at least one occasion, were examined and studied using a semi-structured interview. Ninety-five percent of the patients had experimented with another drug of abuse at least once in their lifetime. Ecstasy was mainly self-administered at disco clubs, and reported acute psychoactive effects confirmed previous reports. Fifty-three percent of the total sample were found to be affected by one or more psychopathological problems; the most frequent were depression, psychotic disorders, cognitive disturbances, bulimic episodes, impulse control disorders, panic disorders, social phobia. Those who were free from any psychopathological problem, compared to the others, had taken a smaller number of MDMA tablets in their lifetime, for a shorter duration and with a lower frequency. Again, they were less likely to have used alcohol together with ecstasy but more likely to have used opiates. Longer-term, larger dosage (acute or cumulative) MDMA consumers were found to be at high risk of developing psychopathological disturbances. The results are discussed, taking into account both the ecstasy suggested serotonin (5-hydroxytryptamine) neurotoxicity and the various methodological issues pertaining to this kind of large-scale clinical study describing people for whom MDMA is far from being the only drug of abuse

MH  - Adult

MH  - Comparative Study

MH  - Dose-Response Relationship,Drug

MH  - Female

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Male

MH  - Mental Disorders

MH  - chemically induced

MH  - psychology

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Retrospective Studies

MH  - Serotonin

MH  - metabolism

MH  - Street Drugs

MH  - Substance-Related Disorders

MH  - Time Factors

RP  - NOT IN FILE

NT  - UI - 99004279LA - EngRN - 0 (Hallucinogens)RN - 0 (Street Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEDA - 19981230IS - 0376-8716SB - MCY - IRELANDJC - EBSAA - AuthorEM - 199903

UR  - PM:0009788011

SO  - Drug Alcohol Depend 1998 Sep 1 ;52(1):85-90

 

90

UI  - 67

AU  - Shankaran M

AU  - Gudelsky GA

AD  - College of Pharmacy, University of Cincinnati, OH 45267-0004, USA

TI  - Effect of 3,4-methylenedioxymethamphetamine (MDMA) on hippocampal dopamine and serotonin

AB  - The 3,4-methylenedioxymethamphetamine (MDMA)-induced increase in the extracellular concentration of dopamine and the long-term depletion of 5-HT were studied in the hippocampus of the rat brain. MDMA produced a dose-dependent increase in the extracellular concentration of dopamine in the hippocampus, as well as in the striatum. The MDMA-induced increase in the extracellular concentration of dopamine in the hippocampus, but not in the striatum, was suppressed in rats treated with the norepinephrine uptake inhibitor, desipramine, and in rats in which noradrenergic neurons in the hippocampus were lesioned with DSP4 (N-(2- chloroethyl)-N-ethyl-2-bromo benzylamine). However, the long- term depletion of 5-HT in the hippocampus produced by MDMA was unaltered in desipramine-treated rats. These results are supportive of the view that the MDMA-induced increase in the extracellular concentration of dopamine in the hippocampus is the result of an enhanced release of dopamine from noradrenergic neurons. In addition, the MDMA-induced depletion of 5-HT in the hippocampus appears not to involve dopamine-initiated processes, because suppression of MDMA- induced dopamine release did not attenuate the long-term depletion of 5- HT in the hippocampus

MH  - Adrenergic Uptake Inhibitors

MH  - pharmacology

MH  - Animal

MH  - Desipramine

MH  - Dopamine

MH  - metabolism

MH  - Dose-Response Relationship,Drug

MH  - Hippocampus

MH  - drug effects

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 99017829LA - EngRN - 0 (Adrenergic Uptake Inhibitors)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-47-5 (Desipramine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)PT - JOURNAL ARTICLEID - DA07427/DA/NIDADA - 19990301IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199905

UR  - PM:0009802829

SO  - Pharmacol Biochem Behav 1998 Dec ;61(4):361-366

 

91

UI  - 75

AU  - Vollenweider FX

AU  - Gamma A

AU  - Liechti M

AU  - Huber T

AD  - Psychiatric University Hospital Zurich, Research Department, Zurich, Switzerland

TI  - Psychological and cardiovascular effects and short-term sequelae of MDMA ("ecstasy") in MDMA-naive healthy volunteers [see comments]

AB  - 3, 4-methylenedioxymethamphetamine (MDMA, "Ecstasy") is a recreational drug reported to produce a different psychological profile than that of classic hallucinogens and stimulants. It has, therefore, been tentatively classified into a novel pharmacological class termed entactogens. This double-blind placebo-controlled study examined the effects of a typical recreational dose of MDMA (1.7 mg/kg) in 13 MDMA- naive healthy volunteers. MDMA produced an effective state of enhanced mood, well-being, and increased emotional sensitiveness, little anxiety, but no hallucinations or panic reactions. Mild depersonalization and derealization phenomena occurred together with moderate thought disorder, first signs of loss of body control, and alterations in the meaning of percepts. Subjects also displayed changes in the sense of space and time, heightened sensory awareness, and increased psychomotor drive. MDMA did not impair selective attention as measured by the Stroop test. MDMA increased blood pressure moderately, with the exception of one subject who showed a transient hypertensive reaction. This severe increase in blood pressure indicates that the hypertensive effects of MDMA, even at recreational doses, should not be underestimated, particularly in subjects with latent cardiovascular problems. Most frequent acute somatic complaints during the MDMA challenge were jaw clenching, lack of appetite, impaired gait, and restless legs. Adverse sequelae during the following 24 hours included lack of energy and appetite, feelings of restlessness, insomnia, jaw clenching, occasional difficulty concentrating, and brooding. The present findings are consistent with the hypothesis that MDMA produces a different psychological profile than classic hallucinogens or psychostimulants

MH  - Adult

MH  - Affect

MH  - drug effects

MH  - Anorexia

MH  - chemically induced

MH  - Blood Pressure

MH  - Body Temperature

MH  - Bruxism

MH  - Comparative Study

MH  - Double-Blind Method

MH  - Fatigue

MH  - Female

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Male

MH  - Middle Age

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Reaction Time

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 98384700LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - CLINICAL TRIALPT - JOURNAL ARTICLEDA - 19981125IS - 0893-133XSB - MCY - UNITED STATESJC - ADQAA - AuthorEM - 199901RO - M:LC2

UR  - PM:0009718588

SO  - Neuropsychopharmacology 1998 Oct ;19(4):241-251

 

92

UI  - 82

AU  - Zheng Y

AU  - Laverty R

AD  - Department of Pharmacology, University of Otago, P.O. Box 913, Dunedin, New Zealand

TI  - Role of brain nitric oxide in (+/-)3,4-methylenedioxymethamphetamine (MDMA)-induced neurotoxicity in rats

AB  - The role of nitric oxide (NO) in the long-term serotoninergic neurotoxicity induced by (+/-)3,4-methylenedioxymethamphetamine (MDMA) in rats was investigiated. Pretreatment with Nomega-nitro-L-arginine (L- NOARG) (10 mg kg-1), a nitric oxide synthase (NOS) inhibitor, partially protected against long-term serotonin (5-HT) depletion induced by MDMA (40 mg kg-1) in frontal cortex and parietal cortex, but not in other brain regions examined. Brain NOS activities in these two regions were significantly elevated at 6 h after MDMA administration. Moreover, L- NOARG pretreatment caused significant inhibition of brain NOS activity but did not affect the acute 5-HT and dopamine (DA) changes or the hyperthermia induced by MDMA. These results suggest that it is the NOS inhibitory properties of L-NOARG, rather than its effects on the acute monoamine changes or the hyperthermia induced by MDMA, that are responsible for the prevention of neurotoxicity. The regional differences on the protection of L-NOARG and on the activation of NOS by MDMA indicate the unequal role that NO may play in MDMA-induced neurotoxicity in different brain regions. Copyright 1998 Elsevier Science B.V. All rights reserved

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - Enzyme Activation

MH  - Enzyme Inhibitors

MH  - pharmacology

MH  - Hydroxyindoleacetic Acid

MH  - metabolism

MH  - Indazoles

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - toxicity

MH  - Nerve Degeneration

MH  - chemically induced

MH  - enzymology

MH  - Nerve Tissue Proteins

MH  - Nitric Oxide

MH  - physiology

MH  - Nitric-Oxide Synthase

MH  - Nitroarginine

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Serotonin Agents

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 98288185LA - EngRN - EC 1.14.13.- (neural constitutive nitric oxide synthase)RN - EC 1.14.13.39 (Nitric-Oxide Synthase)RN - 0 (Enzyme Inhibitors)RN - 0 (Indazoles)RN - 0 (Nerve Tissue Proteins)RN - 0 (Serotonin Agents)RN - 10102-43-9 (Nitric Oxide)RN - 2149-70-4 (Nitroarginine)RN - 2942-42-9 (7-nitroindazole)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - JOURNAL ARTICLEDA - 19980819IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199810

UR  - PM:0009622646

SO  - Brain Res 1998 Jun 8 ;795(1-2):257-263

 

93

UI  - 102

AU  - Baker LE

AU  - Virden TB

AU  - Miller ME

AU  - Sullivan CL

AD  - Department of Psychology, Western Michigan University, Kalamazoo 49008, USA

TI  - Time course analysis of the discriminative stimulus effects of the optical isomers of 3,4-methylenedioxymethamphetamine (MDMA)

AB  - The present study examined the discriminative stimulus effects of the MDMA optical isomers administered at different presession injection intervals. In the first experiment, male Sprague-Dawley rats were trained in a two-lever, food-reinforced operant procedure to discriminate either (+)-MDMA (1.25 mg/kg) or (-)-MDMA (3.50 mg kg) at either 20 or 90 min following injection. Animals administered (+)-MDMA or saline 90 min before training sessions failed to attain the discrimination criteria after 73 training sessions, whereas (-)-MDMA successfully established discriminative stimulus control at both the 20 min and the 90 min postinjection intervals. (+)-Amphetamine did not substitute for either isomer, although a significant amount of drug- appropriate responding occurred in animals trained to discriminate (+)- MDMA at 20 min and (-)-MDMA at 90 min. Sch 39166 partially reduced the discrimination of (+)-MDMA at 20 min and (-)-MDMA at 90 min, although this effect was not dose dependent. Sch 39166 had no effect on animals trained to discriminate (-)-MDMA at 20 min. Haloperidol did not alter the discrimination of (+)-MDMA at 20 min but partially reduced the discriminative stimulus control of (-)-MDMA at 20 min and (-)-MDMA at 90 min. Fenfluramine substituted for both isomers of MDMA. Pirenpirone completely blocked the discriminative stimulus effects of (-)-MDMA at 20 min, although (+)-MDMA at 20 min and (-)-MDMA at 90 min were only partly blocked. WAY 100,135 had little effect on drug-appropriate responding; however, the discrimination of (+)-MDMA at 20 min was partly reduced by this 5-HT1A antagonist. In a second experiment, rats trained to discriminate (+)-MDMA (1.5 mg/kg) or (-)-MDMA (3.0 mg/kg) from saline were administered substitution tests with both isomers 20, 60, 90 and 120 min after injection. Results confirmed those of the first experiment that (+)-MDMA appears to have a shorter duration of action than (-)-MDMA. These results are discussed in light of the training doses employed

MH  - Amphetamine

MH  - pharmacology

MH  - Animal

MH  - Discrimination (Psychology)

MH  - drug effects

MH  - Dose-Response Relationship,Drug

MH  - Hallucinogens

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Stereoisomerism

MH  - Time Factors

RP  - NOT IN FILE

NT  - UI - 97444080LA - EngRN - 0 (Hallucinogens)RN - 300-62-9 (Amphetamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19971201IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199802

UR  - PM:0009300612

SO  - Pharmacol Biochem Behav 1997 Oct ;58(2):505-516

 

94

UI  - 105

AU  - Baker LE

AU  - Taylor MM

AD  - Department of Psychology, Western Michigan University, Kalamazoo 49008, USA

TI  - Assessment of the MDA and MDMA optical isomers in a stimulant- hallucinogen discrimination

AB  - The phenylisopropylamine derivatives 3,4-methylenedioxymethamphetamine (MDMA) and 3,4-methylenedioxyamphetamine (MDA) have been compared to both psychostimulants and hallucinogens in drug discrimination investigations. The stereoisomers of these compounds, in particular those of MDA, appear to produce differential effects. Previous studies have demonstrated that animals trained to discriminate amphetamine from vehicle generalize to the S(+)-isomers but not the R(-)-isomers of MDA and MDMA while animals trained to discriminate LSD from saline generalize to R(-)-MDA and neither isomer of MDMA. However, animals trained to discriminate mescaline from vehicle generalize to both stereoisomers of these phenylisopropylamine derivatives. The present study consisted of two experiments in which a three-choice drug discrimination procedure was employed to compare the stereoisomers of MDA and MDMA to both amphetamine and either mescaline (experiment one) or LSD (experiment two). Sixteen male Sprague-Dawley rats were trained to discriminate S(+)-amphetamine (1.0 mg/kg) and mescaline (12.5 mg/kg) and eight rats were trained to discriminate S(+)-amphetamine (1.0 mg/kg) and LSD (0.08 mg/kg) from saline in three-choice, food reinforced drug discrimination procedures. Substitution tests were administered with the isomers of MDA and MDMA. In the second experiment, substitution tests were also administered with lower doses of each training compound and with the stimulant cocaine and the hallucinogen 2,5-dimethoxy-4-methylphenylisopropylamine (DOM). In both experiments, all of the isomers produced very few responses on the S(+)- amphetamine lever. In the first experiment, R(-)-MDA and R(-)-MDMA produced nearly complete substitution for mescaline. The results of the second experiment revealed partial substitution for LSD with both isomers of MDMA and S(+)-MDA, and nearly complete substitution with R(- )MDA for LSD. The present findings do not support previous reports that S(+)-MDMA and S(+)-MDMA substitute for S(+)-amphetamine. The three- lever drug discrimination procedure may provide a more sensitive behavioral assay in which to examine the discriminative stimulus effects of drugs with compound stimulus properties

MH  - Animal

MH  - Cocaine

MH  - pharmacology

MH  - Discrimination Learning

MH  - drug effects

MH  - physiology

MH  - Dom

MH  - Food

MH  - Generalization (Psychology)

MH  - Hallucinogens

MH  - Lysergic Acid Diethylamide

MH  - Male

MH  - Mescaline

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Narcotics

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Reinforcement (Psychology)

MH  - Stereoisomerism

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 97403645LA - EngRN - 0 (Hallucinogens)RN - 0 (Narcotics)RN - 15588-95-1 (DOM)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-36-2 (Cocaine)RN - 50-37-3 (Lysergic Acid Diethylamide)RN - 54-04-6 (Mescaline)PT - JOURNAL ARTICLEDA - 19971016IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199712

UR  - PM:0009259001

SO  - Pharmacol Biochem Behav 1997 Aug ;57(4):737-748

 

95

UI  - 109

AU  - Cohen RS

AU  - Cocores J

AD  - Fairleigh Dickinson, University Madison, New Jersey, USA

TI  - Neuropsychiatric manifestations following the use of 3,4- methylenedioxymethamphetamine (MDMA: "Ecstasy")

AB  - 1. The recurring side-effects associated with MDMA consumption are reviewed. 2. The recreational use of "Ecstasy" has been implicated in the onset of various psychological, neurological, and organic complications. A table has been employed to depict the deleterious reactions that have occurred following MDMA ingestion. 3. An original case report is presented in which an individual developed perpetual neuropsychiatric symptomatology after having consumed MDMA. This case indicates that MDMA may induce long lasting effects, even after one exposure

MH  - Adolescence

MH  - Brain Diseases

MH  - chemically induced

MH  - Case Report

MH  - Human

MH  - Male

MH  - Mental Disorders

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - Time Factors

RP  - NOT IN FILE

NT  - UI - 97337413LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19970917IS - 0278-5846SB - MCY - ENGLANDJC - Q45AA - AuthorEM - 199711

UR  - PM:0009194153

SO  - Prog Neuropsychopharmacol Biol Psychiatry 1997 May ;21(4):727-734

 

96

UI  - 106

AU  - Colado MI

AU  - O'Shea E

AU  - Granados R

AU  - Murray TK

AU  - Green AR

AD  - Departamento de Farmacologia, Facultad de Medicina, Universidad Complutense, Madrid, Spain

TI  - In vivo evidence for free radical involvement in the degeneration of rat brain 5-HT following administration of MDMA ('ecstasy') and p- chloroamphetamine but not the degeneration following fenfluramine

AB  - 1. Administration of 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') to several species results in a long lasting neurotoxic degeneration of 5-hydroxytryptaminergic neurones in several regions of the brain. We have now investigated whether this degeneration is likely to be the result of free radical-induced damage. 2. Free radical formation can be assessed by measuring the formation of 2,3- and 2,5- dihydroxybenzoic acid (2,3-DHBA and 2,5-DHBA) from salicylic acid. An existing method involving implantation of a probe into the hippocampus and in vivo microdialysis was modified and validated. 3. Administration of MDMA (15 mg kg-1, i.p.) to Dark Agouti (DA) rats increased the formation of 2,3-DHBA (but not 2,5-DHBA) for at least 6 h. Seven days after this dose of MDMA, the concentration of 5-hydroxytryptamine (5- HT) and 5-hydroxyindoleacetic acid (5-HIAA) was reduced by over 50% in hippocampus, cortex and striatum, reflecting neurotoxic damage. There was no change in the concentration of dopamine or 3,4- dihydroxyphenylacetic acid (DOPAC) in the striatum. 4. p- Chloroamphetamine (PCA), another compound which produces a neurotoxic loss of cerebral 5-HT content, when given at a dose of 5 mg kg-1 also significantly increased the formation of 2.3-DHBA (but not 2,5-DHBA) in the dialysate for over 4.5 h. post-injection starting 2 h after treatment. 5. In contrast, fenfluramine administration (15 mg kg-1, i.p.) failed to increase the 2,3-DHBA or 2,5-DHBA concentration in the dialysate. A single fenfluramine injection nevertheless also markedly decreased the concentration of 5-HT and 5-HIAA in the hippocampus, cortex and striatum seven days later. 6. When rats pretreated with fenfluramine (15 mg kg-1, i.p.) seven days earlier were given MDMA (15 mg kg-1, i.p.) no increase in 2,3-DHBA was seen in the dialysate from the hippocampal probe. This indicates that the increase in free radical formation following MDMA is occurring in 5-HT neurones which have been damaged by the prior fenfluramine injection. 7. Administration of the free radical scavenging agent alpha-phenyl-N-tert-butyl nitrone (PBN; 120 mg kg-1, i.p.) 10 min before and 120 min after an MDMA (15 mg kg-1, i.p.) injection prevented the acute rise in the 2,3-DHBA concentration in the dialysate and attenuated by 30% the long term damage to hippocampal 5-HT neurones (as indicated by a smaller MDMA-induced decrease in both the concentration of 5-HT and 5-HIAA and also the binding of [3H]-paroxetine). 8. These data indicate that a major mechanism by which MDMA and PCA induce damage to 5- hydroxytryptaminergic neurones in rat brain is by increasing the formation of free radicals. These probably result from the degradation of catechol and quinone metabolites of these substituted amphetamines. In contrast, fenfluramine induces damage by another mechanism not involving free radicals; a proposal supported by some of our earlier indirect studies. 9. We suggest that these different modes of action render untenable the recent suggestion that MDMA will not be neurotoxic in humans because fenfluramine appears safe at clinical doses

MH  - p-Chloroamphetamine

MH  - toxicity

MH  - Animal

MH  - Biogenic Monoamines

MH  - metabolism

MH  - Body Temperature

MH  - drug effects

MH  - Brain Chemistry

MH  - Fenfluramine

MH  - Free Radical Scavengers

MH  - pharmacology

MH  - Free Radicals

MH  - Hippocampus

MH  - Male

MH  - Microdialysis

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Nerve Degeneration

MH  - Paroxetine

MH  - Rats

MH  - Serotonin Agents

MH  - Serotonin Uptake Inhibitors

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 97365718LA - EngRN - 0 (Biogenic Monoamines)RN - 0 (Free Radical Scavengers)RN - 0 (Free Radicals)RN - 0 (Serotonin Agents)RN - 0 (Serotonin Uptake Inhibitors)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 458-24-2 (Fenfluramine)RN - 61869-08-7 (Paroxetine)RN - 64-12-0 (p-Chloroamphetamine)PT - JOURNAL ARTICLEDA - 19970915IS - 0007-1188SB - MCY - ENGLANDJC - B00AA - AuthorEM - 199711

UR  - PM:0009222545

SO  - Br J Pharmacol 1997 Jul ;121(5):889-900

 

97

UI  - 108

AU  - Colado MI

AU  - O'Shea E

AU  - Granados R

AU  - Misra A

AU  - Murray TK

AU  - Green AR

AD  - Departamento de Farmacologia, Facultad de Medicina, Universidad Complutense, Madrid, Spain

TI  - A study of the neurotoxic effect of MDMA ('ecstasy') on 5-HT neurones in the brains of mothers and neonates following administration of the drug during pregnancy

AB  - 1. It is well established that 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') is neurotoxic and produces long term degeneration of cerebral 5-hydroxytryptamine (5-HT) nerve terminals in many species. Since MDMA is used extensively as a recreational drug by young people, it is being ingested by many women of child bearing age. We have therefore examined the effect of administering high doses of MDMA to rats during pregnancy on the cerebral content of both the dams and the neonates. 2. MDMA (20 mg kg-1, s.c.) was injected twice daily on days 14-17 of the gestation period. The initial dose produced a marked hyperthermic response in the dam which was progressively attenuated in both peak height and area under the curve following further doses of the drug. The body weight of the dams decreased during the period of treatment. 3. There was a modest decrease in litter size (-20%) of the MDMA-treated dams. 4. The concentration of 5-HT and its metabolite 5- HIAA was decreased by over 65% in the hippocampus and striatum and 40% in the cortex of the dams 1 week after parturition. In contrast, the content of 5-HT and 5-HIAA in the dorsal telencephalon of the pups of the MDMA-treated dams was the same as that seen in tissue from pups born to control animals. 5. Administration of MDMA (40 mg kg-1, s.c.) to adult rats increased thiobarbituric acid reacting substances (TBARS) in cortical tissue 3 h and 6 h later, indicating increased lipid peroxidation. No increase in TBARS was seen in the cortical tissue of 7- 10 day neonates injected with this dose of MDMA 3 h or 6 h earlier. 6. The data suggest that exposure to MDMA in utero during the maturation phase does not produce damage to 5-HT nerve terminals in the foetal rat brain, in contrast to the damage seen in the brains of the mothers. This may be due to MDMA being metabolized to free radical producing entities in the adult brain but not in the immature brain or, alternatively, to more effective or more active free radical scavenging mechanisms being present in the immature brain

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - Body Weight

MH  - Brain

MH  - Dopamine

MH  - metabolism

MH  - Female

MH  - Hydroxyindoleacetic Acid

MH  - Lipid Peroxidation

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Neurons

MH  - Pregnancy

MH  - Rats

MH  - Rats,Wistar

MH  - Serotonin

MH  - Serotonin Agents

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 97351873LA - EngRN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - JOURNAL ARTICLEDA - 19970925IS - 0007-1188SB - MCY - ENGLANDJC - B00AA - AuthorEM - 199711

UR  - PM:0009208155

SO  - Br J Pharmacol 1997 Jun ;121(4):827-833

 

98

UI  - 103

AU  - Curran HV

AU  - Travill RA

AD  - Department of Psychology, University College London, UK. v.curran@ucl.ac.uk

TI  - Mood and cognitive effects of +/-3,4-methylenedioxymethamphetamine (MDMA, 'ecstasy'): week-end 'high' followed by mid-week low

AB  - AIMS: Recreational use of +/-3,4-methylenedioxymethamphetamine (MDMA, 'ecstasy') is widespread. The present study aimed to examine both the acute and residual effects of this drug on users' mood and cognitive function. DESIGN AND PARTICIPANTS: A parallel group design was used to compare 12 participants who reported having taken MDMA with 12 participants who reported having consumed only alcohol, on the relevant night (day 1). These same participants were then re-assessed the following day (day 2) and again mid-week (day 5). FINDINGS: Acute effects of MDMA broadly replicated previous findings. MDMA users rated elevated mood on day 1 but significantly low mood on day 5, at which point some participants scored within the range for clinical depression. In contrast, the alcohol group showed less pronounced changes, which followed a U-shaped curve over days with the lowest point being day 2. The MDMA group also showed significant impairments on an attentional/working memory task, compared with alcohol users. CONCLUSIONS: Weekend use of MDMA may lead to depressed mood mid-week. Possible mechanisms underlying the findings are discussed in terms of temporary depletion of serotonin, serotonergic neurotoxity and psychological aspects of mood change

MH  - Adult

MH  - Affect

MH  - drug effects

MH  - Alcohol Drinking

MH  - psychology

MH  - Cognition

MH  - Comparative Study

MH  - Female

MH  - Follow-Up Studies

MH  - Hallucinogens

MH  - pharmacology

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Substance-Related Disorders

RP  - NOT IN FILE

NT  - UI - 97438553LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19970923IS - 0965-2140CY - ENGLANDJC - BM3AA - AuthorEM - 199711

UR  - PM:0009293041

SO  - Addiction 1997 Jul ;92(7):821-831

 

99

UI  - 110

AU  - De S

AU  - Kelly JP

AU  - Harkin AJ

AU  - Leonard BE

AD  - Department of Pharmacology, University College, Galway, Ireland

TI  - An appraisal of the pharmacological and toxicological effects of a single oral administration of 3,4-methylenedioxymethamphetamine (MDMA) in the rat

AB  - This study examined some acute pharmacological and toxicological effects of 3,4 methylenedioxymethamphetamine (MDMA, "Ecstasy") over a range of doses (20, 40, 80, 160 and 320 mg/kg orally) in adult female rats. Deaths were observed from the 40 mg/kg MDMA group onwards. Reductions in body weight change, food and water intake were found in the 80 mg/kg group, whilst food intake alone was reduced in the 20 and 40 mg/kg groups. Significant hyperthermic responses were found over the first 8 hr following MDMA administration which were dose-related. A significant hyperactivity of approximately 9 hr duration was observed in the 20 mg/kg and 40 mg/kg groups, whereas there was evidence of a serotonin syndrome in the higher dosage groups. Thus, acute oral administration of MDMA results in a variety of measurable responses. The cause of death in this study is probably a combination of serotonin syndrome and hyperthermia

MH  - Administration,Oral

MH  - Animal

MH  - Body Temperature

MH  - Dose-Response Relationship,Drug

MH  - Drug Administration Schedule

MH  - Female

MH  - Hallucinogens

MH  - pharmacology

MH  - toxicity

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Rectum

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 97325545LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19970718IS - 0901-9928SB - MCY - DENMARKJC - PHTAA - AuthorEM - 199709

UR  - PM:0009181598

SO  - Pharmacol Toxicol 1997 May ;80(5):207-210

 

100

UI  - 94

AU  - Dinse H

AD  - Abteilung fur Anasthesiologie und Intensivmedizin, Berufsgenossenschaftliche Unfall-klinik Tubingen

TI  - [Ecstasy (MDMA) intoxication. An overview]

AB  - The increased consumption of "ecstasy" (MDMA, 3,4-methylenedioxy- methamphetamine) has also increased the number of life-threatening intoxications. From a Medline search of the years 1992-1996, reports were registered and evaluated. Besides cerebral, cardiorespiratory, renal, and hepatic symptoms, hyperthermia syndromes such as malignant hyperthermia, neuroleptic malignant syndrome, or the serotonin syndrome were common. In addition to a discussion of the intoxication symptoms and their acute and intensive-care therapy, the psychological and physiological effects of "ecstasy" will be described. Some historical considerations of the topic are included in this review

MH  - Emergency Medical Services

MH  - English Abstract

MH  - Hallucinogens

MH  - pharmacology

MH  - poisoning

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Overdose

MH  - therapy

RP  - NOT IN FILE

NT  - UI - 97454907LA - GerRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19971119IS - 0003-2417SB - MCY - GERMANYJC - 4MYAA - AuthorEM - 199801

UR  - PM:0009382208

SO  - Anaesthesist 1997 Aug ;46(8):697-703

 

101

UI  - 119

AU  - Frederick DL

AU  - Paule MG

AD  - Division of Neurotoxicology, National Center for Toxicological Research/FDA, Jefferson, AR 72079-9502, USA

TI  - Effects of MDMA on complex brain function in laboratory animals

AB  - This review surveys experiments that have examined the effects of acute and chronic MDMA exposure on schedule-controlled operant behaviors thought to engender responses that reflect the expression of complex brain functions. Such functions include time estimation, short-term memory, learning, motivation, and color and position discrimination. Recent experiments conducted in the Behavioral Toxicology Laboratory at the National Center for Toxicological Research concerning MDMA's acute and long-term effects on rhesus monkey performance in an operant test battery are compared to previous studies involving the effects of MDMA on operant behaviors. Results of these experiments suggest that when given acutely, MDMA disrupts complex brain functions associated with learning and time estimation more than those associated with short-term memory and visual discrimination, and that behavioral tasks requiring relatively high rates of responding are particularly sensitive to the disruptive effects of MDMA. Repeated exposure to doses of MDMA sufficient to produce long-lasting changes in brain neurotransmitter systems results in residual effects (e.g. tolerance, sensitivity) on behavioral task performance when subjects are subsequently challenged with acute MDMA, whereas baseline (non-challenged) performance of these tasks after such exposure generally remains unchanged. Although the experiments described herein were conducted on a relatively small number of non-human subjects, they raise the possibility that long-term effects on cognitive processes may also occur in humans exposed to repeated or acute high doses of MDMA

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - physiology

MH  - Dose-Response Relationship,Drug

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 97147305LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19970411IS - 0149-7634SB - MCY - UNITED STATESJC - OA7AA - AuthorEM - 199706

UR  - PM:0008994210

SO  - Neurosci Biobehav Rev 1997 Jan ;21(1):67-78

 

102

UI  - 91

AU  - Gartside SE

AU  - McQuade R

AU  - Sharp T

AD  - University of Oxford Department of Clinical Pharmacology, Radcliffe Infirmary, UK

TI  - Acute effects of 3,4-methylenedioxymethamphetamine (MDMA) on 5-HT cell firing and release: comparison between dorsal and median raphe 5-HT systems

AB  - It is proposed that 3,4-methylenedioxymethamphetamine (MDMA; Ecstasy) is more toxic to 5-HT neurones projecting from the dorsal raphe nucleus (DRN) than to those from the median raphe nucleus (MRN). Since increased 5-HT release has been associated with MDMA-induced neurotoxicity, MDMA may have a DRN-selective 5-HT releasing effect. Here we have compared the effects of acute MDMA on DRN and MRN 5-HT pathways using in vivo electrophysiological and neurochemical techniques. MDMA inhibited the firing of 5-HT neurones in both the DRN and the MRN, and did so with similar potency (ED50 values, 0.589 +/- 0.151 (8) and 0.588 +/- 0.207 (6) mg/kg i.v., respectively). In both nuclei this inhibitory effect was reversed by the selective 5-HT1A receptor antagonist, WAY 100635 (0.1 mg/kg i.v.). Microdialysis measurements were made in the frontal cortex and dorsal hippocampus, regions which receive a DRN- and an MRN-selective 5-HT innervation, respectively. A dose of 1 mg/kg i.v. MDMA increased extracellular 5-HT 3-fold in both the frontal cortex and dorsal hippocampus. A higher dose (3 mg/kg i.v.) increased 5-HT levels 8-fold in both regions. Overall, our data suggest that MDMA releases 5-HT from the cell body and terminal regions of both DRN and MRN 5-HT pathways, and does so in a qualitatively and quantitatively similar fashion. We conclude that any DRN-selectivity in the neurotoxic effects of MDMA is not due to a DRN- selective, acute 5-HT releasing action of the drug

MH  - Chromatography,High Pressure Liquid

MH  - Comparative Study

MH  - Electric Stimulation

MH  - Electrochemistry

MH  - Electrophysiology

MH  - Hippocampus

MH  - drug effects

MH  - metabolism

MH  - Microdialysis

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Neurons

MH  - Piperazines

MH  - Prefrontal Cortex

MH  - Pyridines

MH  - Raphe Nuclei

MH  - cytology

MH  - physiology

MH  - Serotonin

MH  - Serotonin Agents

MH  - Serotonin Antagonists

MH  - Stereotaxic Techniques

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 98176618LA - EngRN - 0 (Piperazines)RN - 0 (Pyridines)RN - 0 (Serotonin Agents)RN - 0 (Serotonin Antagonists)RN - 146714-97-8 (WAY 100635)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEDA - 19980505IS - 0028-3908SB - MCY - ENGLANDJC - NZBAA - AuthorEM - 199807

UR  - PM:0009517441

SO  - Neuropharmacology 1997 Nov ;36(11-12):1697-1703

 

103

UI  - 95

AU  - Huether G

AU  - Zhou D

AU  - Ruther E

AD  - Psychiatrische Klinik, Universitat Gottingen, Federal Republic of Germany

TI  - Causes and consequences of the loss of serotonergic presynapses elicited by the consumption of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") and its congeners

AB  - The massive and prolonged stimulation of serotonin (5-HT)-release and the increased dopaminergic activity are responsible for the acute psychomimetic and psychostimulatory effects of 3,4-methylenedioxy- methamphetamine (MDMA, "ecstasy") and its congeners. In vulnerable subjects, at high doses or repeated use, and under certain unfavorable conditions (crowding, high ambient temperature), severe, in some cases fatal, averse systemic reactions (hyperthermia, serotonin-syndrome) may occur during the first few hours. Animal experiments revealed the existence of similar differences in vulnerability and similar dose- and context-related influences on a similar sequence of acute responses. The severity of these acute systemic responses is closely related to the severity of the long-term damage to 5-HT axon terminals caused by the administration of substituted amphetamines. Attempts to identify the mechanisms involved in this selective degeneration of 5-HT presynapses brought to light a multitude of different factors and conditions which either attenuate or potentiate the loss of 5-HT terminals caused by MDMA and related amphetamine derivatives. These puzzling observations suggest that the degeneration of 5-HT presynapses represents only the final step in a sequence of events which compromise the ability of 5-HT terminals to maintain their functional and structural integrity. Substituted amphetamines selectively tax energy metabolism in 5-HT presynapses through their ability to exchange with 5- HT and to dissipate transmembrane ion gradients. The active carrier systems in the vesicular and presynaptic membrane operate at a permanently activated state. The resulting energy deficit can no longer adequately restored by the 5-HT presynapses when their availability of substrates for ATP production is additionally reduced by the hyperthermic and other energy consuming reactions which are elicited by the systemic administration of substituted amphetamines. The exhaustion of energy in 5-HT nerve terminals compromised all energy-requiring endogenous mechanisms involved in the regulation of transmembrane-ion exchange, internal Ca(++)-homeostasis, prevention of oxidative stress, detoxification, and repair. Above a critical threshold the failure of these self-protective mechanisms will lead to the degeneration of the 5- HT axon terminals. Based on the role of 5-HT as a global modulatory transmitter-system involved in the stabilization and integration of impulse flow between distributed multifocal neuronal networks, the partial loss of 5-HT presynapses must be expected to impair the ability of these networks to maintain the integrity of signal flow pattern, and increase the likelihood of switching to unstable information processing. Behavioral responding may therefore become more dominated by activities generated in individual networks, and hitherto "buffered" personality traits and predisposition may become manifested as defined psychiatric syndromes in certain predisposed subjects

MH  - Amphetamine-Related Disorders

MH  - metabolism

MH  - pathology

MH  - physiopathology

MH  - Animal

MH  - Energy Metabolism

MH  - drug effects

MH  - Hallucinogens

MH  - administration & dosage

MH  - pharmacology

MH  - toxicity

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - Nerve Degeneration

MH  - Presynaptic Terminals

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

MH  - Synaptic Transmission

RP  - NOT IN FILE

NT  - UI - 98113680LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19980226IS - 0300-9564SB - MCY - AUSTRIAJC - CIJAA - AuthorEM - 199804

UR  - PM:0009451711

SO  - J Neural Transm 1997  ;104(8-9):771-794

 

104

UI  - 116

AU  - Kikura R

AU  - Nakahara Y

AU  - Mieczkowski T

AU  - Tagliaro F

AD  - National Institute of Health Sciences, Tokyo, Japan

TI  - Hair analysis for drug abuse. XV. Disposition of 3, 4- methylenedioxymethamphetamine (MDMA) and its related compounds into rat hair and application to hair analysis for MDMA abuse

AB  - In order to clarify the mechanism of drug incorporation into hair, disposition of 3,4-methylenedioxyamphetamine (MDA), 3,4- methylenedioxymethamphetamine (MDMA), 3,4- methylenedioxyethylamphetamine (MDEA), 3-methoxy-4,5- methylenedioxyamphetamine (MMDA) and metabolites of MDMA, 4-hydroxy-3- methoxyamphetamine (HMAP) and 4-hydroxy-3-methoxymethamphetamine (HMMA), into hair was investigated with an animal model. After the intraperitoneal administration of those six drugs to pigmented hairy rats (5 mg/kg/day, 10 days, n = 3), the parent compounds and their metabolites in the rat plasma (5, 15, 30, 60, 120, 360 min after administration) and in the newly grown rat hair for 4 weeks were determined by GC/MS-SIM. When the ratio of hair concentration to area under the concentration versus time curves (AUCs) in plasma was represented as an index of incorporation rate (ICR) of drugs into hair, the order of ICRs was HMAP < MDA < HMMA < MDMA < MDEA < MMDA. In the comparison between MDA, MDMA and MDEA, their ICRs increased according to the length of carbon branches from proton to ethyl at the N position. From the point of view that the ICRs of MMDA was 2.3 times as much as that of MDA, the methoxy group on the benzene ring seemed to serve as a positive factor for the ICR. However, the ICRs of 4-hydroxy- 3-methoxy compounds, HMAP and HMMA, were lower in comparison with those of MDA and MDMA, respectively. On the other hand, the ICRs of MDA, MDMA and MDEA were 5.5-6.1 times larger than those of amphetamine, methamphetamine and ethylamphetamine, suggesting that the methylenedioxy group on the benzene ring raises their ICRs very positively. Moreover, in order to apply the results from the animal experiments to human cases, the scalp hair samples of seven MDMA abusers were analyzed. MDMA and its metabolites, MDA; were simultaneously detected in all the samples by GC/MS. In the two samples, MDEA was found in addition to MDMA and MDA. It was shown that a hair sample is a good specimen for the confirmation of retrospective use of methylenedioxyamphetamines

MH  - Amphetamines

MH  - pharmacokinetics

MH  - Animal

MH  - Comparative Study

MH  - Hair

MH  - metabolism

MH  - Hallucinogens

MH  - Human

MH  - Lactates

MH  - Male

MH  - Mass Fragmentography

MH  - Methamphetamine

MH  - analogs & derivatives

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Substance Abuse Detection

MH  - methods

MH  - Substance-Related Disorders

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 97195370LA - EngRN - 0 (Amphetamines)RN - 0 (Hallucinogens)RN - 0 (Lactates)RN - 117652-28-5 (4-hydroxy-3-methoxymethamphetamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 515-30-0 (atrolactic acid)RN - 537-46-2 (Methamphetamine)RN - 82801-81-8 (3,4-methylenedioxyethamphetamine)PT - JOURNAL ARTICLEDA - 19970328IS - 0379-0738SB - MCY - IRELANDJC - F49AA - AuthorEM - 199706

UR  - PM:0009042722

SO  - Forensic Sci Int 1997 Jan 17 ;84(1-3):165-177

 

105

UI  - 118

AU  - Koch S

AU  - Galloway MP

AD  - Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, USA

TI  - MDMA induced dopamine release in vivo: role of endogenous serotonin

AB  - Acting as a substrate at the serotonin (5-HT) transporter, (+)-MDMA (3,4-methylenedioxymethamphetamine), is a potent releaser of 5-HT and causes toxicity to 5-HT neurons after repeated exposure. (+)-MDMA also releases dopamine (DA), although with less potency. Since we have shown previously that the intrastriatal application of 5-HT facilities DA release, it was hypothesized that increased release of striatal 5-HT after MDMA may influence extracellular levels of DA. Using microdialysis in vivo, we found that (+)-MDMA (4.7 mumol/kg, i.v.) administration increased extracellular striatal DA levels to 501% of control (p < 0.01, n = 12). However, in the presence of fluoxetine (14.4 mumol/kg, s.c.), which prevents (+)-MDMA effects on 5-HT release, the (+)-MDMA-induced increase in DA was significantly less (to 375% of control, p < 0.05, vs. no fluoxetine, n = 8). In vitro studies with striatal slices, to test drug selectivity, showed that (+)-MDMA (0.3-3 microM) increased extracellular levels of both DA and 5-HT in a dose- dependent manner. Fluoxetine (3 microM) completely blocked the effects of (+)-MDMA on 5-HT release, but did not alter (+)-MDMA-induced DA release in vitro. The selective DA transport inhibitor GBR-12909 (1 microM), blocked (+)-MDMA's effect on DA release. It is concluded that 5-HT release after (+)-MDMA treatment partially contributes to (+)- MDMA's effect on DA release in vivo

MH  - Animal

MH  - Chromatography,High Pressure Liquid

MH  - Dopamine

MH  - metabolism

MH  - Dopamine Uptake Inhibitors

MH  - pharmacology

MH  - Fluoxetine

MH  - In Vitro

MH  - Ketanserin

MH  - Male

MH  - Microdialysis

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Neostriatum

MH  - drug effects

MH  - Piperazines

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Serotonin Agents

MH  - Serotonin Antagonists

MH  - Serotonin Uptake Inhibitors

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 97346660LA - EngRN - 0 (Dopamine Uptake Inhibitors)RN - 0 (Piperazines)RN - 0 (Serotonin Agents)RN - 0 (Serotonin Antagonists)RN - 0 (Serotonin Uptake Inhibitors)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 54910-89-3 (Fluoxetine)RN - 67469-78-7 (GBR 12909)RN - 74050-98-9 (Ketanserin)PT - JOURNAL ARTICLEID - NIDA-04120DA - 19970903IS - 0300-9564SB - MCY - AUSTRIAJC - CIJAA - AuthorEM - 199711

UR  - PM:0009203077

SO  - J Neural Transm 1997  ;104(2-3):135-146

 

106

UI  - 104

AU  - Kramer HK

AU  - Poblete JC

AU  - Azmitia EC

AD  - Department of Psychiatry, New York University Medical Center, NY 10016, USA

TI  - Activation of protein kinase C (PKC) by 3,4- methylenedioxymethamphetamine (MDMA) occurs through the stimulation of serotonin receptors and transporter

AB  - This report further characterizes the intermediate metabolic effects of the psychotropic amphetamine derivative, 3,4- methylenedioxymethamphetamine (MDMA or "ecstasy"), on the activity of second messenger-dependent kinases. Previous work has demonstrated that two injections of MDMA (20 mg/kg) elicits a prolonged translocation of the calcium and phospholipid-dependent enzyme, protein kinase C (PKC) in rats. However, because MDMA has actions at the 5-HT transporter and 5-HT2A/2C receptors, our experiments were directed at uncovering which of these many sites may be involved in this second messenger dependent response. A single injection of MDMA produced a time- and dose- dependent increase in the density of cortical and hippocampal PKC (as measured by 3H-phorbol 12,13-dibutyrate (PDBu) binding sites. MDMA- mediated PKC translocation was long-lasting and remained above control (saline-treated rats) for up to 24 h after injection. This effect was mimicked by another substituted amphetamine, p-chloroamphetamine (pCA), but with a temporal-response curve that was to the left of MDMA's. However, pure uptake inhibitors like fluoxetine, cocaine, and the selective 5-HT2A/2C agonist, DOB, were unable to produce a long-lasting translocation of PKC binding sites in rat cortex. Fluoxetine, a selective serotonin uptake inhibitor (SSRI) and ketanserin a 5-HT2A antagonist, attenuated PKC translocation by MDMA with differing efficacies; however, both compounds completely prevented the loss of 5- HT uptake sties after multiple doses of MDMA. These results suggest that MDMA increases PKC translocation by two interrelated mechanisms that involve 5-HT2A/2C receptors and the 5-HT transporter. This pathway appears to include: (1) the drug binding to the 5-HT transporter, (2) the release of cytosolic 5-HT stores into the extracellular space, and (3) the activation of post-synaptic 5-HT2A/2C receptors linked to G- protein-mediated phospholipid hydrolysis

MH  - Animal

MH  - Binding Sites

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - Brain Stem

MH  - Carrier Proteins

MH  - Cerebral Cortex

MH  - Comparative Study

MH  - Enzyme Activation

MH  - Female

MH  - Fluoxetine

MH  - pharmacology

MH  - Hippocampus

MH  - Ketanserin

MH  - Membrane Glycoproteins

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Phorbol 12,13-Dibutyrate

MH  - Protein Kinase C

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Receptors,Serotonin

MH  - Serotonin Agents

MH  - Serotonin Uptake Inhibitors

RP  - NOT IN FILE

NT  - UI - 97418518LA - EngRN - EC 2.7.1.- (Protein Kinase C)RN - 0 (serotonin transporter)RN - 0 (Carrier Proteins)RN - 0 (Membrane Glycoproteins)RN - 0 (Receptors, Serotonin)RN - 0 (Serotonin Agents)RN - 0 (Serotonin Uptake Inhibitors)RN - 37558-16-0 (Phorbol 12,13-Dibutyrate)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 54910-89-3 (Fluoxetine)RN - 74050-98-9 (Ketanserin)PT - JOURNAL ARTICLEDA - 19980108IS - 0893-133XSB - MCY - UNITED STATESJC - ADQAA - AuthorEM - 199803

UR  - PM:0009272479

SO  - Neuropsychopharmacology 1997 Sep ;17(3):117-129

 

107

UI  - 111

AU  - LeSage M

AU  - Poling A

AD  - Department of Psychology, Western Michigan University, Kalamazoo 49008, USA

TI  - MDMA and d-amphetamine produce comparable effects in pigeons performing under a multiple fixed-ratio interresponse-time-greater-than-t schedule of food delivery

AB  - The purpose of this study was to gain further information about the behavioral effects of (+/-) 3.4-methylenedioxymethamphetamine (MDMA) on schedule-controlled responding. MDMA (0.32, 0.56, 1.0, 3.2, 5.6, and 10 mg/kg) and d-amphetamine (0.32, 0.56, 1.0, 3.2, 5.6, and 10 mg/kg) were administered to pigeons performing under a multiple fixed-ratio 30 (FR 30) interresponse-time-greater-than-15-s (IRT > 15-s) schedule of food delivery. In general, both drugs had no significant effect on response rates under the IRT > 15-s component at doses that decreased rates under the FR component. Results of the present experiment indicate that under some conditions MDMA and d-amphetamine produce similar, and rate- dependent, effects

MH  - Animal

MH  - Central Nervous System Stimulants

MH  - pharmacology

MH  - Conditioning,Operant

MH  - drug effects

MH  - Dextroamphetamine

MH  - Drug Screening

MH  - Food

MH  - Hallucinogens

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Pigeons

MH  - Reaction Time

MH  - Reinforcement Schedule

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 97307378LA - EngRN - 0 (Central Nervous System Stimulants)RN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 51-64-9 (Dextroamphetamine)PT - JOURNAL ARTICLEID - DA07869-01A4/DA/NIDADA - 19970730IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199710

UR  - PM:0009164569

SO  - Pharmacol Biochem Behav 1997 May ;57(1-2):173-177

 

108

UI  - 117

AU  - Lin HQ

AU  - Jackson DM

AU  - Atrens DM

AU  - Christie MJ

AU  - McGregor IS

AD  - Department of Pharmacology, University of Sydney, Australia

TI  - Serotonergic modulation of 3,4-methylenedioxymethamphetamine (MDMA)- elicited reduction of response rate but not rewarding threshold in accumbal self-stimulation

AB  - In a fixed interval 5-s rate-frequency function paradigm with rats, 3,4- methylenedioxymethamphetamine (MDMA; 0.5, 2 and 4 mg/kg) dose- dependently decreased response rate for nucleus accumbens self- stimulation while both D-amphetamine (0.3 and 1 mg/kg) and cocaine (5 and 15 mg /kg) increased response rates. The highest doses of MDMA caused a cessation of responding in many of the rats tested, but in those rats that continued to respond a significant reduction in frequency threshold for self-stimulation was seen. Cocaine and amphetamine dose-dependently reduced frequency threshold in all rats tested. The non-specific serotonin antagonist, methysergide (5 mg/kg), reversed the inhibitory effects of MDMA on response rates and caused all rats to respond following MDMA (4 mg/kg). Methysergide did not affect MDMA's threshold-lowering properties and when administered alone methysergide had not effect on self-stimulation. These results suggest serotonergic involvement in the performance but not reinforcement- modulating effect of MDMA in the self-stimulation paradigm

MH  - Animal

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Nucleus Accumbens

MH  - drug effects

MH  - Rats

MH  - Rats,Wistar

MH  - Reward

MH  - Self Stimulation

MH  - Sensory Thresholds

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 97179111LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEDA - 19970416IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199706

UR  - PM:0009027397

SO  - Brain Res 1997 Jan 9 ;744(2):351-357

 

109

UI  - 100

AU  - Mallick A

AU  - Bodenham AR

AD  - Academic Unit of Anaesthesia, Leeds General Infirmary

TI  - MDMA induced hyperthermia: a survivor with an initial body temperature of 42.9 degrees C

AB  - A young male survived hyperpyrexia (42.9 degrees C) following MDMA ("Ecstasy") ingestion. He developed convulsions, rhabdomyolysis, metabolic acidosis, and respiratory failure. This was successfully managed by assisted ventilation, aggressive fluid therapy, and the early administration of dantrolene, in addition to cooling measures. This is the first report of a survivor with such a severe hyperpyrexia

MH  - Adult

MH  - Blood Gas Analysis

MH  - Body Temperature

MH  - Case Report

MH  - Dantrolene

MH  - therapeutic use

MH  - Emergency Service,Hospital

MH  - Fever

MH  - chemically induced

MH  - diagnosis

MH  - drug therapy

MH  - Hallucinogens

MH  - Human

MH  - Male

MH  - Muscle Relaxants,Central

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Substance-Related Disorders

MH  - complications

RP  - NOT IN FILE

NT  - UI - 97461666LA - EngRN - 0 (Hallucinogens)RN - 0 (Muscle Relaxants, Central)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 7261-97-4 (Dantrolene)PT - JOURNAL ARTICLEDA - 19971031IS - 1351-0622SB - MCY - ENGLANDJC - B0UAA - AuthorEM - 199801

UR  - PM:0009315942

SO  - J Accid Emerg Med 1997 Sep ;14(5):336-338

 

110

UI  - 97

AU  - Mann H

AU  - Ladenheim B

AU  - Hirata H

AU  - Moran TH

AU  - Cadet JL

AD  - Molecular Neuropsychiatry Section, NIDA, Addiction Research Center, Baltimore, MD 21224, USA

TI  - Differential toxic effects of methamphetamine (METH) and methylenedioxymethamphetamine (MDMA) in multidrug-resistant (mdr1a) knockout mice

AB  - The toxic effects of methamphetamine (METH) (2.5, 5.0 and 10.0 mg/kg) and methylenedioxymethamphetamine (MDMA) (5.0, 10.0 and 20.0 mg/kg) on dopaminergic systems were assessed in the striatum and of the nucleus accumbens in mdr1a wild-type and knockout mice. METH caused significant dose-dependent decreases of dopamine (DA) and DA transporters (DAT) in the striatum and the nucleus accumbens (NAc) of both wild-type and knockout mice. The lowest doses of METH (2.5 mg/kg) caused only small changes in the wild-type, but marked. decreases in the mdr1a knockout mice. The two higher doses (5 mg/kg and 10 mg/kg) caused similar changes in both strains of mice. In contrast to METH, MDMA caused greater percentage decreases in DAT in the wild-type mice. For example, the lowest dose (5 mg/kg) caused significant decreases in DAT in the NAc of wild-type but not of mdr1a knockout mice. The highest dose (20 mg/kg) caused similar changes in both the strains. These results suggest that METH and MDMA interact differentially with P- glycoproteins. These observations document, for the first time, a role for these proteins in the entry of METH and MDMA into the brain via the blood-brain barrier, with P-glycoprotein possibly facilitating the entry of MDMA but interfering with that of METH into the brain

MH  - Animal

MH  - Binding Sites

MH  - drug effects

MH  - Corpus Striatum

MH  - metabolism

MH  - Dopamine

MH  - Dose-Response Relationship,Drug

MH  - Genes,Mdr

MH  - genetics

MH  - Male

MH  - Methamphetamine

MH  - poisoning

MH  - Mice

MH  - Mice,Knockout

MH  - Mice,Mutant Strains

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Nucleus Accumbens

MH  - Serotonin Agents

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 98040360LA - EngRN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 51-61-6 (Dopamine)RN - 537-46-2 (Methamphetamine)PT - JOURNAL ARTICLEID - HD 24605/HD/NICHDDA - 19971223IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199802

UR  - PM:0009374204

SO  - Brain Res 1997 Sep 26 ;769(2):340-346

 

111

UI  - 113

AU  - Montgomery H

AU  - Myerson S

TI  - 3,4-methylenedioxymethamphetamine (MDMA, or "ecstasy") and associated hypoglycemia [letter]

MH  - Acute Disease

MH  - Adult

MH  - Case Report

MH  - Dantrolene

MH  - adverse effects

MH  - Female

MH  - Fever

MH  - chemically induced

MH  - Hallucinogens

MH  - poisoning

MH  - Human

MH  - Hypoglycemia

MH  - Muscle Relaxants,Central

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rhabdomyolysis

RP  - NOT IN FILE

NT  - UI - 97249064LA - EngRN - 0 (Hallucinogens)RN - 0 (Muscle Relaxants, Central)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 7261-97-4 (Dantrolene)PT - LETTERDA - 19970424IS - 0735-6757SB - MCY - UNITED STATESJC - AA2EM - 199706

UR  - PM:0009115539

SO  - Am J Emerg Med 1997 Mar ;15(2):218

 

112

UI  - 99

AU  - Nakahara Y

AU  - Kikura R

AD  - National Institute of Health Sciences, Tokyo, Japan

TI  - Hair analysis for drugs of abuse. XVIII. 3,4- Methylenedioxymethamphetamine (MDMA) disposition in hair roots and use in identification of acute MDMA poisoning

AB  - Disposition of 3,4-methylenedioxymethamphetamine (MDMA) in hair roots was studied using rats and the hair root samples were evaluated to prove acute MDMA poisoning. The back hair of male pigmented hairy rats (n = 6) was shaved and 5 d later the animals were intraperitoneally administered with acute poisonous doses (20, 40, 60, 80 and 100 mg/kg) of MDMA. Roots of the hairs were then plucked out with a hair nipper 5 min and, 0.5, 1, 2, 6 and 24 h after injection. The hair root samples were, directly or after being washed with detergent, extracted with methanol-5 N HCl (20:1) under ultrasonication in ice-cold water for 4 h. After filtration and evaporation, the residue was derivatized with pentafluoropropionic anhydride and analyzed by GC/MS. From all samples including the 5 min sample, MDMA was detected at high concentrations (up to 156 ng/mg) accompanied by 3,4-methylenedioxyamphetamine (MDA). Some of the animals died within 2 h after administration, but in the surviving rats the MDMA concentrations in the hair roots increased up to 6 h and then slowly decreased until 24 h. The remaining MDMA after washing apparently increased from 13-31% at 0.5 h to 51-83% at 24 h in the surviving rats. These facts show that most of drugs in the hair roots are not yet immobilized in the early stage and are thereafter gradually incorporated into the hair shaft. Increase of the MDMA concentration stopped soon after death of the animal, probably due to the cessation of hair growth. Although the ratios of MDA/MDMA steadily increased over time, those after death plateaued, probably due to the cessation of metabolism after death. It was clearly shown that MDMA is more quickly incorporated into and more firmly retained in hair than methamphetamine (MA) by comparing their disposition in hair roots

MH  - Acute Disease

MH  - Animal

MH  - Disease Models,Animal

MH  - Dose-Response Relationship,Drug

MH  - Hair

MH  - chemistry

MH  - Hallucinogens

MH  - poisoning

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Substance-Related Disorders

MH  - diagnosis

RP  - NOT IN FILE

NT  - UI - 97473094LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19971201IS - 0918-6158SB - MCY - JAPANJC - BPZAA - AuthorEM - 199802

UR  - PM:0009331978

SO  - Biol Pharm Bull 1997 Sep ;20(9):969-972

 

113

UI  - 107

AU  - Poland RE

AU  - Lutchmansingh P

AU  - McCracken JT

AU  - Zhao JP

AU  - Brammer GL

AU  - Grob CS

AU  - Boone KB

AU  - Pechnick RN

AD  - Department of Psychiatry, Harbor-UCLA Medical Center, Torrance 90509, USA

TI  - Abnormal ACTH and prolactin responses to fenfluramine in rats exposed to single and multiple doses of MDMA

AB  - The present study examined the persistent functional consequences associated with exposure to single and multiple doses of (+/-) 3,4- methylenedioxymethamphetamine (MDMA) as reflected by the neuroendocrine responses to d,l-fenfluramine (FEN). Adult male rats were administered a single dose of MDMA (20 mg/kg, s.c.) and challenged 2 weeks later with saline or FEN (2, 4, 6 and 8 mg/kg, s.c.). The corticotropin (ACTH) response to FEN (6 and 8 mg/kg) was blunted and the prolactin response to FEN (4 and 6 mg/kg) was enhanced in MDMA pre-treated rats. The ACTH and prolactin responses to FEN (6 mg/kg, s.c.) were then evaluated 4, 8 and 12 months after exposure to single and multiple doses MDMA (20 mg/kg, s.c. and 20 mg/kg, s.c., bid, x 4 days, respectively). The ACTH response to FEN was significantly reduced at 4 and 8 months in both MDMA treatment groups, and at 12 months in the multiple dose group only. In contrast, the prolactin response to FEN was enhanced in both groups of MDMA treated rats at 4 months, but only in the multiple dose group at 8 months. By 12 months, the prolactin response to FEN had normalized. Following multiple doses of MDMA, 5-HT concentrations were reduced significantly in the frontal cortex at 4 and 12 months. The results indicate that exposure to single or multiple doses of MDMA can produce functional alterations which can persist for months, whereas the biochemical sequelae were less robust and shorter lived

MH  - Animal

MH  - Cerebral Cortex

MH  - drug effects

MH  - Corticotropin

MH  - blood

MH  - metabolism

MH  - Dose-Response Relationship,Drug

MH  - Fenfluramine

MH  - pharmacology

MH  - Hallucinogens

MH  - Hippocampus

MH  - Hypothalamus

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Prolactin

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Serotonin Agents

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 97370396LA - EngRN - 0 (Hallucinogens)RN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 458-24-2 (Fenfluramine)RN - 50-67-9 (Serotonin)RN - 9002-60-2 (Corticotropin)RN - 9002-62-4 (Prolactin)PT - JOURNAL ARTICLEID - DA06863/DA/NIDAID - MH00534/MH/NIMHID - MH00722/MH/NIMHDA - 19970827IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199710

UR  - PM:0009226745

SO  - Psychopharmacology (Berl) 1997 Jun ;131(4):411-419

 

114

UI  - 101

AU  - Schwartz RH

AU  - Miller NS

AD  - University of Virginia School of Medicine, Charlottesville, Virginia, USA

TI  - MDMA (ecstasy) and the rave: a review

MH  - Adolescence

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - poisoning

MH  - diagnosis

MH  - therapy

MH  - Street Drugs

MH  - Substance Abuse Detection

RP  - NOT IN FILE

NT  - UI - 97456227LA - EngRN - 0 (Street Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19971014IS - 0031-4005SB - ASB - MCY - UNITED STATESJC - OXVEM - 199712

UR  - PM:0009310529

SO  - Pediatrics 1997 Oct ;100(4):705-708

 

115

UI  - 115

AU  - Simantov R

AU  - Tauber M

AD  - Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel

TI  - The abused drug MDMA (Ecstasy) induces programmed death of human serotonergic cells

AB  - The widely abused amphetamine analog 3,4-methylenedioxymethamphetamine (MDMA, also called "ecstasy") induces hallucination and psychostimulation, as well as long-term neuropsychiatric behaviors such as panic and psychosis. In rodents and monkeys, MDMA is cytotoxic to serotonergic neurons, but this is less clear with humans. Herein, MDMA was cytotoxic to human serotonergic JAR cells; it altered the cell cycle, increased G2/M phase arrest, and induced DNA fragmentation in a cycloheximide-sensitive way. This apoptosis was not observed in nonserotonergic human NMB cells. The stereospecific effect of amphetamines in JAR cells, and the key role of NO and dopamine in MDMA- induced apoptosis were determined. The relevancy of MDMA-induced cell death to drug users is discussed

MH  - Apoptosis

MH  - drug effects

MH  - Catecholamines

MH  - physiology

MH  - Cell Cycle

MH  - Cell Survival

MH  - Choriocarcinoma

MH  - DNA Fragmentation

MH  - Female

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - toxicity

MH  - Nitric Oxide

MH  - Serotonin Agents

MH  - Support,Non-U.S.Gov't

MH  - Tumor Cells,Cultured

MH  - Uterine Neoplasms

RP  - NOT IN FILE

NT  - UI - 97192137LA - EngRN - 0 (Catecholamines)RN - 0 (Serotonin Agents)RN - 10102-43-9 (Nitric Oxide)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19970311IS - 0892-6638SB - MSB - XCY - UNITED STATESJC - FASAA - AuthorEM - 199705

UR  - PM:0009039956

SO  - FASEB J 1997 Feb ;11(2):141-146

 

116

UI  - 112

AU  - Spatt J

AU  - Glawar B

AU  - Mamoli B

TI  - A pure amnestic syndrome after MDMA ("ecstasy") ingestion [letter]

MH  - Administration,Oral

MH  - Adult

MH  - Amnesia

MH  - chemically induced

MH  - Case Report

MH  - Female

MH  - Globus Pallidus

MH  - pathology

MH  - Hallucinogens

MH  - poisoning

MH  - Human

MH  - Magnetic Resonance Imaging

MH  - N-Methyl-3,4-methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 97252590LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - LETTERDA - 19970424IS - 0022-3050SB - MCY - ENGLANDJC - JBBEM - 199706

UR  - PM:0009120467

SO  - J Neurol Neurosurg Psychiatry 1997 Apr ;62(4):418-419

 

117

UI  - 114

AU  - Thomasius R

AU  - Schmolke M

AU  - Kraus D

AD  - Psychiatrische und Nerven- und Poliklinik der Universitat Hamburg

TI  - [MDMA ("Ecstasy") use--an overview of psychiatric and medical sequelae (see comments)]

AB  - Epidemiological research and Substance Abuse Warning Systems point to a sharp increase in the use of "Ecstasy" (MDMA), as well as to structural changes in the drug scene in and outside Europe. For some consumers, "Ecstasy" opens the door to the abuse of other illegal substances. Since the mid-eighties psychiatric complications and consequences of the abuse of MDMA have been reported in at least 48 cases. It is necessary to differentiate between acute psychiatric complications, which subside completely when the level of intoxication comes down, toxic psychoses and long-term psychiatric diseases as a consequence of substance abuse. The latter involve atypical and paranoid psychoses, depressions, panic disorders, depersonalisation and behavioural disorders. Convulsive seizures are among the most common problems involving the central nervous system. Furthermore, there have been reports on cerebrovascular accidents and intracranial haemorrhages. Literature reports on at least 53 cases of medical complications in abusers of MDMA, 14 of which came to a lethal end. Research still blatantly lacks prospective epidemiological and clinical studies on a sufficiently large scale to identify different developments of dependency and predictors of harmful and unhealthy consumption

MH  - Brain

MH  - drug effects

MH  - English Abstract

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - Neurologic Examination

MH  - Psychoses,Substance-Induced

MH  - diagnosis

MH  - psychology

MH  - Seizures

MH  - chemically induced

MH  - Substance-Related Disorders

RP  - NOT IN FILE

NT  - UI - 97240864LA - GerRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19970522IS - 0720-4299SB - MCY - GERMANYJC - F67AA - AuthorEM - 199707RO - M:CNR

UR  - PM:0009157047

SO  - Fortschr Neurol Psychiatr 1997 Feb ;65(2):49-61

 

118

UI  - 72

AU  - Tretter F

TI  - [Entactogenic drugs "ecstasy" (MDMA), "eve" (MDE) and other ring- substituted methamphetamine derivatives. A new class of substances among illegal designer drugs? (letter; comment)]

MH  - Designer Drugs

MH  - adverse effects

MH  - Human

MH  - Methamphetamine

MH  - analogs & derivatives

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Psychoses,Substance-Induced

MH  - etiology

MH  - Risk Factors

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 98403276LA - GerRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 537-46-2 (Methamphetamine)PT - COMMENTPT - LETTERDA - 19981028IS - 0028-2804SB - MCY - GERMANYJC - NWSEM - 199901RO - M:CNR

UR  - PM:0009732739

SO  - Nervenarzt 1997 Nov ;68(11):922-923

 

119

UI  - 98

AU  - Yeh SY

AD  - Molecular Neuropsychiatry Section, National Institute on Drug Abuse, National Institute of Health, Baltimore, MD 21224, USA

TI  - Effects of salicylate on 3,4-methylenedioxymethamphetamine (MDMA)- induced neurotoxicity in rats

AB  - The drug 3,4-methylenedioxymethamphetamine (MDMA) is a serotonergic neurotoxicant that causes hyperthermia and depletion of serotonin (5- HT) and 5-hydroxy-indole-3-acetic acid (5-HIAA) in the central nervous system. Formation of neurotoxic metabolites of MDMA, e.g., 2,4,5- trihydroxy-methamphetamine and 2,4,5-trihydroxyamphetamine, involves hydroxyl and/or superoxide free radicals. The present study was designed to determine whether the hydroxyl free-radical-trapping agent salicylate could provide protection against MDMA neurotoxicity in rats. In the acute studies, sodium salicylate (12.5-400 mg/kg, calculated as free acid) was injected interperitoneally (i.p.) 1 h before subcutaneous (s.c.) injections of MDMA (20 mg/kg as base). In the chronic studies, sodium salicylate (3.1-100 mg/kg) was injected i.p. 1 h before repeated s.c. injections of MDMA (10 mg/kg as base, twice daily, at 0830 and 1730 h for 4 consecutive days). Repeated MDMA administration depleted contents of 5-HT and 5-HIAA in the frontal cortex, hippocampus and striatum. Coadministration of salicylate plus MDMA did not significantly alter MDMA-induced depletion of 5-HT and 5- HIAA in these tissues. Thus, salicylate, a hydroxyl free-radical- trapping agent, does not protect against MDMA-induced hyperthermia and depletion of 5-HT and 5-HIAA. These observations suggest that MDMA- induced neurotoxicity may occur mainly through the production of superoxide or other radicals rather than hydroxyl free radicals. Salicylate actually potentiated MDMA-induced hyperthermia and lethality, findings that might be of clinical relevance

MH  - Adrenergic Uptake Inhibitors

MH  - toxicity

MH  - Animal

MH  - Biogenic Monoamines

MH  - metabolism

MH  - Body Temperature

MH  - drug effects

MH  - Brain Chemistry

MH  - Free Radical Scavengers

MH  - administration & dosage

MH  - pharmacology

MH  - Hydroxyl Radical

MH  - Injections,Intraperitoneal

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Nervous System Diseases

MH  - chemically induced

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Salicylic Acids

MH  - Superoxides

RP  - NOT IN FILE

NT  - UI - 97469600LA - EngRN - 0 (Adrenergic Uptake Inhibitors)RN - 0 (Biogenic Monoamines)RN - 0 (Free Radical Scavengers)RN - 0 (Salicylic Acids)RN - 11062-77-4 (Superoxides)RN - 3352-57-6 (Hydroxyl Radical)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 69-72-7 (Salicylic Acid)PT - JOURNAL ARTICLEDA - 19980206IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199804

UR  - PM:0009329062

SO  - Pharmacol Biochem Behav 1997 Nov ;58(3):701-708

 

120

UI  - 138

AU  - Baker LE

AU  - Makhay MM

AD  - Department of Psychology, Western Michigan University, Kalamazoo 49008, USA

TI  - Effects of (+)-fenfluramine on 3,4-methylenedioxymethamphetamine (MDMA) discrimination in rats

AB  - This study examined the effects of a presumed neurotoxic dose regimen of (+)-fenfluramine on the discrimination of MDMA and (+)-amphetamine in male Sprague-Dawley rats trained to discriminate 1.5 mg/kg MDMA from saline in a two-choice operant task. Substitution tests were conducted with saline, several doses of MDMA (0.19-1.5 mg/kg), and (+)- amphetamine (0.125-1.0 mg/kg) prior to and again following the administration of (+)-fenfluramine (4.0 mg/kg twice a day for 4 days; n = 11) or a similar pattern of saline injections (n = 10). During pretreatment substitution tests, lower doses of MDMA elicited drug- appropriate responding in a dose-dependent manner, although none of these doses substituted for the training dose. Likewise, no dose of (+)- amphetamine substituted for the training drug during pretreatment substitution tests. The discrimination of MDMA was disrupted in some animals following (+)-fenfluramine treatment, but with subsequent training, discrimination criteria were met. In posttreatment substitution tests, the lowest dose of MDMA produced significantly higher drug-appropriate responding in (+)-fenfluramine treated animals but not in saline-treated animals. The amount of drug-appropriate responding during posttreatment substitution tests with (+)-amphetamine varied little from pretreatment substitution tests in saline-treated animals, but was greater at all doses in (+)-fenfluramine-treated animals; the highest dose of (+)-amphetamine substituted for MDMA subsequent to (+)-fenfluramine treatment. These results support previous findings that the long-lasting serotonergic effects of fenfluramine may have functional consequences that can be detected using a drug discrimination procedure. Specifically, serotonin depletion may unmask or strengthen the stimulant-like effects of MDMA

MH  - Animal

MH  - Dextroamphetamine

MH  - pharmacology

MH  - Discrimination (Psychology)

MH  - drug effects

MH  - Dopamine Agents

MH  - Dose-Response Relationship,Drug

MH  - Fenfluramine

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Reinforcement Schedule

MH  - Serotonin Agents

RP  - NOT IN FILE

NT  - UI - 96403880LA - EngRN - 0 (Dopamine Agents)RN - 0 (Serotonin Agents)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 458-24-2 (Fenfluramine)RN - 51-64-9 (Dextroamphetamine)PT - JOURNAL ARTICLEDA - 19970116IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199703

UR  - PM:0008808158

SO  - Pharmacol Biochem Behav 1996 Feb ;53(2):455-461

 

121

UI  - 140

AU  - Bitsch A

AU  - Thiel A

AU  - Rieckmann P

AU  - Prange H

AD  - Department of Neurology, Georg August University, Gottingen, Germany

TI  - Acute inflammatory CNS disease after MDMA ('ecstasy')

MH  - Acute Disease

MH  - Adult

MH  - Case Report

MH  - Central Nervous System Diseases

MH  - chemically induced

MH  - diagnosis

MH  - Hallucinogens

MH  - adverse effects

MH  - chemistry

MH  - Human

MH  - Inflammation

MH  - Magnetic Resonance Imaging

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 97018104LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19970103IS - 0014-3022SB - MCY - SWITZERLANDJC - ENFEM - 199703

UR  - PM:0008864721

SO  - Eur Neurol 1996  ;36(5):328-329

 

122

UI  - 120

AU  - Centini F

AU  - Masti A

AU  - Barni C

AD  - Department of Legal Medicine, University of Siena, Italy

TI  - Quantitative and qualitative analysis of MDMA, MDEA, MA and amphetamine in urine by headspace/solid phase micro-extraction (SPME) and GC/MS

AB  - The results of qualitative and quantitative analysis of some amphetamines and their analogs isolated from urine samples by solid phase micro-extraction with polydimethylsiloxane fibers are reported. The analytical method employed was gas-chromatography/mass spectrometry of head space samples

MH  - Hallucinogens

MH  - urine

MH  - Human

MH  - Mass Fragmentography

MH  - methods

MH  - Methamphetamine

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 97185216LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 537-46-2 (Methamphetamine)RN - 82801-81-8 (3,4-methylenedioxyethamphetamine)PT - JOURNAL ARTICLEDA - 19970311IS - 0379-0738SB - MCY - IRELANDJC - F49AA - AuthorEM - 199705

UR  - PM:0009032950

SO  - Forensic Sci Int 1996 Dec 27 ;83(3):161-166

 

123

UI  - 135

AU  - Cohen RS

TI  - Adverse symptomatology and suicide associated with the use of methylenedioxymethamphetamine (MDMA; "Ecstasy")

MH  - Adolescence

MH  - Adult

MH  - Case Report

MH  - Combined Modality Therapy

MH  - Depressive Disorder

MH  - chemically induced

MH  - psychology

MH  - rehabilitation

MH  - Female

MH  - Hallucinogens

MH  - administration & dosage

MH  - adverse effects

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Substance-Related Disorders

MH  - Suicide

RP  - NOT IN FILE

NT  - UI - 96301309LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19961002IS - 0006-3223SB - MCY - UNITED STATESJC - A3SEM - 199612

UR  - PM:0008731525

SO  - Biol Psychiatry 1996 May 1 ;39(9):819-820

 

124

UI  - 127

AU  - Cook TM

TI  - Cerebral oedema after MDMA ("ecstasy") and unrestricted water intake. Values for plasma osmolality may have been wrong [letter; comment]

MH  - Brain Edema

MH  - chemically induced

MH  - Drinking

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Osmolar Concentration

MH  - Sodium

MH  - blood

RP  - NOT IN FILE

NT  - UI - 96407758LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 7440-23-5 (Sodium)PT - COMMENTPT - LETTERDA - 19961024IS - 0959-8138SB - ASB - MSB - XCY - ENGLANDJC - BMJEM - 199612RO - M:LC1

UR  - PM:0008811775

SO  - BMJ 1996 Sep 14 ;313(7058):689

 

125

UI  - 128

AU  - Dar KJ

AU  - McBrien ME

AD  - New York Hospital-Cornell Medical Center, 1520 East 70th Street, Starr 505, New York, NY 10021, USA

TI  - MDMA induced hyperthermia: report of a fatality and review of current therapy

AB  - Ingestion of 3,4-methylene dioxymethamphetamine (MDMA), commonly known as "Ecstasy", can produce toxicity that is characterised by hyperthermia, coagulopathy, rhabdomyolysis and renal failure. We report a fatality associated with MDMA ingestion and briefly review the current literature on MDMA-induced hyperthermia

MH  - Adolescence

MH  - Blood Coagulation Disorders

MH  - chemically induced

MH  - Case Report

MH  - Dantrolene

MH  - therapeutic use

MH  - Fatal Outcome

MH  - Fever

MH  - drug therapy

MH  - Hallucinogens

MH  - poisoning

MH  - Human

MH  - Kidney Failure,Acute

MH  - Male

MH  - Muscle Relaxants,Central

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rhabdomyolysis

RP  - NOT IN FILE

NT  - UI - 97061411LA - EngRN - 0 (Hallucinogens)RN - 0 (Muscle Relaxants, Central)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 7261-97-4 (Dantrolene)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW OF REPORTED CASESDA - 19970218IS - 0342-4642SB - MCY - UNITED STATESJC - H2JAA - AuthorEM - 199704

UR  - PM:0008905441

SO  - Intensive Care Med 1996 Sep ;22(9):995-996

 

126

UI  - 139

AU  - Elk C

AD  - Pennsylvania State University, USA

TI  - MDMA (Ecstacy): useful information for health professionals involved in drug education programs

AB  - 3,4-Methylenedioxymethamphetamine (MDMA; "Ecstacy") is an amphetamine derivative that is related chemically to both amphetamines and hallucinogens. Despite reports of an increase in MDMA usage among adolescents and young adults in the past decade, systematic scientific information concerning MDMA and its effects remains insufficient, thus limiting or eliminating MDMA from inclusion in the drug education curriculum

MH  - Adult

MH  - Hallucinogens

MH  - chemistry

MH  - poisoning

MH  - therapeutic use

MH  - Health Education

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Substance-Related Disorders

MH  - epidemiology

MH  - prevention & control

RP  - NOT IN FILE

NT  - UI - 97224673LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19970410IS - 0047-2379CY - UNITED STATESJC - JL7AA - AuthorEM - 199706

UR  - PM:0009071057

SO  - J Drug Educ 1996  ;26(4):349-356

 

127

UI  - 125

AU  - Finch E

AU  - Sell L

AU  - Arnold D

TI  - Cerebral oedema after MDMA ("ecstasy") and unrestricted water intake. Drug workers emphasise that water is not an antidote to drug [letter; comment]

MH  - Antidotes

MH  - Brain Edema

MH  - chemically induced

MH  - Drinking

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Water

RP  - NOT IN FILE

NT  - UI - 96407760LA - EngRN - 0 (Antidotes)RN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 7732-18-5 (Water)PT - COMMENTPT - LETTERDA - 19961024IS - 0959-8138SB - ASB - MSB - XCY - ENGLANDJC - BMJEM - 199612RO - M:LC1

UR  - PM:0008811777

SO  - BMJ 1996 Sep 14 ;313(7058):690

 

128

UI  - 141

AU  - Fineschi V

AU  - Masti A

AD  - Department of Forensic Science, University of Siena, Policlinico Le Scotte, Italy

TI  - Fatal poisoning by MDMA (ecstasy) and MDEA: a case report

AB  - The first observation of lethal recreational use of MDMA (ecstasy) and MDEA in Italy is reported, together with extensive toxicological and histopathological documentation. Findings such as disseminated intravascular coagulation, rarely reported before, are colocated in the framework of the toxic syndrome for a better definition of criteria for forensic diagnosis

MH  - Capillaries

MH  - pathology

MH  - Designer Drugs

MH  - pharmacokinetics

MH  - poisoning

MH  - Fluorescent Antibody Technique

MH  - Hallucinogens

MH  - Human

MH  - Kidney Tubules

MH  - Lung

MH  - blood supply

MH  - Mass Fragmentography

MH  - Myoglobinuria

MH  - blood

MH  - chemically induced

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Overdose

MH  - Pulmonary Embolism

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 96285881LA - EngRN - 0 (Designer Drugs)RN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 82801-81-8 (3,4-methylenedioxyethamphetamine)PT - JOURNAL ARTICLEDA - 19961002IS - 0937-9827SB - MCY - GERMANYJC - AX1AA - AuthorEM - 199612

UR  - PM:0008721431

SO  - Int J Legal Med 1996  ;108(5):272-275

 

129

UI  - 134

AU  - Gouzoulis-Mayfrank E

AU  - Hermle L

AU  - Kovar KA

AU  - Sass H

AD  - Psychiatrische Klinik, Medizinische Einrichtungen der RWTH, Aachen

TI  - [Entactogenic drugs "ecstasy" (MDMA), "eve" (MDE) and other ring- substituted methamphetamine derivatives. A new class of substances among illegal designer drugs? (see comments)]

AB  - The widely used recreational drugs 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy) and 3,4-methylenedioxyethamphetamine (MDE, Eve) occupy an intermediate position between stimulants and hallucinogens. Besides stimulation similar to that caused by amphetamines, they usually induce a pleasant, easily controllable emotional state with relaxation, fearlessness and feelings of happiness, but they sometimes also have stronger, hallucinogenic, effects. A number of pharmacological studies support the hypothesis that these drugs make up a distinct class of psychoactive substances, which have been designated "entactogens." On the drug scene, MDMA and MDE are considered "safe." However, this view must be corrected. Complications are rare, but potentially devastating ([long-lasting anxiety and depressive syndromes in chronic users, fatalities with hyperpyrexia, rhabdomyolysis and DIC syndrome (disseminated instravascular coagulation), possible hepatotoxicity]. Moreover, the clinical relevance of animal studies showing neurotoxic effects of MDMA on central serotonergic pathways is still not clear

MH  - Animal

MH  - Designer Drugs

MH  - adverse effects

MH  - English Abstract

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Risk Factors

MH  - Substance Withdrawal Syndrome

MH  - diagnosis

MH  - Substance-Related Disorders

MH  - psychology

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 97128124LA - GerRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 82801-81-8 (3,4-methylenedioxyethamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19970129IS - 0028-2804SB - MCY - GERMANYJC - NWSAA - AuthorEM - 199704RO - M:CNR

UR  - PM:0009005345

SO  - Nervenarzt 1996 May ;67(5):369-380

 

130

UI  - 124

AU  - Helmlin HJ

AU  - Bracher K

AU  - Bourquin D

AU  - Vonlanthen D

AU  - Brenneisen R

AD  - Institute of Pharmacy, University of Bern, Switzerland

TI  - Analysis of 3,4-methylenedioxymethamphetamine (MDMA) and its metabolites in plasma and urine by HPLC-DAD and GC-MS [see comments]

AB  - In Europe, the compound 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy, Adam), in addition to cannabis, is the most abused illicit drug at all-night "techno" parties. Methods for the determination of MDMA and its metabolites, 4-hydroxy-3-methoxymethamphetamine (HMMA), 3,4-dihydroxy-methamphetamine (HHMA), 3,4-methylenedioxyamphetamine (MDA), 4-hydroxy-3-methoxyamphetamine (HMA), and 3,4- dihydroxyamphetamine (HHA), in biological fluids were established. Plasma and urine samples were collected from two patients in a controlled clinical study over periods of 9 and 22 h, respectively. MDMA and MDA were determined in plasma and urine by reversed-phase high- performance liquid chromatography with diode array detection (HPLC-DAD) after solid-phase extraction on cation-exchange columns. Acidic or enzymatic hydrolysis was necessary to detect HMMA, HMA, HHMA, and HHA, which are mainly excreted as glucuronides. Gas chromatography-mass spectrometry (GC-MS) was used for confirmation. Sample extraction and on-disc derivatization with heptafluorobutyric anhydride (HFBA) were performed on Toxi-Lab SPEC solid-phase extraction concentrators. After administration of a single oral dose of 1.5 mg/kg body weight MDMA, peak plasma levels of 331 ng/ml MDMA and 15 ng/mL MDA were measured after 2 h and 6.3 h, respectively. Peak concentrations of 28.1 micrograms/mL MDMA in urine appeared after 21.5 h. Up to 2.3 micrograms/mL MDA, 35.1 micrograms/mL HMMA, and 2.1 micrograms/mL HMA were measured within 16-21.5 h. Conjugated HMMA and HHMA are the main urinary metabolites of MDMA

MH  - Administration,Oral

MH  - Adolescence

MH  - Adult

MH  - Chromatography,High Pressure Liquid

MH  - Deoxyepinephrine

MH  - analogs & derivatives

MH  - blood

MH  - urine

MH  - Female

MH  - Fluorocarbons

MH  - chemistry

MH  - Hallucinogens

MH  - administration & dosage

MH  - Human

MH  - Hydrolysis

MH  - Ion Exchange Resins

MH  - Male

MH  - Mass Fragmentography

MH  - Methamphetamine

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Reference Standards

MH  - Support,Non-U.S.Gov't

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 97044609LA - EngRN - 0 (Fluorocarbons)RN - 0 (Hallucinogens)RN - 0 (Ion Exchange Resins)RN - 117652-28-5 (4-hydroxy-3-methoxymethamphetamine)RN - 15398-87-5 (alpha-methylepinine)RN - 336-59-4 (heptafluorobutyric anhydride)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 501-15-5 (Deoxyepinephrine)RN - 537-46-2 (Methamphetamine)RN - 555-64-6 (alpha-methyldopamine)PT - CLINICAL TRIALPT - CONTROLLED CLINICAL TRIALPT - JOURNAL ARTICLEDA - 19970130IS - 0146-4760SB - MCY - UNITED STATESJC - K4RAA - AuthorEM - 199704RO - M:LC2

UR  - PM:0008889680

SO  - J Anal Toxicol 1996 Oct ;20(6):432-440

 

131

UI  - 136

AU  - Holden R

AU  - Jackson MA

TI  - Near-fatal hyponatraemic coma due to vasopressin over-secretion after "ecstasy" (3,4-MDMA) [letter]

MH  - Adult

MH  - Case Report

MH  - Coma

MH  - chemically induced

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Hyponatremia

MH  - Male

MH  - Serotonin Agents

MH  - Vasopressins

MH  - secretion

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 96185286LA - EngRN - 0 (Hallucinogens)RN - 0 (Serotonin Agents)RN - 0 (Vasopressins)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - LETTERDA - 19960517IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199607

UR  - PM:0008606600

SO  - Lancet 1996 Apr 13 ;347(9007):1052

 

132

UI  - 131

AU  - Kehne JH

AU  - Ketteler HJ

AU  - McCloskey TC

AU  - Sullivan CK

AU  - Dudley MW

AU  - Schmidt CJ

AD  - Hoechst Marion Roussel, Inc., Cincinnati, OH 45215, USA

TI  - Effects of the selective 5-HT2A receptor antagonist MDL 100,907 on MDMA- induced locomotor stimulation in rats

AB  - (+/-)3,4-Methylenedioxymethamphetamine (MDMA) releases dopamine and serotonin in vivo and stimulates locomotor activity. Previous work demonstrated that MDMA-stimulated dopamine release could be reduced by the selective 5-HT2A receptor antagonist [R-(+)-a- (2,3- dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidinem ethanol] (MDL 100,907). In the present study MDL 100,907 significantly reduced MDMA-stimulated locomotion without affecting basal levels of locomotion. Other agents with 5-HT2A antagonist activity (ritanserin, clozapine, MDL 28,133A, or methiothepin), as well as agents that block 5-HT1A-(propranolol), D2-(haloperidol), or D1 receptors (SCH 23390) also reduced MDMA-stimulated locomotion. Intraventricularly administered 5,7-dihydroxytryptamine decreased regional 5-HT levels and attenuated MDMA-stimulated locomotion. These data support the conclusion that serotonin released onto 5-HT2A receptors contributes to MDMA-stimulated locomotion and suggest that MDMA-stimulated locomotion may be useful as an in vivo behavioral measure of 5-HT2A antagonism. The data also support previous reports of contributions of 5-HT1A, D1 and D2 receptors to MDMA-stimulated locomotion. A preliminary time- course analysis indicating time-dependent contributions of different receptors to MDMA-stimulated locomotion suggests the potential utility of this model for characterizing potential atypical antipsychotic compounds

MH  - Animal

MH  - Brain Chemistry

MH  - drug effects

MH  - Clozapine

MH  - pharmacology

MH  - Comparative Study

MH  - Dopamine Antagonists

MH  - Fluorobenzenes

MH  - Male

MH  - Methiothepin

MH  - Motor Activity

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - antagonists & inhibitors

MH  - Piperidines

MH  - Presynaptic Terminals

MH  - metabolism

MH  - Rats

MH  - Receptors,Neurotransmitter

MH  - Ritanserin

MH  - Serotonin

MH  - Serotonin Agents

MH  - Serotonin Antagonists

MH  - Stimulation,Chemical

MH  - 5,7-Dihydroxytryptamine

RP  - NOT IN FILE

NT  - UI - 96437738LA - EngRN - 0 (Dopamine Antagonists)RN - 0 (Fluorobenzenes)RN - 0 (Piperidines)RN - 0 (Receptors, Neurotransmitter)RN - 0 (Serotonin Agents)RN - 0 (Serotonin Antagonists)RN - 139290-65-6 (MDL 100907)RN - 20229-30-5 (Methiothepin)RN - 31363-74-3 (5,7-Dihydroxytryptamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 5786-21-0 (Clozapine)RN - 87051-43-2 (Ritanserin)PT - JOURNAL ARTICLEDA - 19961226IS - 0893-133XSB - MCY - UNITED STATESJC - ADQAA - AuthorEM - 199702

UR  - PM:0008840347

SO  - Neuropsychopharmacology 1996 Aug ;15(2):116-124

 

133

UI  - 142

AU  - Keup W

TI  - [MDMA--"ecstasy"]

MH  - Cross-Sectional Studies

MH  - Germany

MH  - epidemiology

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Incidence

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Substance-Related Disorders

MH  - rehabilitation

RP  - NOT IN FILE

NT  - UI - 96158204LA - GerRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19960321IS - 0342-9601CY - GERMANYJC - M5GEM - 199605

UR  - PM:0008583979

SO  - Med Monatsschr Pharm 1996 Jan ;19(1):2-5

 

134

UI  - 122

AU  - Kunsman GW

AU  - Levine B

AU  - Kuhlman JJ

AU  - Jones RL

AU  - Hughes RO

AU  - Fujiyama CI

AU  - Smith ML

AD  - Division of Forensic Toxicology, Office of the Armed Forces Medical Examiner, Armed Forces Institute of Pathology, Washington, DC, USA

TI  - MDA-MDMA concentrations in urine specimens

AB  - Urine specimens collected from active-duty U.S. Army personnel were submitted for analysis to the Tripler Army Medical Center, Forensic Toxicology Drug Testing Laboratory as part of the random drug testing program. During an 18-month drug-screening period, 34 specimens tested positive for amphetamines with the Roche Abuscreen Radioimmunoassay for Methamphetamine (High Specificity); based on gas chromatographic-mass spectrometric (GC-MS) analysis, the presence of 3,4- methylenedioxymethamphetamine (MDMA) was suspected. These samples were subsequently submitted to the Division of Forensic Toxicology, Office of the Armed Forces Medical Examiner, Armed Forces Institute of Pathology for further testing. All 34 samples screened positive using both the Abbott TDx Amphetamine/ Methamphetamine II assay and the Amphetamine class assay. Confirmation and quantitation by GC-MS revealed the presence of both MDMA and 3,4-methylenedioxyamphetamine (MDA) in all samples. The MDMA concentrations ranged from 0.38 to 96.2 mg/L (mean, 13.4 mg/L) and the MDA concentrations ranged from 0.15 to 8.6 mg/L (mean, 1.6 mg/L). The mean ratio of MDA, the N-demethylation metabolite of MDMA, to MDMA was 0.15, similar to the ratio of amphetamine, the N-demethylation metabolite of methamphetamine, to methamphetamine of 0.10. The presence of MDA in urine specimens at a concentration approximately 10-15% that of the MDMA present is consistent with MDMA metabolism, which may be indicative of the use of MDMA only, as compared with the combined use of both drugs

MH  - Designer Drugs

MH  - metabolism

MH  - Female

MH  - Hallucinogens

MH  - urine

MH  - Human

MH  - Immunoassay

MH  - Male

MH  - Mass Fragmentography

MH  - Military Personnel

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Substance Abuse Detection

MH  - Support,Non-U.S.Gov't

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 97088361LA - EngRN - 0 (Designer Drugs)RN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19970226IS - 0146-4760SB - MCY - UNITED STATESJC - K4RAA - AuthorEM - 199705

UR  - PM:0008934299

SO  - J Anal Toxicol 1996 Nov ;20(7):517-521

 

135

UI  - 132

AU  - Malberg JE

AU  - Sabol KE

AU  - Seiden LS

AD  - University of Chicago, Department of Pharmacological and Physiological Sciences, Illinois, USA

TI  - Co-administration of MDMA with drugs that protect against MDMA neurotoxicity produces different effects on body temperature in the rat

AB  - The substituted amphetamine 3,4-methylenedioxymethamphetamine (MDMA) has been shown to be neurotoxic to serotonin (5HT) terminals in the rat, and rat body temperature (TEMP) has been shown to affect this neurotoxicity. This study looked at the effect on CORE TEMP of three drugs that protect against MDMA neurotoxicity in the rat. Male Holtzmann rats were injected with a control saline (SAL) injection or with ketanserin (KET; 6 mg/kg), alpha-methyl-p-tyrosine (AMPT; 75 mg/kg) or fluoxetine (FLUOX; 10 mg/kg) before a 40-mg/kg MDMA or SAL injection. CORE TEMP was recorded throughout the study using a noninvasive peritoneally implanted temperature probe. Rats pretreated with KET had no change in CORE TEMP until MDMA was injected, at which time an immediate hypothermia was seen that continued for 180 minutes, with a peak low of 34.7 degrees C. Rats treated with AMPT had no change in CORE TEMP until the MDMA was injected, at which time an immediate hypothermia was seen that continued for 240 min., with a peak low of 34.3 degrees C. Two weeks later, brain regions were analyzed for 5-HT and 5-hydroxindole acetic acid levels. MDMA produced significant (P < .05) decreases in 5-HT and 5-hydroxindole acetic acid levels in the frontal cortex, somatosensory cortex, striatum and hippocampus, and pretreatment with KET or AMPT prevented these depletions. When rats were given the KET/MDMA or AMPT/MDMA drug injections and warmed to prevent hypothermia, the protection against neurotoxicity was removed, which indicated that the hypothermia mediated the protective effects of KET and AMPT. In comparison with the hypothermia seen with AMPT or KET pretreatment, pretreatment with FLUOX had no effect on CORE TEMP. The rats given the FLUOX/MDMA treatment did not have different CORE TEMPs than rats given SAL/MDMA. The FLUOX pretreatment protected against MDMA- induced 5-HT and 5-hydroxindole acetic acid depletions in the frontal cortex, somatosensory cortex, striatum and hippocampus. This study suggests that a decrease in CORE TEMP may be a mechanism of protection against MDMA neurotoxicity by some drugs but that there is also a mechanism of protection that is independent of a change in body temperature

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - Drug Combinations

MH  - Fluoxetine

MH  - pharmacology

MH  - Ketanserin

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Rats

MH  - Support,U.S.Gov't,P.H.S.

MH  - Tyrosine

RP  - NOT IN FILE

NT  - UI - 96289314LA - EngRN - 0 (Drug Combinations)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 54910-89-3 (Fluoxetine)RN - 55520-40-6 (Tyrosine)RN - 74050-98-9 (Ketanserin)PT - JOURNAL ARTICLEID - DA-07255-01/DA/NIDAID - MA-00085ID - RSA-10562DA - 19960923IS - 0022-3565SB - MCY - UNITED STATESJC - JP3AA - AuthorEM - 199611

UR  - PM:0008764359

SO  - J Pharmacol Exp Ther 1996 Jul ;278(1):258-267

 

136

UI  - 133

AU  - Matthai SM

AU  - Davidson DC

AU  - Sills JA

AU  - Alexandrou D

TI  - Cerebral oedema after ingestion of MDMA ("ecstasy") and unrestricted intake of water [letter] [see comments]

MH  - Adolescence

MH  - Brain Edema

MH  - chemically induced

MH  - Case Report

MH  - Drinking

MH  - Female

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 96233457LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - LETTERDA - 19960719IS - 0959-8138SB - ASB - MSB - XCY - ENGLANDJC - BMJEM - 199609RO - M:LC1

UR  - PM:0008646063

SO  - BMJ 1996 May 25 ;312(7042):1359

 

137

UI  - 130

AU  - McCann UD

AU  - Slate SO

AU  - Ricaurte GA

AD  - Unit on Anxiety Disorders, National Institute of Mental Health, Bethesda, Maryland, USA

TI  - Adverse reactions with 3,4-methylenedioxymethamphetamine (MDMA; 'ecstasy')

AB  - 3,4-Methylenedioxymethamphetamine (MDMA; 'ecstasy') is an increasingly popular recreational drug in the US, Western Europe and Australia. In animals, including nonhuman primates, MDMA is known to damage brain serotonin (5-hydroxytryptamine; 5-HT) neurons. It is not known whether MDMA damages serotonin neurons in the human brain but there is some indication that it may. Although the large majority of individuals who have used MDMA recreationally do not develop acute complications, as the popularity of MDMA has increased, so have reports of adverse nonpsychiatric and psychiatric consequences associated with use of the drug. Further, since manifestations of MDMA-induced serotonin injury might only become apparent with age, or under periods of stress, it is possible that some individuals with no apparent abnormalities might develop complications over time

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - Hallucinogens

MH  - adverse effects

MH  - Heart

MH  - Human

MH  - Mental Disorders

MH  - chemically induced

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Substance-Related Disorders

RP  - NOT IN FILE

NT  - UI - 97038581LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19970108IS - 0114-5916SB - MCY - NEW ZEALANDJC - AHQAA - AuthorEM - 199703

UR  - PM:0008884162

SO  - Drug Saf 1996 Aug ;15(2):107-115

 

138

UI  - 121

AU  - Moore KA

AU  - Mozayani A

AU  - Fierro MF

AU  - Poklis A

AD  - Department of Pathology, Medical College of Virginia, Virginia 23298- 0165, USA

TI  - Distribution of 3,4-methylenedioxymethamphetamine (MDMA) and 3,4- methylenedioxyamphetamine (MDA) stereoisomers in a fatal poisoning

AB  - This communication presents the quantitation and differential distribution of the enantiomers of 3,4-methylenedioxymethamphetamine (MDMA) and its physiologically active metabolite 3,4- methylenedioxyamphetamine (MDA) in a fatal poisoning following insufflation of MDMA, cocaine and heroin. Animal studies have demonstrated the stereoselective pharmacokinetics and neurotoxicity of these compounds; however, enantiomeric distributions have not been reported in humans. Quantitation of MDMA and MDA enantiomer was by gas chromatography/mass spectrometry (GC/MS) following chiral derivatization with N-trifluoroacetyl-L-triproyl chloride (LTPC). The decedents' blood concentration of S(+)-MDMA was slightly less than that of R(-)-MDMA (1.3 vs. 1.6 mg/l, respectively), while the S(+)- and R(-)- MDA blood concentrations were identical (0.8 mg/l). Both primary routes of excretion, bile and urine, had greater concentrations of R(-)-MDMA than the S(+) isomer. These fluids also contained twice the concentration of S(+)-MDA than the R(-)-isomer. These data indicate that S(+)-MDMA is metabolized and eliminated faster than R(-)-MDMA. The results appear to support the findings in animals regarding stereoselective metabolism of MDMA

MH  - Adult

MH  - Case Report

MH  - Cocaine

MH  - poisoning

MH  - Fatal Outcome

MH  - Heroin

MH  - Human

MH  - Male

MH  - Mass Fragmentography

MH  - N-Methyl-3,4- methylenedioxyamphetamine

MH  - blood

MH  - pharmacokinetics

MH  - Narcotics

MH  - Stereoisomerism

MH  - Tissue Distribution

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 97174546LA - EngRN - 0 (Narcotics)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-36-2 (Cocaine)RN - 561-27-3 (Heroin)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19970304IS - 0379-0738SB - MCY - IRELANDJC - F49AA - AuthorEM - 199705

UR  - PM:0009022274

SO  - Forensic Sci Int 1996 Dec 2 ;83(2):111-119

 

139

UI  - 123

AU  - Prada C

AU  - Alvarez FJ

AD  - Departamento de Farmacologia y Terapeutica, Facultad de Medicina, Universidad de Valladolid

TI  - [MDMA or ecstasy: pharmacologic, toxicologic and clinical aspects]

MH  - Animal

MH  - Hallucinogens

MH  - adverse effects

MH  - chemistry

MH  - pharmacology

MH  - therapeutic use

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Substance-Related Disorders

RP  - NOT IN FILE

NT  - UI - 97108067LA - SpaRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19970121IS - 0025-7753SB - MCY - SPAINJC - LTQEM - 199703

UR  - PM:0008999216

SO  - Med Clin (Barc ) 1996 Oct 26 ;107(14):549-555

 

140

UI  - 137

AU  - Reid LD

AU  - Hubbell CL

AU  - Tsai J

AU  - Fishkin MD

AU  - Amendola CA

AD  - Laboratory for Psychopharmacology, Rensselaer Polytechnic Institute, Troy, NY 12180-3590, USA

TI  - Naltrindole, a delta-opioid antagonist, blocks MDMA's ability to enhance pressing for rewarding brain stimulation

AB  - Twelve rats were each fixed with a chronically indwelling bipolar electrode for stimulation of the medial forebrain bundle as it courses through the hypothalamus. These rats were trained to press a bar for intracranial stimulation of 0.3-s trains of 60 Hz sine waves for 10 min daily at three intensities. One intensity was just above threshold for maintaining pressing, one intensity was a high intensity that sustained considerable pressing, but not maximum pressing, and the other was intermediate to the others. After stable rates of pressing were obtained, rats received MDMA daily. MDMA significantly increased rates of pressing. Prior to a day when rats received MDMA, they also received an injection of naltrindole, a selective delta-opioid receptor antagonist. Naltrindole blocked MDMA's enhancement of pressing for reinforcing brain stimulation

MH  - Animal

MH  - Brain

MH  - physiology

MH  - Electric Stimulation

MH  - Male

MH  - Medial Forebrain Bundle

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - antagonists & inhibitors

MH  - pharmacology

MH  - Naltrexone

MH  - analogs & derivatives

MH  - Narcotic Antagonists

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Receptors,Opioid,delta

MH  - Reward

MH  - Self Stimulation

MH  - drug effects

MH  - Serotonin Agents

RP  - NOT IN FILE

NT  - UI - 96403883LA - EngRN - 0 (Narcotic Antagonists)RN - 0 (Receptors, Opioid, delta)RN - 0 (Serotonin Agents)RN - 111555-53-4 (naltrindole)RN - 16590-41-3 (Naltrexone)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19970116IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199703

UR  - PM:0008808161

SO  - Pharmacol Biochem Behav 1996 Feb ;53(2):477-480

 

141

UI  - 129

AU  - White SR

AU  - Obradovic T

AU  - Imel KM

AU  - Wheaton MJ

AD  - Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman 99164, USA

TI  - The effects of methylenedioxymethamphetamine (MDMA, "Ecstasy") on monoaminergic neurotransmission in the central nervous system

AB  - Methylenedioxymethamphetamine (MDMA, Ecstasy) is a popular recreationally used drug among young people in Europe and North America. The recent surge in use of MDMA and increasing concerns about possible toxic effects of the drug have inspired a great deal of research into the mechanisms by which the drug may affect the central nervous system. This paper reviews studies on the neurochemical, behavioral and neurophysiological effects of MDMA, with emphasis on MDMA effects in regions of the brain that have been implicated in reward. Experiments in awake, behaving laboratory animals have demonstrated that single injections of MDMA increase extracellular levels of the neurotransmitters dopamine (DA) and serotonin (5HT) in the nucleus accumbens and in several other brain regions that are important for reward. Most of the behavioral and electrophysiological changes that have been reported to date for single doses of MDMA appear to be mediated by this MDMA-induced increase in extracellular DA and 5HT. As an example, MDMA-induced hyperthermia and locomotor hyperactivity in laboratory animals can be blocked by administering drugs that prevent MDMA-induced 5HT release and can be attenuated by administering 5HT receptor antagonists, whereas effects of MDMA on delayed reinforcement tasks appear to be mediated by MDMA-induced increases in extracellular DA. Similarly, the effects of MDMA on neuronal excitability in the nucleus accumbens and in several other brain regions can be prevented by administering drugs that block MDMA- induced 5HT release and can be attenuated by depleting brain DA levels or by administering either DA D1 receptor antagonists or 5HT receptor antagonists. In addition to the acute effects of MDMA, it is now well established that repeated or high-dose administration of MDMA is neurotoxic to a subpopulation of 5HT-containing axons that project to the forebrain in laboratory animals. Recent studies have shown that this neurotoxic effect of MDMA is associated with long-duration changes in both DA and 5HT neurotransmission in the nucleus accumbens. Whether these long-duration changes in neurotransmission might be related to reports of depression and other psychopathologies by some frequent users of MDMA remains to be determined. Methylene-dioxymethamphetamine has been found to increase extracellular levels of norepinephrine and to alter brain levels of several neuropeptides as well as altering levels of DA and 5HT. Much additional research is required to understand the multiple ways in which this complex drug may alter neurotransmission in the brain, both acutely and in the long term

MH  - Action Potentials

MH  - drug effects

MH  - Animal

MH  - Brain

MH  - physiopathology

MH  - Brain Damage,Chronic

MH  - chemically induced

MH  - Dopamine

MH  - physiology

MH  - Fever

MH  - Guinea Pigs

MH  - Haplorhini

MH  - Hippocampus

MH  - Human

MH  - Hyperkinesis

MH  - Hypoglossal Nerve

MH  - Motor Neurons

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - pharmacology

MH  - Neurons

MH  - pathology

MH  - Nucleus Accumbens

MH  - Prefrontal Cortex

MH  - Raphe Nuclei

MH  - Rats

MH  - Reward

MH  - Serotonin

MH  - Street Drugs

MH  - Substance-Related Disorders

MH  - Support,U.S.Gov't,P.H.S.

MH  - Synaptic Transmission

MH  - Tegmentum Mesencephali

RP  - NOT IN FILE

NT  - UI - 97051257LA - EngRN - 0 (Street Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, ACADEMICID - DA-08116/DA/NIDADA - 19970219IS - 0301-0082SB - MCY - ENGLANDJC - Q3RAA - AuthorEM - 199704

UR  - PM:0008895996

SO  - Prog Neurobiol 1996 Aug ;49(5):455-479

 

142

UI  - 126

AU  - Wilkins B

TI  - Cerebral oedema after MDMA ("ecstasy") and unrestricted water intake. Hyponatraemia must be treated with low water input [letter; comment]

MH  - Brain Edema

MH  - chemically induced

MH  - Drinking

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Hyponatremia

MH  - therapy

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Water

MH  - administration & dosage

RP  - NOT IN FILE

NT  - UI - 96407759LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 7732-18-5 (Water)PT - COMMENTPT - LETTERDA - 19961024IS - 0959-8138SB - ASB - MSB - XCY - ENGLANDJC - BMJEM - 199612RO - M:LC1

UR  - PM:0008811776

SO  - BMJ 1996 Sep 14 ;313(7058):689-690

 

143

UI  - 148

AU  - Broening HW

AU  - Bowyer JF

AU  - Slikker W

AD  - Interdisciplinary Toxicology Program, University of Arkansas for Medical Sciences, Little Rock, USA

TI  - Age-dependent sensitivity of rats to the long-term effects of the serotonergic neurotoxicant (+/-)-3,4-methylenedioxymethamphetamine (MDMA) correlates with the magnitude of the MDMA-induced thermal response

AB  - The effects of developmental age on (+/-)-3,4- methylenedioxymethamphetamine (MDMA)-induced reductions in 5- hydroxytryptamine (5-HT) content and 5-HT reuptake sites were investigated in conjunction with the effects of developmental age on MDMA-induced thermoregulatory responses. MDMA was administered to rats at postnatal days (PND) 10, 40 and 70 in a range of ambient temperature environments (10 degrees C, 25 degrees C and 33 degrees C). Animals were monitored for alterations in body temperature and sacrificed 1 week after MDMA administration. MDMA administration at PND 10 did not result in persistent reductions in 5-HT content or 5-HT reuptake sites in frontal cortex, nor could a hyperthermic response be elicited. In contrast, MDMA administration at PND 40 and PND 70 resulted in a hypothermic response in cold environments (10 degrees C) and a hyperthermic response in warm environments (> or = 25 degrees C). When hypothermia was observed after MDMA (10 degrees C environment), long- term reductions in 5-HT content and 5-HT reuptake sites were significantly attenuated or abolished. Conversely, when a hyperthermic response was observed (25 degrees C and 33 degrees C environments), long-term MDMA-induced reductions in 5-HT content and 5-HT reuptake sites were significantly enhanced. Thus, thermal responses significantly correlated with MDMA-induced reductions in 5-HT content and 5-HT reuptake sites. These experiments demonstrate a role for hyperthermia in the expression of serotonergic neurotoxicity after MDMA administration

MH  - Aging

MH  - physiology

MH  - Animal

MH  - Body Temperature Regulation

MH  - drug effects

MH  - Brain

MH  - metabolism

MH  - Dose-Response Relationship,Drug

MH  - Female

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - toxicity

MH  - Neurotoxins

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Serotonin Uptake Inhibitors

MH  - Synaptic Transmission

MH  - Temperature

MH  - Time Factors

RP  - NOT IN FILE

NT  - UI - 96017362LA - EngRN - 0 (Neurotoxins)RN - 0 (Serotonin Uptake Inhibitors)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEDA - 19951121IS - 0022-3565SB - MCY - UNITED STATESJC - JP3AA - AuthorEM - 199601

UR  - PM:0007562567

SO  - J Pharmacol Exp Ther 1995 Oct ;275(1):325-333

 

144

UI  - 147

AU  - Cadet JL

AU  - Ladenheim B

AU  - Hirata H

AU  - Rothman RB

AU  - Ali S

AU  - Carlson E

AU  - Epstein C

AU  - Moran TH

AD  - Molecular Neuropsychiatry Section, NIH/NIDA, Baltimore, Maryland 21224, USA

TI  - Superoxide radicals mediate the biochemical effects of methylenedioxymethamphetamine (MDMA): evidence from using CuZn- superoxide dismutase transgenic mice

AB  - The subacute and long-term biochemical effects of methylenedioxymethamphetamine (MDMA) were assessed in homozygous and heterozygous transgenic (Tg) mice that carry the complete sequence of the human copper-zinc (CuZn) superoxide dismutase (SOD) gene. Non- transgenic (Non-Tg) mice showed significant decreased in striatal dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) levels both at 24 h and at 2 weeks after a single injection of MDMA (50 mg/kg). Heterozygous SOD-Tg mice showed DA depletion only at the 24 h time point. In contrast, homozygous SOD-Tg mice show no DA or DOPAC depletion at either the 24 h or at the 2 week time points. Moreover, three injections of MDMA (50 mg/kg) given 24 h apart also caused marked reduction of striatal DA and DOPAC in Non-Tg mice when these substances were measured 2 weeks after the last MDMA injection. That injection schedule also caused small decreases in DA levels in the heterozygous animals but no changes in the homozygous mice; DOPAC levels were not affected in the heterozygous nor in the homozygous SOD-Tg mice. Furthermore, the multiple injection schedule caused significant decreases in DA and DOPAC in female Non-Tg mice but not in the two strains of transgenic mice. Neither the single dose nor the multiple dose schedule of MDMA injections affected striatal serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) levels in any of the three strains of mice. These results support previous observations that MDMA-induced biochemical effects are observed in the DA systems of mice, whereas these effects are seen in the 5-HT systems of rats. The present observations also document for the first time a role for the production of superoxide radicals in these effects of MDMA. These mice are an important tool for dissecting pathways involved in drug-induced neurotoxicity

MH  - Animal

MH  - Autoradiography

MH  - Cocaine

MH  - analogs & derivatives

MH  - pharmacokinetics

MH  - Corpus Striatum

MH  - metabolism

MH  - Dopamine

MH  - Female

MH  - Human

MH  - Male

MH  - Mice

MH  - Mice,Transgenic

MH  - genetics

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Receptors,Dopamine

MH  - Superoxide Dismutase

MH  - Superoxides

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

MH  - Tissue Distribution

MH  - 3,4-Dihydroxyphenylacetic Acid

RP  - NOT IN FILE

NT  - UI - 96119012LA - EngRN - EC 1.15.1.1 (Superoxide Dismutase)RN - 0 (Receptors, Dopamine)RN - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)RN - 11062-77-4 (Superoxides)RN - 146145-21-3 (RTI 121)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-36-2 (Cocaine)RN - 51-61-6 (Dopamine)PT - JOURNAL ARTICLEID - HD 24605/HD/NICHDID - AG-08938/AG/NIADA - 19960319IS - 0887-4476SB - MCY - UNITED STATESJC - VFLAA - AuthorEM - 199605

UR  - PM:0008584978

SO  - Synapse 1995 Oct ;21(2):169-176

 

145

UI  - 143

AU  - Cohen RS

AD  - Department of Psychology Fairleigh Dickinson University, Madison, NJ USA

TI  - Subjective reports on the effects of the MDMA ('ecstasy') experience in humans

AB  - 1. The objective of this paper was to provide an understanding of methylenedioxymethamphetamine (MDMA) use. This investigation provides the subjective effects that were reported by MDMA users. 2. There were a total of (500) humans who participated in this study. 3. Using a survey device, data from users were collected. Symptomatology associated with both the consumption of MDMA and its residual effects are documented. 4. Tables have been constructed to present prevalent psychological and physical side-effects associated with MDMA intake. 5. The results suggest that MDMA has significant implications with various psychological disorders and physical manifestations

MH  - Adolescence

MH  - Adult

MH  - Anxiety

MH  - chemically induced

MH  - Behavior

MH  - drug effects

MH  - Depression

MH  - Female

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Paranoid Disorders

MH  - Questionnaires

RP  - NOT IN FILE

NT  - UI - 96256069LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19960926IS - 0278-5846SB - MCY - ENGLANDJC - Q45AA - AuthorEM - 199611

UR  - PM:0008787037

SO  - Prog Neuropsychopharmacol Biol Psychiatry 1995 Nov ;19(7):1137-1145

 

146

UI  - 153

AU  - Colado MI

AU  - Williams JL

AU  - Green AR

AD  - Astra Neuroscience Research Unit, London

TI  - The hyperthermic and neurotoxic effects of 'Ecstasy' (MDMA) and 3,4 methylenedioxyamphetamine (MDA) in the Dark Agouti (DA) rat, a model of the CYP2D6 poor metabolizer phenotype

AB  - 1. The effect of administration of 3,4-methylenedioxymethamphetamine (MDMA or 'Ecstasy') and its N-demethylated product, 3,4- methylenedioxyamphetamine (MDA) on both rectal temperature and long term neurotoxic loss of cerebral 5-hydroxytryptamine (5-HT) has been studied in male and female Dark Agouti (DA) rats. The female metabolizes debrisoquine more slowly than the male and its use has been suggested as a model of the human debrisoquine 4-hydroxylase poor metabolizer phenotype. 2. A novel h.p.l.c. method was developed and used to measure plasma MDMA and MDA concentrations in the DA rats. 3. The hyperthermic response following MDMA was enhanced in female rats. Plasma MDMA concentrations were also 57% higher than in males 45 min post-injection, while plasma concentrations of MDA were 48% lower. 4. Plasma concentrations of MDMA and MDA in male rats were unaffected by pretreatment with proadifen (15 mg kg-1) or quinidine (60 mg kg-1), but the hyperthermic response to MDMA (10 mg kg-1, i.p.) was enhanced by quinidine pretreatment. 5. The hyperthermic response following MDA was greater in male DA rats, despite plasma drug concentrations being 40% higher in females 60 min after injection. 6. Seven days after a single dose of MDMA (10 mg kg-1, i.p.) there was a substantial loss in the concentration of 5-HT and 5-hydroxyindoleacetic acid (5-HIA) in cortex and hippocampus. [3H]-paroxetine binding was also decreased by 27% in the cortex, indicating that the amine loss reflected a neurodegenerative change. MDMA (5 mg kg-1, i.p.) was without effect on brain 5-HT content.(ABSTRACT TRUNCATED AT 250 WORDS)

MH  - Animal

MH  - Body Temperature Regulation

MH  - drug effects

MH  - Brain

MH  - metabolism

MH  - Cytochrome P-450

MH  - Female

MH  - Fever

MH  - chemically induced

MH  - Human

MH  - Hydroxyindoleacetic Acid

MH  - Hydroxylases

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - blood

MH  - pharmacology

MH  - toxicity

MH  - Paroxetine

MH  - Phenotype

MH  - Proadifen

MH  - Quinidine

MH  - Rats

MH  - Rectum

MH  - Serotonin

MH  - Serotonin Agents

MH  - Sex Factors

MH  - Support,Non-U.S.Gov't

MH  - Tritium

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 96001984LA - EngRN - EC 1.14. (Hydroxylases)RN - EC 1.14.99.- (Cytochrome P-450 CYP2D6)RN - 0 (Serotonin Agents)RN - 10028-17-8 (Tritium)RN - 302-33-0 (Proadifen)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 56-54-2 (Quinidine)RN - 61869-08-7 (Paroxetine)RN - 9035-51-2 (Cytochrome P-450)PT - JOURNAL ARTICLEDA - 19951201IS - 0007-1188SB - MCY - ENGLANDJC - B00AA - AuthorEM - 199602

UR  - PM:0007582557

SO  - Br J Pharmacol 1995 Aug ;115(7):1281-1289

 

147

UI  - 157

AU  - Cook A

TI  - Ecstasy (MDMA): alerting users to the dangers

AB  - In this paper, the author outlines the chemical make-up of the recreational drug ecstasy, and describes signs and symptoms of intoxication which are especially useful to A&E nurses. He describes the effects of the drug on the users, and suggests advice which should be given to users on admission

MH  - Emergency Nursing

MH  - Female

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - pharmacology

MH  - Street Drugs

MH  - Substance-Related Disorders

MH  - physiopathology

MH  - psychology

RP  - NOT IN FILE

NT  - UI - 95249424LA - EngRN - 0 (Street Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19950601IS - 0029-6589SB - NCY - ENGLANDJC - O9UAA - AuthorEM - 199508

UR  - PM:0007731854

SO  - Nurs Times 1995 Apr 19 ;91(16):32-33

 

148

UI  - 145

AU  - Dafters RI

AD  - Department of Psychology, Glasgow University, Scotland

TI  - Hyperthermia following MDMA administration in rats: effects of ambient temperature, water consumption, and chronic dosing

AB  - In two experiments it was found that the hyperthermia which follows MDMA ("Ecstasy") results from an interaction of direct pharmacological effect of the drug and the prevailing environmental conditions in which it is administered. In Experiment 1, rats given fixed doses of either 2.5, 5.0 or 7.5 mg/kg MDMA or saline were injected on different days at ambient temperatures (Ta's) of 11, 24, and 30 degrees C. At each Ta drinking water was freely available following dosing on one session and temporarily unavailable on a second. The hyperthermic and hyperkinetic responses were monitored using remote biotelemetry. Experiment 2 used a between-subject design in which each group of rats received a standard 7.5 mg/kg dose of MDMA administered at only one of the three levels of Ta(24 degrees C) and at only one level of the water-availability factor. Dosing in some groups was continued for a further 13 days to test for tolerance or sensitization effects. Ambient temperature significantly affected the magnitude of the hyperthermia but not the hyperkinesis. Water deprivation during the drugged period significantly augmented the hyperthermia, but only in the high Ta (30 degrees C.) condition. Chronic dosing produced sensitization of both hyperthermic and hyperkinetic responses. The findings indicate that ambient temperature, water consumption and frequency of drug use affect the hyperthermia which follows MDMA administration

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - Drinking

MH  - physiology

MH  - Fever

MH  - chemically induced

MH  - physiopathology

MH  - Hyperkinesis

MH  - psychology

MH  - Male

MH  - Motor Activity

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - administration & dosage

MH  - pharmacology

MH  - Rats

MH  - Rats,Wistar

MH  - Telemetry

MH  - Temperature

RP  - NOT IN FILE

NT  - UI - 96141264LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19960314IS - 0031-9384SB - MCY - UNITED STATESJC - P72AA - AuthorEM - 199605

UR  - PM:0008577883

SO  - Physiol Behav 1995 Nov ;58(5):877-882

 

149

UI  - 151

AU  - Fischer C

AU  - Hatzidimitriou G

AU  - Wlos J

AU  - Katz J

AU  - Ricaurte G

AD  - Department of Neurology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21224, USA

TI  - Reorganization of ascending 5-HT axon projections in animals previously exposed to the recreational drug (+/-)3,4-methylenedioxymethamphetamine (MDMA, "ecstasy")

AB  - The recreational drug (+/)3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") is a methamphetamine derivative that selectively destroys central 5-HT axons and axon terminals in animals and, possibly, humans. The fate of 5-HT neurons following MDMA injury is uncertain. In particular, while it is known that central 5-HT axons can undergo regenerative sprouting after MDMA injury, it has not been determined whether they reestablish the original innervation pattern. To address this question, the present studies examined 5-HT innervation patterns in animals lesioned with MDMA 12-18 months previously. Both rodents (rats) and nonhuman primates (squirrel monkeys) were examined, since there is indication that serotonergic recovery after MDMA injury may be species dependent. 5-HT axon projections were studied neurochemically, autoradiographically and immunocytochemically. In both rodents and nonhuman primates previously lesioned with MDMA, substantial serotonergic axonal sprouting was observed. However, in a few rats and in most squirrel monkeys, the reinnervation pattern was highly abnormal: distant targets (e.g., dorsal neocortex) remained denervated, while some proximal targets (e.g., amygdala, hypothalamus) were reinnervated or hyperinnervated. Although the specific determinants of axonal recovery after MDMA injury remain to be identified, it appears that axons which initially sustain more severe damage, are longer, or are more highly arborized have low probability of recovering. The observation that some brain regions remain denervated, while others are reinnervated or hyperinnervated suggests that, under some circumstances, MDMA injury can lead to a lasting reorganization of ascending 5-HT axon projections. Such lasting changes in brain innervation, documented here in MDMA-treated animals, may have implications for humans using MDMA recreationally

MH  - Afferent Pathways

MH  - drug effects

MH  - physiopathology

MH  - Animal

MH  - Autoradiography

MH  - Axons

MH  - physiology

MH  - Brain

MH  - pathology

MH  - Immunohistochemistry

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Nerve Regeneration

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Saimiri

MH  - Serotonin

MH  - Support,U.S.Gov't,P.H.S.

MH  - Synaptic Transmission

MH  - Time Factors

RP  - NOT IN FILE

NT  - UI - 95370916LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEID - DA05707/DA/NIDAID - DA06275/DA/NIDADA - 19950920IS - 0270-6474SB - MCY - UNITED STATESJC - JDFAA - AuthorEM - 199511

UR  - PM:0007643196

SO  - J Neurosci 1995 Aug ;15(8):5476-5485

 

150

UI  - 150

AU  - Frederick DL

AU  - Ali SF

AU  - Slikker W

AU  - Gillam MP

AU  - Allen RR

AU  - Paule MG

AD  - Division of Neurotoxicology, National Center for Toxicological Research/FDA, Jefferson, AR 72079-9502, USA

TI  - Behavioral and neurochemical effects of chronic methylenedioxymethamphetamine (MDMA) treatment in rhesus monkeys

AB  - Effects of chronic treatment with the putative serotonergic neurotoxicant MDMA were assessed in rhesus macaques using behavior in an operant test battery (OTB) designed to model aspects of time estimation, short-term memory, motivation, learning, and color and position discrimination. After an initial acute dose-response assessment, escalating doses of MDMA (0.10-20.0 mg/kg, im, twice daily, for 14 consecutive days at each dose) were administered, followed by three additional acute dose-response assessments. In general, tolerance to MDMA's acute effects was evident in all OTB tasks by the second week of repeated exposure to each individual MDMA dose and as doses escalated. Baseline OTB performance after chronic treatment was not significantly altered. Residual behavioral tolerance to MDMA's acute effects, however, was evident in all OTB tasks but was least pronounced in the motivation task. Monkeys were sacrificed (21 months after chronic treatment) and brains were dissected into several regions for neurochemical analyses. Serotonin (5-HT), 5-hydroxyindoleacetic acid (5- HIAA), dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) were analyzed via HPLC. Although MDMA-treated monkeys tended to have lower 5-HT concentrations in the frontal cortex, chronic MDMA treatment had no significant effects on 5-HT concentrations in any brain area sampled. Hippocampal 5-HIAA concentration, 5-HT uptake sites, and turnover of 5-HT of MDMA-treated monkeys were significantly lower than control values. DA concentrations in the CN of MDMA-treated monkeys were significantly greater than control values. No significant effects on DA concentrations were noted in any other brain area sampled. The absence of significant decreases in 5-HT and the general increase in DA concentrations are dissimilar to neurochemical effects reported after a short course of MDMA treatment at relatively high doses. These data suggest that chronic administration of gradually increasing doses of MDMA results in long- lasting tolerance to the drugs acute effects on the complex brain functions modeled in the OTB. It is uncertain, however, if such tolerance is related to the observed decreases in uptake sites and turnover of 5-HT in the hippocampus of these monkeys

MH  - Animal

MH  - Biogenic Amine Neurotransmitters

MH  - metabolism

MH  - Brain

MH  - drug effects

MH  - Conditioning,Operant

MH  - Dose-Response Relationship,Drug

MH  - Drug Tolerance

MH  - Homovanillic Acid

MH  - Hydroxyindoleacetic Acid

MH  - Macaca mulatta

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Psychomotor Performance

MH  - Reinforcement Schedule

MH  - Serotonin Agents

MH  - Time Factors

MH  - 3,4-Dihydroxyphenylacetic Acid

RP  - NOT IN FILE

NT  - UI - 96105915LA - EngRN - 0 (Biogenic Amine Neurotransmitters)RN - 0 (Serotonin Agents)RN - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)RN - 306-08-1 (Homovanillic Acid)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - JOURNAL ARTICLEDA - 19960222IS - 0892-0362SB - MCY - UNITED STATESJC - NATAA - AuthorEM - 199604

UR  - PM:0008551999

SO  - Neurotoxicol Teratol 1995 Sep ;17(5):531-543

 

151

UI  - 155

AU  - Frederick DL

AU  - Gillam MP

AU  - Allen RR

AU  - Paule MG

AD  - Division of Neurotoxicology, National Center for Toxicological Research/FDA, Jefferson, AR 72079-9502, USA

TI  - Acute effects of methylenedioxymethamphetamine (MDMA) on several complex brain functions in monkeys

AB  - The effects of MDMA were assessed in rhesus macaques using behavior in an operant test battery (OTB) consisting of five food-reinforced tasks designed to model aspects of time estimation, short-term memory, and attention, motivation, learning, and color and position discrimination. Testing occurred 30 min after intramuscular, injections of MDMA (0.0, 0.1, 0.3, and 1.0 mg/kg). The behavioral endpoints monitored included percent task completed, response rate or latency, and response accuracy. Percent task completed was significantly decreased in the time estimation, learning, and motivation tasks at 1.0 mg/kg as compared to saline controls. Response accuracies in the time estimation and learning tasks were also decreased at 1.0 mg/kg. Response rate was decreased at 1.0 mg/kg in the motivation task but was not significantly affected in any other tasks. No behavioral endpoints were significantly affected in the short-term memory and attention and color and position discrimination tasks at any dose tested. Results indicate that time estimation, motivation, and learning are more sensitive to the acute effects of MDMA than are short-term memory and attention and color and position discrimination

MH  - Animal

MH  - Attention

MH  - drug effects

MH  - Color Perception

MH  - Conditioning,Operant

MH  - Discrimination (Psychology)

MH  - Dose-Response Relationship,Drug

MH  - Macaca mulatta

MH  - Male

MH  - Memory,Short-Term

MH  - Mental Processes

MH  - Motivation

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Support,Non-U.S.Gov't

MH  - Time Perception

RP  - NOT IN FILE

NT  - UI - 95396850LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19951011IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199512

UR  - PM:0007667344

SO  - Pharmacol Biochem Behav 1995 Jun ;51(2-3):301-307

 

152

UI  - 149

AU  - Galloway G

AU  - Shulgin AT

AU  - Kornfeld H

AU  - Frederick SL

TI  - Amphetamine, not MDMA, is associated with intracranial hemorrhage [letter; comment]

MH  - Amphetamine

MH  - adverse effects

MH  - Case Report

MH  - Central Nervous System Stimulants

MH  - Cerebral Hemorrhage

MH  - etiology

MH  - Female

MH  - Hallucinogens

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Overdose

MH  - Substance-Related Disorders

MH  - complications

RP  - NOT IN FILE

NT  - UI - 96127009LA - EngRN - 0 (Central Nervous System Stimulants)RN - 0 (Hallucinogens)RN - 300-62-9 (Amphetamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - COMMENTPT - LETTERDA - 19960320IS - 1351-0622SB - MCY - ENGLANDJC - B0UEM - 199605RO - M:LC2

UR  - PM:0008581263

SO  - J Accid Emerg Med 1995 Sep ;12(3):231-232

 

153

UI  - 154

AU  - Green AR

AU  - Cross AJ

AU  - Goodwin GM

AD  - MRC Brain Metabolism Unit, Royal Edinburgh Hospital, UK

TI  - Review of the pharmacology and clinical pharmacology of 3,4- methylenedioxymethamphetamine (MDMA or "Ecstasy")

AB  - 3,4-Methylenedioxymethamphetamine (MDMA or "Ecstasy") was first synthesised 80 years ago, but has recently received prominence as an illegally synthesised recreational drug of abuse. There is a widely held belief among misusers that it is safe. In the last 2-3 years there have been a number of reports of the drug producing severe acute toxicity and death and there are concerns that it may cause long term toxic damage to 5-hydroxytryptamine (5-HT) nerve terminals. There is a considerable literature on the acute pharmacological effects of MDMA in experimental animals, and this is reviewed. The drug produces both hyperthermia and the "serotonin syndrome", a series of behavioural changes which result from increased 5-HT function. Acute clinical toxicity problems following MDMA ingestion also include hyperthermia and the appearance of the serotonin syndrome. The hyperthermia appears to precipitate other severe clinical problems and the outcome can be fatal. In agreement with others, we suggest that the recent increase in the number of reports of MDMA toxicity probably results from the widespread use of the drug at all night dance parties or "raves". The phenomenon of amphetamine aggregation toxicity in mice was reported 40 years ago. If applicable to MDMA-induced toxicity in humans, all the conditions necessary to induce or enhance toxicity are present at raves: crowded conditions (aggregation), high ambient temperature, loud noise and dehydrated subjects. Administration of MDMA to rodents and non-human primates results in a long term neurotoxic decrease in 5-HT content in several brain regions and there is clear biochemical and histological evidence that this reflects neurodegeneration of 5-HT terminals. Unequivocal data demonstrating that similar changes occur in human brain do not exist, but limited and indirect clinical evidence gives grounds for concern. There are also data suggesting that long term psychiatric changes can occur, although there are problems of interpretation and these are reviewed. Suggestions for the rational treatment of the acute toxicity are made on the basis of both pharmacological studies in animals and current clinical practice. Cases presenting clinically are usually emergencies and unlikely to allow carefully controlled studies. Proposals include decreasing body temperature (possibly with ice), the use of dantrolene and anticonvulsant and sedative medication, particularly benzodiazepines. The use of neuroleptics requires care because of the theoretical risk of producing the neuroleptic malignant syndrome and the possibility of precipitating seizures. In rats, chlormethiazole antagonises the hyperthermia produced by MDMA and has been shown clinically to block MDMA-induced convulsive activity

MH  - Animal

MH  - Behavior,Animal

MH  - drug effects

MH  - Fever

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Serotonin

MH  - Tryptophan

RP  - NOT IN FILE

NT  - UI - 95406391LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 73-22-3 (Tryptophan)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, ACADEMICDA - 19951018IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199512

UR  - PM:0007675958

SO  - Psychopharmacology (Berl) 1995 Jun ;119(3):247-260

 

154

UI  - 152

AU  - McConn UD

AU  - Ricaurte GA

TI  - On the neurotoxicity of MDMA and related amphetamine derivatives [letter]

MH  - Amphetamines

MH  - toxicity

MH  - Hallucinogens

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Substance-Related Disorders

MH  - physiopathology

RP  - NOT IN FILE

NT  - UI - 96015234LA - EngRN - 0 (Amphetamines)RN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - LETTERDA - 19951219IS - 0271-0749SB - MCY - UNITED STATESJC - HUDEM - 199602

UR  - PM:0007593721

SO  - J Clin Psychopharmacol 1995 Aug ;15(4):295-296

 

155

UI  - 144

AU  - Meehan SM

AU  - Gordon TL

AU  - Schechter MD

AD  - Department of Pharmacology, Northeastern Ohio Universities College of Medicine, Rootstown 44272, USA

TI  - MDMA (Ecstasy) substitutes for the ethanol discriminative cue in HAD but not LAD rats

AB  - Selectively bred high- and low-alcohol-drinking (HAD/LAD) rats were trained to discriminate the interoceptive stimuli produced by IP- administered 600 mg/kg ethanol (10% w/v in a two-lever, food-motivated operant task. Once criterion discrimination was attained, animals were tested with 3.0, 1.5, 1.0, and 0.5 mg/kg MDMA. Although no differences in alcohol discrimination were observed between the HAD and LAD animals, the HAD line was significantly more sensitive than the LAD line to the effects of MDMA. These results provide additional information to the growing body of evidence suggesting serotonergic mediation of some of the behavioral effects of ethanol

MH  - Alcohol Drinking

MH  - genetics

MH  - psychology

MH  - Animal

MH  - Central Nervous System Depressants

MH  - pharmacology

MH  - Comparative Study

MH  - Cues

MH  - Discrimination (Psychology)

MH  - drug effects

MH  - Discrimination Learning

MH  - Dose-Response Relationship,Drug

MH  - Ethanol

MH  - Generalization,Stimulus

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Piperazines

MH  - Rats

MH  - Serotonin Agents

MH  - Serotonin Agonists

RP  - NOT IN FILE

NT  - UI - 96161345LA - EngRN - 0 (Central Nervous System Depressants)RN - 0 (Piperazines)RN - 0 (Serotonin Agents)RN - 0 (Serotonin Agonists)RN - 15532-75-9 (1-(3-trifluoromethylphenyl)piperazine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 64-17-5 (Ethanol)PT - JOURNAL ARTICLEDA - 19960403IS - 0741-8329SB - MCY - UNITED STATESJC - AG9AA - AuthorEM - 199606

UR  - PM:0008590621

SO  - Alcohol 1995 Nov ;12(6):569-572

 

156

UI  - 158

AU  - Sprague JE

AU  - Nichols DE

AD  - Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, IN 47907, USA

TI  - Inhibition of MAO-B protects against MDMA-induced neurotoxicity in the striatum

AB  - The effects of the MAO-B inhibitors, L-deprenyl and MDL-72974 on MDMA- induced serotonergic neurotoxicity in rats were examined. MDMA alone produced a significant decrease in the number of 5-HT uptake sites, measured as a decrease in the Bmax for binding of [3H]paroxetine, and in 5-HT and 5-HIAA levels in the striatum. L-Deprenyl and MDL-72974 attenuated this MDMA-induced decrease in serotonergic markers. The data suggest a key role for MAO-B in the expression of the neurotoxicity produced by MDMA in the striatum

MH  - Animal

MH  - Corpus Striatum

MH  - drug effects

MH  - metabolism

MH  - Hydroxyindoleacetic Acid

MH  - Male

MH  - Monoamine Oxidase Inhibitors

MH  - pharmacology

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - toxicity

MH  - Paroxetine

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Selegiline

MH  - Serotonin

MH  - Sodium Chloride

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 95343079LA - EngRN - 0 (Monoamine Oxidase Inhibitors)RN - 14611-51-9 (Selegiline)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 61869-08-7 (Paroxetine)RN - 7647-14-5 (Sodium Chloride)PT - JOURNAL ARTICLEID - DA04758/DA/NIDADA - 19950823IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199510

UR  - PM:0007542394

SO  - Psychopharmacology (Berl) 1995 Apr ;118(3):357-359

 

157

UI  - 156

AU  - White SR

AU  - Harris GC

AU  - Imel KM

AU  - Wheaton MJ

AD  - Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman 99164, USA

TI  - Inhibitory effects of dopamine and methylenedioxymethamphetamine (MDMA) on glutamate-evoked firing of nucleus accumbens and caudate/putamen cells are enhanced following cocaine self-administration

AB  - Rats were allowed to self-administer cocaine during a 3-h session for 15 days. One to 11 days after the last cocaine exposure, rats were anesthetized with urethane and effects of microiontophoretically- applied dopamine on glutamate-evoked firing of neurons in the nucleus accumbens and in the caudate/putamen were tested. Dopamine produced a dose-dependent inhibition of glutamate-evoked firing in both the nucleus accumbens and the caudate/putamen of rats that had been repeatedly exposed to self-administered cocaine and in control rats. However, the DA-induced inhibition was significantly greater in the group that had self-administered cocaine. The cocaine self- administration group was significantly sensitized to the inhibitory effects of dopamine in both early (1-3 day) and later (9-11 days) periods of cocaine abstinence. Following cessation of repeated cocaine self-administration sessions, nucleus accumbens cells were also sensitized to the inhibitory effects of methylenedioxymethamphetamine (MDMA), a drug that increases extracellular levels of DA and serotonin in the nucleus accumbens. This sensitization to DA- and MDMA-induced inhibition in the nucleus accumbens and in the striatum indicates that long-term neuroadaptations occur in these regions of the nervous system following repeated exposure to self-administered cocaine

MH  - Animal

MH  - Brain

MH  - cytology

MH  - drug effects

MH  - physiology

MH  - Caudate Nucleus

MH  - Cocaine

MH  - pharmacology

MH  - Dopamine

MH  - Dopamine Uptake Inhibitors

MH  - Dose-Response Relationship,Drug

MH  - Glutamic Acid

MH  - Iontophoresis

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Neurons

MH  - Nucleus Accumbens

MH  - Putamen

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Self Administration

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 96031794LA - EngRN - 0 (Dopamine Uptake Inhibitors)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-36-2 (Cocaine)RN - 51-61-6 (Dopamine)RN - 56-86-0 (Glutamic Acid)PT - JOURNAL ARTICLEID - DA08116/DA/NIDADA - 19951106IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199601

UR  - PM:0007552276

SO  - Brain Res 1995 May 29 ;681(1-2):167-176

 

158

UI  - 146

AU  - Wichems CH

AU  - Hollingsworth CK

AU  - Bennett BA

AD  - Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27157-1083, USA

TI  - Release of serotonin induced by 3,4-methylenedioxymethamphetamine (MDMA) and other substituted amphetamines in cultured fetal raphe neurons: further evidence for calcium-independent mechanisms of release

AB  - The substituted amphetamines 3,4-methylenedioxymethamphetamine (MDMA), 3,4-methylenedioxyamphetamine (MDA), p-chloro-amphetamine (PCA) and fenfluramine (FEN) all exert their effects by releasing serotonin (5- HT) from presynaptic nerve terminals. In the current study, we examined the ability of these agents to induce the release of 5-HT in culture fetal raphe neurons. The data indicate that the rank order of release potencies for these agents was (+/-)PCA>(+)MDMA=(+)MDA=(+/-)FEN. Studies examining the role fo calcium in 5-HT release demonstrate that preventing calcium influx with L- and N-type calcium channel blockers inhibits potassium-stimulated release of -3H-5-HT but has no effect on release induced by the substituted amphetamines. Furthermore, omitting calcium from the extracellular media or depleting the vesicular pool of neurotransmitter with continual potassium stimulation did not affect the release of -3H-5-HT induced by these compounds. Administration of fluoxetine prior to the substituted amphetamines significantly attenuated the releasing effects of these agents, while producing no effect on potassium-stimulated release. These results are consistent with the notion that the amphetamines induce release of cytoplasmic 5- HT via the plasma membrane transporter

MH  - Amphetamine

MH  - pharmacology

MH  - Animal

MH  - Calcium

MH  - Cells,Cultured

MH  - drug effects

MH  - Dose-Response Relationship,Drug

MH  - Fenfluramine

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Potassium Chloride

MH  - Raphe Nuclei

MH  - metabolism

MH  - Rats

MH  - Serotonin

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 96113777LA - EngRN - 300-62-9 (Amphetamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 458-24-2 (Fenfluramine)RN - 50-67-9 (Serotonin)RN - 7440-70-2 (Calcium)RN - 7447-40-7 (Potassium Chloride)PT - JOURNAL ARTICLEID - NIDA 05073ID - NIDA 06634ID - NIDA 07246DA - 19960312IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199605

UR  - PM:0008574641

SO  - Brain Res 1995 Oct 9 ;695(1):10-18

 

159

UI  - 159

AU  - Bronson ME

AU  - Barrios-Zambrano L

AU  - Jiang W

AU  - Clark CR

AU  - DeRuiter J

AU  - Newland MC

AD  - Department of Pharmacal Sciences, Auburn University, AL 36849-5503

TI  - Behavioral and developmental effects of two 3,4- methylenedioxymethamphetamine (MDMA) derivatives

AB  - The effects of 3,4-methylenedioxymethamphetamine (MDMA or 'ecstacy') and two structurally related compounds, N-methyl-1-(3,4- methylenedioxyphenyl)-1-ethanamine (MDM1EA) and N-methyl-1-(3,4- methylenedioxyphenyl)-3-butanamine (HMDMA) were examined in two preparations: (i) a drug discrimination procedure in MDMA-trained rats and (ii) the chicken embryo, for determination of the direct effects of these compounds on the developing organism. The highest doses of MDM1EA and HMDMA partially substituted for MDMA, whereas higher (30-60 mg/kg) doses of HMDMA evoked clonic seizures in a separate group of rats. In chicken embryos MDMA had no effect on body, brain or liver weight, while the highest dose of MDM1EA decreased body weight and the 2 lowest doses of HMDMA increased body weight. All doses of HMDMA decreased liver weight (expressed as % body weight) when compared with contemporaneous water-treated controls. Taken together, the results of these experiments suggest that structurally related compounds share some stimulus properties with MDMA and may therefore share abuse liability. Furthermore, both MDMA-related compounds produced adverse effects on the developing organism, whereas MDMA did not

MH  - Abnormalities,Drug-Induced

MH  - etiology

MH  - Animal

MH  - Appetitive Behavior

MH  - drug effects

MH  - Arousal

MH  - Body Weight

MH  - Brain

MH  - Chick Embryo

MH  - Designer Drugs

MH  - pharmacology

MH  - toxicity

MH  - Discrimination Learning

MH  - Dose-Response Relationship,Drug

MH  - Liver

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - Organ Weight

MH  - Rats

MH  - Structure-Activity Relationship

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 95196522LA - EngRN - 0 (Designer Drugs)RN - 121734-64-3 (3,4-methylenedioxyphenyl-1-ethanamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 92279-87-3 (N-methyl-3,4-methylenedioxyphenylisobutylamine)PT - JOURNAL ARTICLEID - DA06637/DA/NIDADA - 19950420IS - 0376-8716SB - MCY - IRELANDJC - EBSAA - AuthorEM - 199506

UR  - PM:0007889806

SO  - Drug Alcohol Depend 1994 Dec ;36(3):161-166

 

160

UI  - 165

AU  - Cadet JL

AU  - Ladenheim B

AU  - Baum I

AU  - Carlson E

AU  - Epstein C

AD  - Molecular Neuropsychiatry Section, NIH/NIDA, Addiction Research Center, Baltimore, MD 21224

TI  - CuZn-superoxide dismutase (CuZnSOD) transgenic mice show resistance to the lethal effects of methylenedioxyamphetamine (MDA) and of methylenedioxymethamphetamine (MDMA)

AB  - We have used female and male transgenic (Tg) mice that carry the complete sequence of the human copper-zinc (CuZn) superoxide dismutase (SOD) gene in order to assess the lethal effects of methylenedioxyamphetamine (MDA) and methylenedioxymethamphetamine (MDMA). In contrast to non-Tg mice, both heterozygous and homozygous SOD-Tg mice showed resistance to the lethal effects of both drugs. Females of both SOD-Tg and non-Tg strains were somewhat more resistant to the effects of these drugs in comparison to males. In general, homozygous animals show greater resistance to the effects of the two drugs. These results suggest that the acute lethal effects of amphetamine-substituted analogs might involve the intracellular overproduction of the superoxide radicals secondary to hypoxic injury. The gender differences suggest that there might be hormonal-free radical scavenger interactions that offer better protection to female mice. This might be related both to the lifespan of and to the lower prevalence of Parkinson's disease in women. Future studies will need to address these issues further

MH  - Animal

MH  - Female

MH  - Human

MH  - Injections,Intraperitoneal

MH  - Male

MH  - Mice

MH  - Mice,Transgenic

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - administration & dosage

MH  - toxicity

MH  - Oxygen Consumption

MH  - drug effects

MH  - Sex Characteristics

MH  - Superoxide Dismutase

MH  - genetics

MH  - Superoxides

MH  - metabolism

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 95112024LA - EngRN - EC 1.15.1.1 (Superoxide Dismutase)RN - 11062-77-4 (Superoxides)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEID - AG-08938/AG/NIADA - 19950206IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199504

UR  - PM:0007812784

SO  - Brain Res 1994 Aug 29 ;655(1-2):259-262

 

161

UI  - 182

AU  - Colado MI

AU  - Green AR

AD  - Astra Neuroscience Research Unit, London

TI  - A study of the mechanism of MDMA ('ecstasy')-induced neurotoxicity of 5- HT neurones using chlormethiazole, dizocilpine and other protective compounds

AB  - 1. An investigation has been made in rats into the neurotoxic effect of the relatively selective 5-hydroxytryptamine (5-HT) neurotoxin, 3,4- methylenedioxymethamphetamine (MDMA or 'Ecstasy') using chlormethiazole and dizocilpine, both known neuroprotective compounds and also gamma- butyrolactone, ondansetron and pentobarbitone. 2. Administration of MDMA (20 mg kg-1, i.p.) resulted in a 50% loss of cortical and hippocampal 5-HT and 5-hydroxyindole acetic acid (5-HIAA) 4 days later. This reflects the long term neurotoxic loss of 5-HT that occurs. Injection of gamma-butyrolactone (GBL; 400 mg kg-1, i.p.) 5 min before and 55 min after the MDMA provided substantial protection. Pentobarbitone (25 mg kg-1, i.p.) using the same dose regime was also protective, but ondansetron (0.5 mg kg-1 or 0.1 mg kg-1, i.p.) was without effect. 3. MDMA (20 mg kg-1) had no significant effect on striatal dopamine concentration 4 days later but did produce a small decrease in 3,4-dihydroxyphenylacetic acid (DOPAC) content. There were few significant changes in rats given MDMA plus GBL, ondansetron or pentobarbitone. 4. A single injection of MDMA (20 mg kg-1, i.p.) resulted in a greater than 80% depletion of 5-HT in hippocampus and cortex 4 h later, reflecting the initial rapid release that had occurred. None of the neuroprotective compounds (chlormethiazole, 50 mg kg-1; dizocilpine, 1 mg kg-1; GBL, 400 mg kg-1; pentobarbitone, 25 mg kg-1) given 5 min before and 55 min after the MDMA injection, altered the degree of 5-HT loss. 5. Acute MDMA injection increased striatal dopamine content (28%) and decreased the DOPAC content. In general, administration of the drugs under investigation did not significantly alter these MDMA-induced changes. Both chlormethiazole and GBL produced a greater increase in dopamine than MDMA alone, but this was apparently an additive effect to the action of either drug alone.(ABSTRACT TRUNCATED AT 250 WORDS)

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - Chlormethiazole

MH  - administration & dosage

MH  - pharmacology

MH  - Comparative Study

MH  - Designer Drugs

MH  - toxicity

MH  - Dizocilpine Maleate

MH  - Dopamine

MH  - Hydroxyindoleacetic Acid

MH  - Male

MH  - Ondansetron

MH  - Pentobarbital

MH  - Rats

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

MH  - 3,4-Dihydroxyphenylacetic Acid

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - 4-Butyrolactone

RP  - NOT IN FILE

NT  - UI - 94282439LA - EngRN - 0 (Designer Drugs)RN - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 533-45-9 (Chlormethiazole)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 76-74-4 (Pentobarbital)RN - 77086-22-7 (Dizocilpine Maleate)RN - 96-48-0 (4-Butyrolactone)RN - 99614-02-5 (Ondansetron)PT - JOURNAL ARTICLEDA - 19940725IS - 0007-1188SB - MCY - ENGLANDJC - B00AA - AuthorEM - 199409

UR  - PM:0007516800

SO  - Br J Pharmacol 1994 Jan ;111(1):131-136

 

162

UI  - 171

AU  - Cuomo MJ

AU  - Dyment PG

AU  - Gammino VM

AD  - Tulane Student Health Center, New Orleans, Louisiana

TI  - Increasing use of "Ecstasy" (MDMA) and other hallucinogens on a college campus

AB  - We conducted a random survey of illicit drug use by undergraduate students at a private southern university in 1990 and compared the results with results from a similar 1986 survey of that college's student population. During the 4 years since the first study, the prevalence of cocaine use declined from 39% to 21%, and use of traditional amphetamines declined from 22% to 12%. No significant differences were found in the use of marijuana--68% in 1986, 64% in 1990--or in use of LSD (lysergic acid diethylamide)--14% in 1986, 17% in 1990. The use of mescaline/psilocybin increased from 8% to 24% and the use of MDMA, known as "Ecstasy" (3,4- methylenedioxymethamphetamine), increased from 16% to 24%. Mescaline/psilocybin and Ecstasy were more likely than the other drugs to have been used first during the students' college years, according to the 1990 study

MH  - Adult

MH  - Cross-Sectional Studies

MH  - Designer Drugs

MH  - Hallucinogens

MH  - Human

MH  - Louisiana

MH  - Questionnaires

MH  - Students

MH  - Substance-Related Disorders

MH  - diagnosis

MH  - Universities

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 94321691LA - EngRN - 0 (Designer Drugs)RN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19940830IS - 0744-8481CY - UNITED STATESJC - H5EAA - AuthorEM - 199411

UR  - PM:0007913938

SO  - J Am Coll Health 1994 May ;42(6):271-274

 

163

UI  - 174

AU  - Dafters RI

AD  - Psychology Department, Glasgow University, UK

TI  - Effect of ambient temperature on hyperthermia and hyperkinesis induced by 3,4-methylenedioxymethamphetamine (MDMA or "ecstasy") in rats

AB  - A stress-free, biotelemetric monitoring technique was used to investigate the effects of ambient temperature (Ta) on the hyperthermic and hyperkinetic effects of 3,4-methylenedioxymethamphetamine. In the first experiment a single injection of 5.0 or 7.5 mg/kg MDMA produced hyperthermia in rats maintained at a Ta of 24 degrees C but hypothermia in rats maintained at a Ta of 11 degrees C for 24 h prior to the injection. In contrast, hyperkinesis was induced at both Tas. In the second experiment, the effects of acute MDMA administration was compared in rats maintained at a standard Ta of 24 degrees C and in rats which were placed in a cool (11 degrees C) room for a brief (90- min) period commencing 30 min after the injection. The brief exposure to the cool environment produced significant attenuation of MDMA- induced hyperthermia but did not affect the magnitude of hyperkinesis. The implications of the results for the understanding of the thermotoxic effects of MDMA in human drug users are discussed

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - Dose-Response Relationship,Drug

MH  - Hyperkinesis

MH  - chemically induced

MH  - psychology

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Rats

MH  - Rats,Wistar

MH  - Telemetry

MH  - Temperature

RP  - NOT IN FILE

NT  - UI - 95158470LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19950316IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199505

UR  - PM:0007855209

SO  - Psychopharmacology (Berl) 1994 Apr ;114(3):505-508

 

164

UI  - 181

AU  - Fernandez PL

TI  - [MDMA (Ecstasy). A designer drug with high toxicity potential]

MH  - Administration,Oral

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - Comparative Study

MH  - Human

MH  - Macaca mulatta

MH  - Mice

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - administration & dosage

MH  - metabolism

MH  - toxicity

MH  - Rats

MH  - Time Factors

RP  - NOT IN FILE

NT  - UI - 95117799LA - SpaRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19950206IS - 0034-0634CY - SPAINJC - 4LMEM - 199504

UR  - PM:0007818035

SO  - An R Acad Nac Med (Madr ) 1994  ;111(3):485-504

 

165

UI  - 180

AU  - Hastings A

AD  - Institute of Transpersonal Psychology, Palo Alto, California 94303

TI  - Some observations on MDMA experiences induced through posthypnotic suggestion

MH  - Adult

MH  - Female

MH  - Human

MH  - Male

MH  - Middle Age

MH  - Relaxation Techniques

MH  - Suggestion

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - adverse effects

MH  - pharmacology

MH  - therapeutic use

RP  - NOT IN FILE

NT  - UI - 94300491LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19940809IS - 0279-1072SB - MCY - UNITED STATESJC - JLPEM - 199410

UR  - PM:0007913132

SO  - J Psychoactive Drugs 1994 Jan ;26(1):77-83

 

166

UI  - 161

AU  - Hewitt KE

AU  - Green AR

AD  - Astra Neuroscience Research Unit, London, U.K

TI  - Chlormethiazole, dizocilpine and haloperidol prevent the degeneration of serotonergic nerve terminals induced by administration of MDMA ('Ecstasy') to rats

AB  - An investigation has been made into the effect of 3,4- methylenedioxymethamphetamine (MDMA or 'Ecstasy') administration on the concentration of 5-hydroxytryptamine (5-HT), uptake of [3H]5-HT and [3H]paroxetine binding in rat cerebral cortex tissue. Four days after 2 injections of MDMA (20 mg/kg i.p., 6 hr apart) the concentrations of 5- HT and its metabolite 5-HIAA were reduced by 60%. The binding of [3H]paroxetine to the presynaptic 5-HT transporter was decreased and high affinity uptake of [3H]5-HT was reduced by a similar amount, indicating neurodegeneration of 5-HT terminals. Pretreatment with chlormethiazole (100 mg/kg i.p.), 10 min before each MDMA injection prevented the decrease in both [3H]parotextine binding and uptake of [3H]5-HT. The loss in 5-HT and 5-HIAA content was also attenuated. Pretreatment with dizocilpine (1 mg/kg i.p.) or haloperidol (2 mg/kg i.p.) also prevented the MDMA-induced loss of [3H]paroxetine binding and attenuated the loss of 5-HT and 5-HIAA content. All three compounds also decreased the degree of hyperthermia that follows MDMA administration, although previous studies suggest that the long term neurodegeneration is not associated with the acute hyperthermic response. These data support the findings of others that MDMA injection produces degeneration of 5-HT nerve terminals in the cortex, confirm that chlormethiazole, dizocilpine and haloperidol attenuate MDMA- induced neurotoxic loss of 5-HT and demonstrate for the first time that these compounds prevent the neurodegeneration of 5-HT nerve terminals that follows MDMA administration

MH  - Animal

MH  - Chlormethiazole

MH  - pharmacology

MH  - Dizocilpine Maleate

MH  - Haloperidol

MH  - Hydroxyindoleacetic Acid

MH  - metabolism

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - antagonists & inhibitors

MH  - Nerve Degeneration

MH  - drug effects

MH  - Nerve Endings

MH  - Neuroprotective Agents

MH  - Radioligand Assay

MH  - Rats

MH  - Serotonin

MH  - Serotonin Uptake Inhibitors

RP  - NOT IN FILE

NT  - UI - 95281103LA - EngRN - 0 (Neuroprotective Agents)RN - 0 (Serotonin Uptake Inhibitors)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 52-86-8 (Haloperidol)RN - 533-45-9 (Chlormethiazole)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 77086-22-7 (Dizocilpine Maleate)PT - JOURNAL ARTICLEDA - 19950626IS - 0028-3908SB - MCY - ENGLANDJC - NZBAA - AuthorEM - 199509

UR  - PM:0007539115

SO  - Neuropharmacology 1994 Dec ;33(12):1589-1595

 

167

UI  - 168

AU  - Leonardi ET

AU  - Azmitia EC

AD  - Department of Biology, New York University, NY 10003

TI  - MDMA (ecstasy) inhibition of MAO type A and type B: comparisons with fenfluramine and fluoxetine (Prozac)

AB  - 3,4-Methylenedioxymethamphetamine (MDMA), a serotonin (5-HT) neurotoxin, has been shown to promote the release of serotonin (5-HT) and block its reuptake. The increased buildup of extracellular 5-HT should normally be degraded by monoamine oxidase (MAO). The effects of both enantiomers of MDMA were examined on MAO-A and monoamine oxidase-B (MAO-B) activity in rat brain homogenates. Both enantiomers competitively inhibited 5-HT catabolism by rat brain MAO-A. The Ki of MDMA for MAO-A was 22 mumol/L. A mixed type of inhibition by MDMA was observed for phenethylamine catabolism by MAO-B for both optical antipodes. Logistical analysis of concentration response curves for MDMA inhibition of MAO-A and MAO-B show an IC50 of 44 mumol/L for inhibition of MAO-A by MDMA. The IC50 value of MDMA inhibition of MAO-B was 370 mumol/L, showing a selective potency for MAO-A inhibition. The MAO inhibitory properties of fenfluramine (FEN) and fluoxetine (FLUOX) were compared to those of MDMA. The rank order potency of these drugs for MAO-A inhibition was MDMA > FLUOX > FEN, whereas for MAO-B inhibition, FLUOX > MDMA > FEN. A combination of FLUOX and MDMA at their respective IC50 did not inhibit MAO activity more than either drug alone at equivalent concentrations. These results indicate that the actions of FEN do not appear to involve MAO inhibition. MDMA (ecstasy) produced a preferential inhibition of MAO-A (IC50 = 44 mumol/L), which should increase extracellular 5-HT.(ABSTRACT TRUNCATED AT 250 WORDS)

MH  - Animal

MH  - Binding,Competitive

MH  - drug effects

MH  - Brain

MH  - enzymology

MH  - Comparative Study

MH  - Drug Interactions

MH  - Fenfluramine

MH  - pharmacology

MH  - Fluoxetine

MH  - In Vitro

MH  - Male

MH  - Monoamine Oxidase Inhibitors

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Phenethylamines

MH  - metabolism

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 95032515LA - EngRN - 0 (Monoamine Oxidase Inhibitors)RN - 0 (Phenethylamines)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 458-24-2 (Fenfluramine)RN - 50-67-9 (Serotonin)RN - 54910-89-3 (Fluoxetine)PT - JOURNAL ARTICLEID - NIDA 271-90-7403DA - 19941212IS - 0893-133XSB - MCY - UNITED STATESJC - ADQAA - AuthorEM - 199502

UR  - PM:0007945733

SO  - Neuropsychopharmacology 1994 Jul ;10(4):231-238

 

168

UI  - 177

AU  - Lin HQ

AU  - McGregor IS

AU  - Atrens DM

AU  - Christie MJ

AU  - Jackson DM

AD  - Department of Pharmacology, University of Sydney, N.S.W., Australia

TI  - Contrasting effects of dopaminergic blockade on MDMA and d-amphetamine conditioned taste aversions

AB  - A series of experiments examined the role of dopamine in the conditioned taste aversion (CTA) produced by 3,4- methylenedioxymethamphetamine (MDMA) and d-amphetamine in rats. The CTA induced by MDMA (1.0 mg/kg) was unaffected by the D1 dopamine receptor antagonist SCH23390 (0.3 or 0.6 mg/kg), the D2 receptor antagonist raclopride (0.3 or 0.6 mg/kg), SCH23390 and raclopride combined (both 0.3 or 0.6 mg/kg), or the D1/D2 receptor antagonist haloperidol (0.4 mg/kg). In contrast, the CTA produced by d-amphetamine (0.5 mg/kg) was attenuated by SCH23390 and raclopride combined (both 0.3 mg/kg) as well as haloperidol (0.4 mg/kg), but not by SCH23390 (0.3 or 0.6 mg/kg) or raclopride (0.3 or 0.6 mg/kg) alone. These results suggest that dopamine plays different roles in MDMA and amphetamine CTAs, and that the D1 and D2 receptors independently mediate the aversive effect of amphetamine in CTA

MH  - Animal

MH  - Avoidance Learning

MH  - drug effects

MH  - Comparative Study

MH  - Dextroamphetamine

MH  - pharmacology

MH  - Haloperidol

MH  - Male

MH  - Rats

MH  - Rats,Wistar

MH  - Receptors,Dopamine

MH  - antagonists & inhibitors

MH  - Receptors,Dopamine D1

MH  - Receptors,Dopamine D2

MH  - Salicylamides

MH  - Sch-23390

MH  - Support,Non-U.S.Gov't

MH  - Taste

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 94195875LA - EngRN - 0 (Receptors, Dopamine D1)RN - 0 (Receptors, Dopamine D2)RN - 0 (Receptors, Dopamine)RN - 0 (Salicylamides)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 51-64-9 (Dextroamphetamine)RN - 52-86-8 (Haloperidol)RN - 84225-95-6 (Raclopride)RN - 87075-17-0 (Sch-23390)PT - JOURNAL ARTICLEDA - 19940502IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199407

UR  - PM:0007908448

SO  - Pharmacol Biochem Behav 1994 Feb ;47(2):369-374

 

169

UI  - 163

AU  - Mannaerts GH

AU  - Luitse JS

AU  - Zandstra DF

AU  - Hoitsma HF

TI  - [Morbidity and mortality due to the use of ecstacy (letter; comment)]

MH  - Adolescence

MH  - Adult

MH  - Female

MH  - Human

MH  - Male

MH  - Middle Age

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - poisoning

MH  - Netherlands

MH  - epidemiology

MH  - therapy

MH  - Prognosis

MH  - Substance-Related Disorders

RP  - NOT IN FILE

NT  - UI - 95059629LA - DutRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - COMMENTPT - LETTERDA - 19941229IS - 0028-2162CY - NETHERLANDSJC - NUKEM - 199502RO - M:CNR

UR  - PM:0007969644

SO  - Ned Tijdschr Geneeskd 1994 Nov 19 ;138(47):2368

 

170

UI  - 175

AU  - McCann UD

AU  - Ridenour A

AU  - Shaham Y

AU  - Ricaurte GA

AD  - Unit on Anxiety and Affective Disorders, National Institute of Mental Health, Bethesda, Maryland 20892

TI  - Serotonin neurotoxicity after (+/-)3,4-methylenedioxymethamphetamine (MDMA; "Ecstasy"): a controlled study in humans

AB  - (+/-)3,4-Methylenedioxymethamphetamine (MDMA; "Ecstasy"), an increasingly popular recreational drug, is known to damage brain serotonin 5-hydroxytryptamine (5-HT) neurons in experimental animals. Whether MDMA is neurotoxic in humans has not been established. Thirty MDMA users and 28 controls were admitted to a controlled inpatient setting for measurement of biologic and behavioral indexes of central 5- HT function. Outcome measures obtained after at least 2 weeks of drug abstinence included concentrations of monoamine metabolites in cerebrospinal fluid (CSF), prolactin responses to L-tryptophan, nociceptive responses to ischemic pain, and personality characteristics in which 5-HT has been implicated (i.e., impulsivity and aggression). Subjects with a history of MDMA exposure had lower levels of CSF 5- hydroxyindoleacetic acid (the major metabolite of 5-HT) than controls (p = .001). Although they resembled controls in their prolactin response to L-tryptophan and their response to ischemic pain, MDMA users had lower scores on personality measures of impulsivity (p = .004) and indirect hostility (p = .009). The CSF findings suggest that 5-HT neurotoxicity may be a potential complication of MDMA use. Further, differences in personality support the view that 5-HT systems are involved in modulating impulsive and aggressive personality traits. Additional studies of MDMA-exposed individuals are needed to confirm and extend the present findings. Such studies could help elucidate the role of 5-HT in normal brain function as well as in neuropsychiatric disease states

MH  - Adult

MH  - Analysis of Variance

MH  - Female

MH  - Homovanillic Acid

MH  - cerebrospinal fluid

MH  - Human

MH  - Hydroxyindoleacetic Acid

MH  - Male

MH  - Middle Age

MH  - Pain

MH  - physiopathology

MH  - Pain Measurement

MH  - Personality Tests

MH  - Prolactin

MH  - blood

MH  - Serotonin

MH  - metabolism

MH  - Street Drugs

MH  - toxicity

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 94296529LA - EngRN - 0 (Street Drugs)RN - 306-08-1 (Homovanillic Acid)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 9002-62-4 (Prolactin)PT - CLINICAL TRIALPT - JOURNAL ARTICLEID - 5MO1RR02719/RR/NCRRID - RO1DA05938/DA/NIDADA - 19940810IS - 0893-133XSB - MCY - UNITED STATESJC - ADQAA - AuthorEM - 199410RO - M:MWS

UR  - PM:0007517677

SO  - Neuropsychopharmacology 1994 Apr ;10(2):129-138

 

171

UI  - 173

AU  - McCoy EP

AU  - Renfrew C

AU  - Johnston JR

AU  - Lavery G

AD  - Royal Victoria Hospital, Balfast, Northern Ireland

TI  - Malignant hyperpyrexia in an MDMA ("Ecstasy") abuser

MH  - Adult

MH  - Case Report

MH  - Diagnosis,Differential

MH  - Hallucinogens

MH  - adverse effects

MH  - Human

MH  - Male

MH  - Malignant Hyperthermia

MH  - drug therapy

MH  - etiology

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Postoperative Complications

MH  - diagnosis

RP  - NOT IN FILE

NT  - UI - 96226877LA - EngRN - 0 (Hallucinogens)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19960726IS - 0041-6193CY - NORTHERN IRELANDJC - WN2EM - 199610

UR  - PM:0008658983

SO  - Ulster Med J 1994 Apr ;63(1):103-107

 

172

UI  - 169

AU  - Miczek KA

AU  - Haney M

AD  - Department of Psychology, Tufts University, Medford, MA 02155

TI  - Psychomotor stimulant effects of d-amphetamine, MDMA and PCP: aggressive and schedule-controlled behavior in mice

AB  - The objective of the present experiments was to characterize psychomotor stimulant effects of d-amphetamine, methylenedioxymethamphetamine (MDMA) and phencyclidine (PCP) on conditioned performance and on aggressive behavior in mice. In a novel protocol with alternating periods of schedule-controlled responding and aggressive behavior toward an intruder it was possible to assess a range of species-specific agonistic acts, postures, and motor activities as well as response rates and patterns engendered by a multiple Fixed Interval (FI) and Fixed Ratio (FR) schedule within the same animal. Initially, it was confirmed that d-amphetamine and, less reliably, MDMA and PCP, increased FI, but not FR responding in mice. In the next experiment, mice confronted an intruder at the midpoint of the 1-h daily session; following the display of aggressive behavior, the rate of FI responding showed an amphetamine-like increase, whereas only a transient change occurred after non-aggressive encounters. Thirdly, using this new protocol, PCP, d-amphetamine and MDMA altered FI and FR responding in a way that was closely similar to the first experiment. Low PCP and d-amphetamine doses increased aggressive behavior erratically in certain individuals, but not reliably for the group. MDMA dose-dependently decreased aggressive behavior, and all drugs disrupted aggressive behavior at higher doses. The characteristic increases in walking and decreases in rearing after higher doses of PCP and d-amphetamine were greatly attenuated when the intruder was present.(ABSTRACT TRUNCATED AT 250 WORDS)

MH  - Aggression

MH  - drug effects

MH  - Animal

MH  - Central Nervous System Stimulants

MH  - pharmacology

MH  - Comparative Study

MH  - Conditioning,Operant

MH  - Dextroamphetamine

MH  - Dose-Response Relationship,Drug

MH  - Male

MH  - Mice

MH  - Motor Activity

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Phencyclidine

MH  - Reinforcement Schedule

MH  - Support,U.S.Gov't,P.H.S.

RP  - NOT IN FILE

NT  - UI - 95175868LA - EngRN - 0 (Central Nervous System Stimulants)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 51-64-9 (Dextroamphetamine)RN - 77-10-1 (Phencyclidine)PT - JOURNAL ARTICLEID - AA05122/AA/NIAAAID - DA02632/DA/NIDADA - 19950324IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199506

UR  - PM:0007871076

SO  - Psychopharmacology (Berl) 1994 Jul ;115(3):358-365

 

173

UI  - 166

AU  - Nash JF

AU  - Roth BL

AU  - Brodkin JD

AU  - Nichols DE

AU  - Gudelsky GA

AD  - Department of Psychiatry, School of Medicine, Case Western Reserve University, Cleveland, OH 44106-5000

TI  - Effect of the R(-) and S(+) isomers of MDA and MDMA on phosphatidyl inositol turnover in cultured cells expressing 5-HT2A or 5-HT2C receptors

AB  - The effect of the R(-) and S(+) isomers of 3,4- methylenedioxyamphetamine (MDA) and its N-methyl analog 3,4- methylenedioxymethamphetamine (MDMA) on [3H]inositol monophosphate accumulation was studied in cells expressing either 5-HT2A or 5-HT2C receptors. The isomers of MDA produced a concentration dependent increase in phosphatidyl inositol (PI) hydrolysis at the 5-HT2A receptors, with the R(-) isomer of MDA being more potent than the S(+) at the 5-HT2A receptor. The R(-) and S(+) isomers of MDMA were significantly less efficacious at the 5-HT2A receptor as compared to MDA; S(+)MDMA had no effect. At the 5-HT2C receptor, both R(-) and S(+)MDA were equipotent at stimulating PI hydrolysis, with the S(+) isomer of MDMA being more efficacious at the 5-HT2C receptor compared with the R(-) isomer. In all cases at both the 5-HT2A and 5-HT2C receptors, the affinities of the isomers of MDMA and MDA were at least 2-3 orders of magnitude less than 5-HT. Despite the weak effect of these compounds at the 5-HT2A and 5-HT2C receptors, these substituted amphetamines do possess intrinsic activity which may contribute to their neurotoxic effects when administered at high doses

MH  - Animal

MH  - Cells,Cultured

MH  - Comparative Study

MH  - Fibroblasts

MH  - drug effects

MH  - metabolism

MH  - Hydrolysis

MH  - Mice

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Phosphatidylinositols

MH  - Receptors,Serotonin

MH  - physiology

MH  - Stereoisomerism

MH  - Structure-Activity Relationship

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - 3T3 Cells

RP  - NOT IN FILE

NT  - UI - 95124589LA - EngRN - 0 (serotonin 2A receptor)RN - 0 (serotonin 2C receptor)RN - 0 (Phosphatidylinositols)RN - 0 (Receptors, Serotonin)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEID - DA 07427/DA/NIDADA - 19950210IS - 0304-3940SB - MCY - IRELANDJC - N7NAA - AuthorEM - 199504

UR  - PM:0007824160

SO  - Neurosci Lett 1994 Aug 15 ;177(1-2):111-115

 

174

UI  - 176

AU  - Padkin A

TI  - Treating MDMA ('Ecstasy') toxicity [letter; comment]

MH  - Animal

MH  - Designer Drugs

MH  - poisoning

MH  - Human

MH  - drug therapy

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 94197341LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - COMMENTPT - LETTERDA - 19940502IS - 0003-2409SB - ASB - MCY - ENGLANDJC - 4MCEM - 199407RO - M:LC2

UR  - PM:0007908506

SO  - Anaesthesia 1994 Mar ;49(3):259

 

175

UI  - 178

AU  - Romano AG

AU  - Harvey JA

AD  - Department of Pharmacology, Medical College of Pennsylvania, Eastern Pennsylvania Psychiatric Institute, Philadelphia 19129

TI  - MDMA enhances associative and nonassociative learning in the rabbit

AB  - The rate of associative learning was assessed in the presence of saline versus methylenedioxymethamphetamine (MDMA) at doses of 0.95, 1.9, and 3.8 mg/kg. The conditioned stimuli (CSs) were lights and tones and the unconditioned stimulus (US) was a corneal air puff. Learning was enhanced by all but the highest dose of drug tested, and the enhancement was most pronounced when light was used as the conditioned stimulus. Nonassociative responding was assessed using unpaired presentations of the lights, tones, and air puffs. MDMA (1.9 mg/kg) produced a slight increase in the percentage of baseline responses but failed to produce an increase in the frequency of nonassociative responding in the presence of the lights or tones. MDMA produced a significant increase in the amplitude of the unconditioned response to the corneal air puff across the 10 sessions. This increase was taken as evidence for sensitization of the unconditioned response, a nonassociative learning phenomenon. In summary, MDMA, like the parent compound methylenedioxyamphetamine (MDA), enhances both conditioned and unconditioned responding. Because this dual effect has not been seen with related psychedelic compounds, the effect appears to be unique to this class of phenylethylamine drugs

MH  - Animal

MH  - Association Learning

MH  - drug effects

MH  - Conditioning,Classical

MH  - Dose-Response Relationship,Drug

MH  - Female

MH  - Male

MH  - Nictitating Membrane

MH  - Physical Stimulation

MH  - Rabbits

MH  - Stimulation,Chemical

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - pharmacology

RP  - NOT IN FILE

NT  - UI - 94195862LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEID - DA04944/DA/NIDADA - 19940502IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199407

UR  - PM:0007908446

SO  - Pharmacol Biochem Behav 1994 Feb ;47(2):289-293

 

176

UI  - 170

AU  - Satchell SC

AU  - Connaughton M

AD  - Department of Geriatrics, Hammersmith Hospital, London

TI  - Inappropriate antidiuretic hormone secretion and extreme rises in serum creatinine kinase following MDMA ingestion

MH  - Adult

MH  - Case Report

MH  - Creatine Kinase

MH  - blood

MH  - Designer Drugs

MH  - adverse effects

MH  - Female

MH  - Human

MH  - Inappropriate ADH Syndrome

MH  - chemically induced

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Seizures

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 95005732LA - EngRN - EC 2.7.3.2 (Creatine Kinase)RN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19941026IS - 0007-1064SB - MCY - ENGLANDJC - BZ5EM - 199501

UR  - PM:0007921509

SO  - Br J Hosp Med 1994 May 4 ;51(9):495

 

177

UI  - 160

AU  - Schifano F

AU  - Magni G

AD  - Addiction Treatment Unit, Local Health Unit No. 21, Padova, Italy

TI  - MDMA ("ecstasy") abuse: psychopathological features and craving for chocolate: a case series

MH  - Adult

MH  - Behavior,Addictive

MH  - metabolism

MH  - psychology

MH  - Cacao

MH  - Case Report

MH  - Female

MH  - Human

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - Serotonin

MH  - Substance-Related Disorders

RP  - NOT IN FILE

NT  - UI - 95161548LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEDA - 19950321IS - 0006-3223SB - MCY - UNITED STATESJC - A3SEM - 199505

UR  - PM:0007858073

SO  - Biol Psychiatry 1994 Dec 1 ;36(11):763-767

 

178

UI  - 162

AU  - Series HG

AU  - Cowen PJ

AU  - Sharp T

AD  - Department of Psychiatry, Warneford Hospital, Oxford, UK

TI  - p-Chloroamphetamine (PCA), 3,4-methylenedioxy-methamphetamine (MDMA) and d-fenfluramine pretreatment attenuates d-fenfluramine-evoked release of 5-HT in vivo

AB  - Previous work has suggested that repeated treatment with substituted amphetamines including PCA, MDMA and d-fenfluramine produces a persistent neurodegeneration which is relatively selective for the fine serotoninergic terminals arising from the dorsal raphe nucleus. The aim of the present study was to investigate whether the acute releasing effect of d-fenfluramine might also be sensitive to lesions produced by PCA, MDMA and d-fenfluramine itself. Basal and 5-HT release evoked by d- fenfluramine or 100 mM KCl was measured by microdialysis in frontal or parietal cortex of rats 2 weeks after they had been treated with a neurodegenerative regime of PCA, MDMA, d-fenfluramine, or vehicle. In frontal cortex of vehicle controls, d-fenfluramine (10 mg/kg IP) and KCl (100 mM via microdialysis probe) evoked an increase in 5-HT of 1740% and 779% of basal, respectively. PCA pretreatment reduced d- fenfluramine-evoked 5-HT release by 90.9% while potassium-evoked release was reduced by only 66.8%. Similar results were obtained in parietal cortex. MDMA (20 mg/kg x 8) and d-fenfluramine (1.25 mg/kg x 8) pretreatment reduced d-fenfluramine-evoked release of 5-HT in frontal cortex by 45.2% and 72.0%, respectively. Overall, the present data are consistent with the hypothesis that the acute release of 5-HT evoked by d-fenfluramine occurs via those terminals destroyed by pretreatment with PCA, MDMA and d-fenfluramine, while KCl evokes release from both PCA-sensitive and PCA-insensitive terminals. The significance of these results for the interpretation of neuroendocrine data from d-fenfluramine challenge tests is discussed

MH  - p-Chloroamphetamine

MH  - pharmacology

MH  - Amphetamines

MH  - Animal

MH  - Cerebral Cortex

MH  - drug effects

MH  - metabolism

MH  - Chromatography,High Pressure Liquid

MH  - Dextroamphetamine

MH  - Fenfluramine

MH  - antagonists & inhibitors

MH  - Hydroxyindoleacetic Acid

MH  - Male

MH  - Microdialysis

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - Potassium

MH  - Raphe Nuclei

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 95215570LA - EngRN - 0 (Amphetamines)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 458-24-2 (Fenfluramine)RN - 50-67-9 (Serotonin)RN - 51-64-9 (Dextroamphetamine)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 64-12-0 (p-Chloroamphetamine)RN - 7440-09-7 (Potassium)PT - JOURNAL ARTICLEDA - 19950428IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199507

UR  - PM:0007535469

SO  - Psychopharmacology (Berl) 1994 Dec ;116(4):508-514

 

179

UI  - 179

AU  - Sprague JE

AU  - Huang X

AU  - Kanthasamy A

AU  - Nichols DE

AD  - Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, IN 47907

TI  - Attenuation of 3,4-methylenedioxymethamphetamine (MDMA) induced neurotoxicity with the serotonin precursors tryptophan and 5- hydroxytryptophan

AB  - Treatment of rats with serotonin (5-HT) precursors tryptophan (TRP, 400 mg/kg) and 5-hydroxytryptophan (5-HTP, 50 mg/kg) was shown to attenuate MDMA (20 mg/kg) induced serotonergic neurotoxicity as measured by [3H]- paroxetine binding in the striatum, hippocampus, and frontal cortex of the rat brain. Hippocampal 5-HT and 5-HIAA levels were also indicative of the protective effects of TRP and 5-HTP. These results suggest that depletion of 5-HT stores is important for MDMA-induced neurotoxicity. The possible significance of this 5-HT depletion in MDMA-induced serotonergic terminal degeneration is also discussed

MH  - Animal

MH  - Brain Diseases

MH  - chemically induced

MH  - metabolism

MH  - prevention & control

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - antagonists & inhibitors

MH  - toxicity

MH  - Nerve Endings

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Support,U.S.Gov't,P.H.S.

MH  - Tryptophan

MH  - pharmacology

MH  - 5-Hydroxytryptophan

RP  - NOT IN FILE

NT  - UI - 95020316LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 56-69-9 (5-Hydroxytryptophan)RN - 73-22-3 (Tryptophan)PT - JOURNAL ARTICLEID - DA04758/DA/NIDADA - 19941025IS - 0024-3205SB - MSB - XCY - ENGLANDJC - L62AA - AuthorEM - 199501

UR  - PM:0007934616

SO  - Life Sci 1994  ;55(15):1193-1198

 

180

UI  - 172

AU  - Steele TD

AU  - McCann UD

AU  - Ricaurte GA

AD  - Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD

TI  - 3,4-Methylenedioxymethamphetamine (MDMA, "Ecstasy"): pharmacology and toxicology in animals and humans

AB  - (+/-)3,4-Methylenedioxymethamphetamine (MDMA, "Ecstasy"), a ring- substituted amphetamine derivative first synthesized in 1914, has emerged as a popular recreational drug of abuse over the last decade. Pharmacological studies indicate that MDMA produces a mixture of central stimulant and psychedelic effects, many of which appear to be mediated by brain monoamines, particularly serotonin and dopamine. In addition to its pharmacologic actions, MDMA has been found to possess toxic activity toward brain serotonin neurones. Serotonergic neurotoxicity after MDMA has been demonstrated in a variety of experimental animals (including non-human primates). In monkeys, the neurotoxic dose of MDMA closely approaches that used by humans. While the possibility that MDMA is also neurotoxic in humans is under investigation, other adverse effects of MDMA in humans have been documented, including various systemic complications and a number of untoward neuropsychiatric sequelae. Notably, many of the adverse neuropsychiatric consequences noted after MDMA involve behavioral domains putatively influenced by brain serotonin (e.g., mood, cognition and anxiety). Given the restricted status of MDMA use, retrospective clinical observations from suspecting clinicians will probably continue to be a primary source of information regarding MDMA's effects in humans. As such, this article is intended to familiarize the reader with the behavioral pharmacology and toxicology of MDMA, with the hope that improved recognition of MDMA-related syndromes will provide insight into the function of serotonin in the human brain, in health as well as disease

MH  - Animal

MH  - Behavior,Animal

MH  - drug effects

MH  - Brain

MH  - Designer Drugs

MH  - pharmacology

MH  - poisoning

MH  - toxicity

MH  - Dopamine

MH  - metabolism

MH  - Human

MH  - Serotonin

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 94319272LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19940831IS - 0965-2140CY - ENGLANDJC - BM3AA - AuthorEM - 199411

UR  - PM:0007913850

SO  - Addiction 1994 May ;89(5):539-551

 

181

UI  - 164

AU  - Szukaj M

AD  - Psychiatrische Klinik und Poliklinik, Westfalischen Wilhelms- Universitat Munster

TI  - [MDMA ("Ecstasy")--a dangerous drug or psychotherapeutic drug?]

AB  - Abuse of 3,4-methylenedioxymethamphetamine (MDMA) is increasing, as is the number of deaths associated with "ecstasy". The history, effects and side effects of this controversial psychotropic substance are presented. Its relevance for clinical practice is shown

MH  - Dose-Response Relationship,Drug

MH  - English Abstract

MH  - Human

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - adverse effects

MH  - therapeutic use

MH  - Psychotherapy

MH  - Substance-Related Disorders

MH  - epidemiology

MH  - etiology

RP  - NOT IN FILE

NT  - UI - 95115819LA - GerRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19950209IS - 0028-2804SB - MCY - GERMANYJC - NWSAA - AuthorEM - 199504

UR  - PM:0007816160

SO  - Nervenarzt 1994 Nov ;65(11):802-805

 

182

UI  - 167

AU  - Wotherspoon G

AU  - Savery D

AU  - Priestley JV

AU  - Rattray M

AD  - Molecular Neuropharmacology Laboratory, UMDS Division of Biochemistry and Molecular Biology, University of London, Guy's Hospital, UK

TI  - Repeated administration of MDMA down-regulates preprocholecystokinin mRNA expression but not tyrosine hydroxylase mRNA expression in neurones of the rat substantia nigra

AB  - The effect of repeated administration of 3,4- methylenedioxymethamphetamine (MDMA) on the expression of tyrosine hydroxylase and preprocholecystokinin (CCK) messenger RNAs in substantia nigra was examined by in situ hybridisation histochemistry. Sections hybridised with 35S-labelled oligonucleotides were subjected to computerised image analysis to determine the density of silver grains above positively labelled cells as an index of steady state mRNA levels. In the substantia nigra pars compacta, CCK mRNA levels were significantly reduced in drug-treated animals 24 h and at 2 weeks after the last dose of MDMA (10 mg/kg i.p., twice daily for 4 days). In the same animals, MDMA caused no change in the level of tyrosine hydroxylase mRNA in this brain region. The results show that MDMA can produce changes in dopamine neurones. Furthermore, since tyrosine hydroxylase and cholecystokinin are co-expressed in substantia nigra pars compacta, these results suggest that the expression of the tyrosine hydroxylase and CCK genes are regulated independently

MH  - Animal

MH  - Cholecystokinin

MH  - genetics

MH  - Down-Regulation (Physiology)

MH  - drug effects

MH  - Genetic Code

MH  - Male

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Neurons

MH  - metabolism

MH  - Protein Precursors

MH  - Rats

MH  - Rats,Wistar

MH  - RNA,Messenger

MH  - biosynthesis

MH  - Substantia Nigra

MH  - cytology

MH  - Support,Non-U.S.Gov't

MH  - Tyrosine 3-Monooxygenase

RP  - NOT IN FILE

NT  - UI - 95075245LA - EngRN - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)RN - 0 (Protein Precursors)RN - 0 (RNA, Messenger)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 89624-02-2 (preprocholecystokinin)RN - 9011-97-6 (Cholecystokinin)PT - JOURNAL ARTICLEDA - 19950105IS - 0169-328XSB - MCY - NETHERLANDSJC - MBRAA - AuthorEM - 199503

UR  - PM:0007984049

SO  - Brain Res Mol Brain Res 1994 Aug ;25(1-2):34-40

 

183

UI  - 190

AU  - Ali SF

AU  - Newport GD

AU  - Scallet AC

AU  - Binienda Z

AU  - Ferguson SA

AU  - Bailey JR

AU  - Paule MG

AU  - Slikker W

AD  - Division of Neurotoxicology, National Center for Toxicological Research, Jefferson, AR 72079-9502

TI  - Oral administration of 3,4-methylenedioxymethamphetamine (MDMA) produces selective serotonergic depletion in the nonhuman primate

AB  - MDMA (3,4-methylenedioxymethamphetamine) has been reported to produce serotonergic depletion in nonhuman primates at doses as low as 2.5 mg/kg (1-2 times the typical human dose). The current study evaluated the dose-response relationships of MDMA (1.25-20.0 mg/kg) using regional concentrations of serotonin (5-HT) and its metabolite, 5- hydroxyindoleacetic acid (5-HIAA), and home cage behavior as endpoints. Adult female rhesus monkeys (n = 16) were treated orally with 0, 1.25, 2.5, or 20.0 mg/kg MDMA twice daily for 4 consecutive days. Eighteen behaviors were measured in the home cage prior to, during, and after MDMA treatment. One month after the last dose, the animals were sacrificed and brains dissected into several regions for neurochemical analyses. 5-HT and 5-HIAA were analyzed via HPLC/EC. The lower doses of MDMA (1.25 and 2.5 mg/kg) did not significantly alter 5-HT or 5-HIAA concentrations in any brain region except hippocampus in which 5-HT concentrations were decreased after 2.5 mg/kg. MDMA at 20.0 mg/kg significantly decreased 5-HT and 5-HIAA concentrations in several cortical and midbrain structures. However, 5-HT and 5-HIAA concentrations in brain stem and hypothalamus were not significantly altered after any dose of MDMA. Combined with previous data from this laboratory, these results indicate that the decreased concentrations of 5-HT and 5-HIAA in selected brain regions show a selective dose- response relationship for MDMA-induced neurotoxicity as measured by serotonergic depletion in the nonhuman primate

MH  - Administration,Oral

MH  - Animal

MH  - Behavior,Animal

MH  - drug effects

MH  - Brain

MH  - metabolism

MH  - Dopamine

MH  - Dose-Response Relationship,Drug

MH  - Female

MH  - Homovanillic Acid

MH  - Hydroxyindoleacetic Acid

MH  - Macaca mulatta

MH  - Serotonin

MH  - 3,4-Dihydroxyphenylacetic Acid

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - administration & dosage

RP  - NOT IN FILE

NT  - UI - 93287943LA - EngRN - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)RN - 306-08-1 (Homovanillic Acid)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - JOURNAL ARTICLEDA - 19930715IS - 0892-0362SB - MCY - UNITED STATESJC - NATAA - AuthorEM - 199309

UR  - PM:0007685472

SO  - Neurotoxicol Teratol 1993 Mar ;15(2):91-96

 

184

UI  - 187

AU  - Allen RP

AU  - McCann UD

AU  - Ricaurte GA

AD  - Department of Neurology, Johns Hopkins University School of Medicine, Francis Scott Key Medical Center, Baltimore, Maryland

TI  - Persistent effects of (+/- )3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") on human sleep

AB  - (+/- )3,4-methylenedioxymethamphetamine (MDMA) is a recreational drug of abuse which damages serotonin neurons in animals. It is not known whether MDMA is also neurotoxic in humans, and if so, whether there are functional consequences. Given the putative role of serotonin in sleep, it was hypothesized that one manifestation of serotonin neurotoxicity in humans might be disturbances of sleep. To determine whether MDMA use has effects on sleep, all-night polysomnograms of 23 MDMA users were compared to those of 22 age- and sex-matched controls. On average, MDMA users had 19 minutes less total sleep and 23.2 minutes less non-REM (NREM) sleep than controls. These statistically significant differences in NREM sleep were due primarily to an average of 37 minutes less stage 2 sleep, with no significant differences noted in stages 1, 3 or 4. Although it is not known whether the alterations in sleep observed in MDMA users are due to serotonin neurotoxicity, the present findings suggest that MDMA use can lead to persistent changes in CNS structures involved in human sleep generation

MH  - Adult

MH  - Amphetamines

MH  - pharmacology

MH  - toxicity

MH  - Comparative Study

MH  - Electroencephalography

MH  - Female

MH  - Human

MH  - Male

MH  - Mental Disorders

MH  - complications

MH  - diagnosis

MH  - Neurons

MH  - drug effects

MH  - Polysomnography

MH  - Psychiatric Status Rating Scales

MH  - Respiration

MH  - Serotonin

MH  - metabolism

MH  - physiology

MH  - Sleep Disorders

MH  - Sleep Stages

MH  - Sleep,Rem

MH  - Substance-Related Disorders

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 94053265LA - EngRN - 0 (Amphetamines)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEID - NIDA DA05707/DA/NIDADA - 19931222IS - 0161-8105SB - MCY - UNITED STATESJC - SWSAA - AuthorEM - 199402

UR  - PM:0007901886

SO  - Sleep 1993 Sep ;16(6):560-564

 

185

UI  - 191

AU  - Colado MI

AU  - Murray TK

AU  - Green AR

AD  - Astra Neuroscience Research Unit, London

TI  - 5-HT loss in rat brain following 3,4-methylenedioxymethamphetamine (MDMA), p-chloroamphetamine and fenfluramine administration and effects of chlormethiazole and dizocilpine

AB  - 1. The present study has investigated whether the neurotoxic effects of the relatively selective 5-hydroxytryptamine (5-HT) neurotoxins, 3,4- methylenedioxymethamphetamine (MDMA or 'Ecstasy'), p-chloroamphetamine (PCA) and fenfluramine on hippocampal and cortical 5-HT terminals in rat brain could be prevented by administration of either chlormethiazole or dizocilpine. 2. Administration of MDMA (20 mg kg-1, i.p.) resulted in an approximate 30% loss of cortical and hippocampal 5- HT and 5-hydroxyindoleacetic acid (5-HIAA) content 4 days later. Injection of chlormethiazole (50 mg kg-1) 5 min before and 55 min after the MDMA provided complete protection in both regions, while dizocilpine (1 mg kg-1, i.p.) protected only the hippocampus. 3. Administration of a single dose of chlormethiazole (100 mg kg-1) 20 min after the MDMA also provided complete protection to the hippocampus but not the cortex. This regime also attenuated the sustained hyperthermia (approx +2.5 degrees C) induced by the MDMA injection. 4. Injection of PCA (5 mg kg-1, i.p.) resulted in a 70% loss of 5-HT and 5-HIAA content in hippocampus and cortex 4 days later. Injection of chlormethiazole (100 mg kg-1, i.p.) or dizocilpine (1 mg kg-1, i.p.) 5 min before and 55 min after the PCA failed to protect against the neurotoxicity, nor was protection afforded by chlormethiazole when a lower dose of PCA (2.5 mg kg-1, i.p.) was given which produced only a 30% loss of 5-HT content.(ABSTRACT TRUNCATED AT 250 WORDS)

MH  - p-Chloroamphetamine

MH  - antagonists & inhibitors

MH  - pharmacology

MH  - toxicity

MH  - Animal

MH  - Behavior,Animal

MH  - drug effects

MH  - Body Temperature

MH  - Brain Chemistry

MH  - Cerebral Cortex

MH  - metabolism

MH  - Chlormethiazole

MH  - Dizocilpine Maleate

MH  - Fenfluramine

MH  - Hippocampus

MH  - Hydroxyindoleacetic Acid

MH  - Male

MH  - Rats

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 93222906LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 458-24-2 (Fenfluramine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 533-45-9 (Chlormethiazole)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 64-12-0 (p-Chloroamphetamine)RN - 77086-22-7 (Dizocilpine Maleate)PT - JOURNAL ARTICLEDA - 19930513IS - 0007-1188SB - MCY - ENGLANDJC - B00AA - AuthorEM - 199307

UR  - PM:0007682129

SO  - Br J Pharmacol 1993 Mar ;108(3):583-589

 

186

UI  - 192

AU  - Finnegan KT

AU  - Calder L

AU  - Clikeman J

AU  - Wei S

AU  - Karler R

AD  - Psychiatry Service, Veterans Administration Medical Center, Salt Lake City, UT 84148

TI  - Effects of L-type calcium channel antagonists on the serotonin- depleting actions of MDMA in rats

AB  - The calcium channel antagonists verapamil nifedipine and flunarizine all increased the threshold for convulsions induced by N-methyl-D- aspartate in rats. By contrast, only flunarizine blocked the long-term serotonin-depleting effects of 3,4-methylenedioxymethamphetamine. Flunarizine was also the only drug that antagonized methamphetamine- induced stereotypy. These findings suggest that calcium influx through L-type channels does not participate in the neurotoxic mechanism of MDMA, and that the neuroprotective actions of flunarizine are probably related to its anti-dopaminergic activity

MH  - Animal

MH  - Brain Chemistry

MH  - drug effects

MH  - Calcium Channel Blockers

MH  - pharmacology

MH  - Cerebral Cortex

MH  - metabolism

MH  - Convulsions

MH  - chemically induced

MH  - prevention & control

MH  - Flunarizine

MH  - Haloperidol

MH  - Hippocampus

MH  - Male

MH  - Methamphetamine

MH  - antagonists & inhibitors

MH  - Nifedipine

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Stereotyped Behavior

MH  - Support,U.S.Gov't,Non-P.H.S.

MH  - Support,U.S.Gov't,P.H.S.

MH  - Verapamil

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 93201244LA - EngRN - 0 (Calcium Channel Blockers)RN - 21829-25-4 (Nifedipine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 52-53-9 (Verapamil)RN - 52-86-8 (Haloperidol)RN - 52468-60-7 (Flunarizine)RN - 537-46-2 (Methamphetamine)PT - JOURNAL ARTICLEID - DA07239/DA/NIDAID - DA00346/DA/NIDADA - 19930416IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199306

UR  - PM:0008095837

SO  - Brain Res 1993 Feb 12 ;603(1):134-138

 

187

UI  - 185

AU  - Gledhill JA

AU  - Moore DF

AU  - Bell D

AU  - Henry JA

TI  - Subarachnoid haemorrhage associated with MDMA abuse [letter]

MH  - Adult

MH  - Aneurysm,Ruptured

MH  - chemically induced

MH  - Case Report

MH  - Female

MH  - Human

MH  - Intracranial Aneurysm

MH  - complications

MH  - Subarachnoid Hemorrhage

MH  - etiology

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - adverse effects

RP  - NOT IN FILE

NT  - UI - 94015113LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - LETTERDA - 19931026IS - 0022-3050SB - MCY - ENGLANDJC - JBBEM - 199401

UR  - PM:0008105032

SO  - J Neurol Neurosurg Psychiatry 1993 Sep ;56(9):1036-1037

 

188

UI  - 184

AU  - Glennon RA

AD  - Department of Medicinal Chemistry, School of Pharmacy, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0540

TI  - MDMA-like stimulus effects of alpha-ethyltryptamine and the alpha-ethyl homolog of DOM

AB  - One-carbon homologation of phenylalkylamine or indolylalkylamine hallucinogens containing an alpha-methyl substituent typically results in a reduction of hallucinogenic potency; however, this same structural change has little to no effect on agents that produce MDMA-like effects. In the present investigation, rats trained to discriminate 1.5 mg/kg of MDMA (3,4-methylenedioxymethamphetamine) from saline vehicle were employed to determine if the alpha-ethyl homologs of the hallucinogens 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM) and alpha-methyltryptamine (alpha-MeT)--that is, alpha-EH DOM (BL-3912) and alpha-EtT, respectively--would produce stimulus effects similar to those of MDMA. Although the MDMA stimulus failed to generalize to DOM (previously published) and alpha-MeT (this study), MDMA stimulus generalization occurred both to alpha-EH DOM (ED50 = 1.3 mg/kg) and alpha-EtT (ED50 = 3.5 mg/kg). A (+)amphetamine stimulus (training dose = 1.0 mg/kg) only partially generalized to these two agents, suggesting that the MDMA stimulus generalization involves more than a simple amphetamine-like action. As such, this is the first demonstration that classical hallucinogens can produce MDMA-like effects upon homologation and that MDMA-like stimulus effects can be associated with an indolylalkylamine. Furthermore, these results continue to support the concept that an intact methylenedioxy ring system, such as that found in MDMA and other MDMA-related agents, is not a structural requirement for drugs to produce MDMA-like effects

MH  - Animal

MH  - Central Nervous System Stimulants

MH  - pharmacology

MH  - Dextroamphetamine

MH  - Discrimination (Psychology)

MH  - drug effects

MH  - Dom

MH  - analogs & derivatives

MH  - Generalization,Stimulus

MH  - Male

MH  - Methyltyrosines

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Support,U.S.Gov't,P.H.S.

MH  - Tryptamines

MH  - Tyrosine 3-Monooxygenase

MH  - antagonists & inhibitors

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 94089807LA - EngRN - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)RN - 0 (Central Nervous System Stimulants)RN - 0 (Methyltyrosines)RN - 0 (Tryptamines)RN - 15588-95-1 (DOM)RN - 2235-90-7 (etryptamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 51-64-9 (Dextroamphetamine)RN - 52842-59-8 (dimoxamine)RN - 658-48-0 (alpha-Methyltyrosine)PT - JOURNAL ARTICLEID - DA 01642/DA/NIDADA - 19940127IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199403

UR  - PM:0007903460

SO  - Pharmacol Biochem Behav 1993 Oct ;46(2):459-462

 

189

UI  - 194

AU  - Krebs KM

AU  - Geyer MA

AD  - Department of Psychology, University of California at San Diego, La Jolla 92093

TI  - Behavioral characterization of alpha-ethyltryptamine, a tryptamine derivative with MDMA-like properties in rats

AB  - Several reports have speculated that the tryptamine-derived drug alpha- ethyltryptamine (AET) may have effects similar to those of the amphetamine-derived drug 3,4-methylenedioxymethamphetamine (MDMA). Indeed, the US Drug Enforcement Administration has recently placed AET on the Schedule I list because of its putative similarity to MDMA. The Behavioral Pattern Monitor, which quantifies locomotor and investigatory responses of rats, was used to characterize the effects of AET in a paradigm that distinguishes between the effects of traditional hallucinogens, amphetamine-like stimulants, and MDMA-like drugs. First, a dose-response study revealed that all doses of AET tested (5, 10, 20 mg/kg) significantly increased locomotor activity. Locomotor hyperactivity is produced by MDMA or amphetamine-like stimulants, but not by classical hallucinogens, such as LSD or mescaline. Additionally, AET significantly decreased measures of investigatory behavior. Similar decreases occur with MDMA or hallucinogen administration. Second, as with MDMA, the locomotor hyperactivity induced by AET was attenuated by pretreatment (10 mg/kg) with the serotonin reuptake inhibitor fluoxetine. Thus, AET, a tryptamine-derived drug, appears to produce an MDMA-like profile of behavioral changes by virtue of releasing presynaptic serotonin

MH  - Animal

MH  - Behavior,Animal

MH  - drug effects

MH  - Exploratory Behavior

MH  - Fluoxetine

MH  - pharmacology

MH  - Male

MH  - Motor Activity

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - antagonists & inhibitors

MH  - pharmacokinetics

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Receptors,Presynaptic

MH  - metabolism

MH  - Receptors,Serotonin

MH  - Serotonin

MH  - Support,U.S.Gov't,P.H.S.

MH  - Tryptamines

RP  - NOT IN FILE

NT  - UI - 95158454LA - EngRN - 0 (Receptors, Presynaptic)RN - 0 (Receptors, Serotonin)RN - 0 (Tryptamines)RN - 2235-90-7 (etryptamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54910-89-3 (Fluoxetine)PT - JOURNAL ARTICLEID - DA02925/DA/NIDAID - MH00188/MH/NIMHDA - 19950316IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199505

UR  - PM:0007855195

SO  - Psychopharmacology (Berl) 1993  ;113(2):284-287

 

190

UI  - 195

AU  - LeSage M

AU  - Clark R

AU  - Poling A

AD  - Department of Psychology, Western Michigan University, Kalamazoo 49008

TI  - MDMA and memory: the acute and chronic effects of MDMA in pigeons performing under a delayed-matching-to-sample procedure

AB  - The purpose of the present study was to examine the acute and chronic effects of (+/-)3,4-methylenedioxy-methamphetamine (MDMA) in pigeons responding under a delayed-matching-to-sample procedure with 0-, 3-, and 6-s delays. In the absence of drug, accuracy (percent correct responses) was inversely related to delay length. When administered pre- chronically, MDMA (0.32-5.6 mg/kg) generally decreased accuracy and response rates at doses of 3.2 mg/kg and above. Although humans report a distinct "hangover" when exposure to MDMA ends, performance of pigeons in the present study did not deteriorate when the chronic regimen ended, indicating an absence of behavioral dependence on the drug. Tolerance developed following chronic exposure to 3.2 mg/kg. In general, greater tolerance occurred at the 0-s delay than at longer delays. Although MDMA is reported to have neurotoxic effects, it does not inevitably produce long-lasting or cumulative behavioral impairment

MH  - Animal

MH  - Conditioning,Operant

MH  - drug effects

MH  - Dose-Response Relationship,Drug

MH  - Drug Tolerance

MH  - Memory

MH  - N-Methyl-3,4-methylenedioxyamphetamine

MH  - pharmacology

MH  - Pigeons

MH  - Support,Non-U.S.Gov't

RP  - NOT IN FILE

NT  - UI - 95132786LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19950223IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199504

UR  - PM:0007831426

SO  - Psychopharmacology (Berl) 1993  ;110(3):327-332

 

191

UI  - 186

AU  - Lin HQ

AU  - Atrens DM

AU  - Christie MJ

AU  - Jackson DM

AU  - McGregor IS

AD  - Department of Pharmacology, University of Sydney, N.S.W., Australia

TI  - Comparison of conditioned taste aversions produced by MDMA and d- amphetamine

AB  - Many drugs of abuse such as d-amphetamine support the development of taste aversion in a conditioned taste aversion paradigm. However, it has yet to be established whether methylenedioxymethamphetamine (MDMA), an amphetamine-like stimulant, has this property. A direct comparison was made between MDMA and d-amphetamine over a dose range of 0.125-2.0 mg/kg (SC). Two pairings of either drug with saccharin produced dose- related taste aversions to saccharin that were retained for at least three successive testing trials. The minimally effective dose was 1 mg/kg for MDMA and 0.5 mg/kg for d-amphetamine. The relative potency of MDMA to amphetamine was 4.5, similar to that previously reported for drug discrimination and self-stimulation

MH  - Animal

MH  - Avoidance Learning

MH  - drug effects

MH  - Comparative Study

MH  - Designer Drugs

MH  - pharmacology

MH  - Dextroamphetamine

MH  - Dose-Response Relationship,Drug

MH  - Male

MH  - Rats

MH  - Rats,Wistar

MH  - Support,Non-U.S.Gov't

MH  - Taste

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 94077881LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 51-64-9 (Dextroamphetamine)PT - JOURNAL ARTICLEDA - 19940110IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199403

UR  - PM:0007902981

SO  - Pharmacol Biochem Behav 1993 Sep ;46(1):153-156

 

192

UI  - 183

AU  - Michel RE

AU  - Rege AB

AU  - George WJ

AD  - Department of Pharmacology, Tulane University School of Medicine, New Orleans, LA 70112

TI  - High-pressure liquid chromatography/electrochemical detection method for monitoring MDA and MDMA in whole blood and other biological tissues

AB  - The drug Ecstasy (3,4-methylenedioxymethamphetamine (MDMA)) is one of several hallucinogenic amphetamine derivatives reported to be serotonergic neurotoxins. The following is a description of a new high- pressure liquid chromatographic (HPLC) analytical method for the analysis of MDMA, 3,4-methylenedioxyamphetamine (MDA) and N-ethyl-3,4- methylenedioxyamphetamine (MDE) from whole blood. Upon separation of MDMA, MDA and MDE by HPLC, quantitation is achieved by use of electrochemical detection. Retention times for MDA, MDMA, and MDE are 6.5, 9.2, and 10.3 min, respectively, allowing for a complete chromatographic run every 15 min. The sensitivity of the method is 1 ng/ml which allows for measurement of MDA, MDMA, or MDE in microsamples of whole blood. The volume of blood required is very small (200 microliters); therefore, there is minimal blood loss in repeated blood sampling from small animals. Assay linearity was demonstrated from 1 ng/ml to at least 1 microgram/ml. The coefficients of variation for both intra-assay and inter-assay comparisons were less than 9%. Other HPLC methods have been previously described for the analysis of amphetamine derivatives, but this new method offers greater sensitivity, rapid turn-around time and ease of use

MH  - Animal

MH  - Chromatography,High Pressure Liquid

MH  - Designer Drugs

MH  - Electrochemistry

MH  - Evaluation Studies

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - blood

MH  - metabolism

RP  - NOT IN FILE

NT  - UI - 94104344LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 82801-81-8 (3,4-methylenedioxyethamphetamine)PT - JOURNAL ARTICLEDA - 19940208IS - 0165-0270SB - MCY - NETHERLANDSJC - K9VAA - AuthorEM - 199404RO - M:RMK

UR  - PM:0007903993

SO  - J Neurosci Methods 1993 Oct ;50(1):61-66

 

193

UI  - 188

AU  - Miller DB

AU  - O'Callaghan JP

AD  - United States Environmental Protection Agency, Health Effects Research Laboratory, Research Triangle Park, North Carolina 27711

TI  - The interactions of MK-801 with the amphetamine analogues D- methamphetamine (D-METH), 3,4-methylenedioxymethamphetamine (D-MDMA) or D-fenfluramine (D-FEN): neural damage and neural protection

MH  - Animal

MH  - Biological Markers

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - pathology

MH  - Cerebral Cortex

MH  - Corpus Striatum

MH  - Dizocilpine Maleate

MH  - pharmacology

MH  - Female

MH  - Fenfluramine

MH  - antagonists & inhibitors

MH  - toxicity

MH  - Glial Fibrillary Acidic Protein

MH  - analysis

MH  - Hippocampus

MH  - Methamphetamine

MH  - Mice

MH  - Mice,Inbred C57BL

MH  - Neurons

MH  - Neurotoxins

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 93290125LA - EngRN - 0 (Biological Markers)RN - 0 (Glial Fibrillary Acidic Protein)RN - 0 (Neurotoxins)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 458-24-2 (Fenfluramine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 537-46-2 (Methamphetamine)RN - 77086-22-7 (Dizocilpine Maleate)PT - JOURNAL ARTICLEID - IAG ND-89-4DA - 19930715IS - 0077-8923SB - MSB - XCY - UNITED STATESJC - 5NMEM - 199309

UR  - PM:0008099774

SO  - Ann N Y Acad Sci 1993 May 28 ;679():321-324

 

194

UI  - 189

AU  - Poklis A

AU  - Fitzgerald RL

AU  - Hall KV

AU  - Saady JJ

AD  - Department of Pathology, Medical College of Virginia Hospitals, Virginia Commonwealth University, Richmond 23298-0597

TI  - EMIT-d.a.u. monoclonal amphetamine/methamphetamine assay. II. Detection of methylenedioxyamphetamine (MDA) and methylenedioxymethamphetamine (MDMA)

AB  - The cross-reactivity, stereoselectivity and clinical performance of the EMIT-d.a.u. monoclonal amphetamine/methamphetamine immunoassay (EM) for the detection of methylenedioxyamphetamine (MDA) and methylenedioxymethamphetamine (MDMA) in urine was evaluated. The cut- off concentrations of racemic MDA and MDMA were found to be approximately 800 ng/ml and 3000 ng/ml, respectively. The EM assay demonstrated a high selectivity for the S(+) isomer of both MDA and MDMA. Urines collected over a 24-h period from rats administered 20 mg i.v. racemic MDMA were all positive when analyzed by the EM assay. The EM was found vastly superior to the EMIT d.a.u. polyclonal amphetamine/methamphetamine assay for the detection of MDA and MDMA. The EM assay displayed sufficient sensitivity for detection of these drugs following clinical intoxication

MH  - Amphetamine

MH  - chemistry

MH  - urine

MH  - Animal

MH  - Cross Reactions

MH  - Designer Drugs

MH  - administration & dosage

MH  - Immunoassay

MH  - Injections,Intravenous

MH  - Male

MH  - Mass Fragmentography

MH  - Rats

MH  - Sensitivity and Specificity

MH  - Stereoisomerism

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 93279618LA - EngRN - 0 (Designer Drugs)RN - 300-62-9 (Amphetamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19930707IS - 0379-0738SB - MCY - SWITZERLANDJC - F49AA - AuthorEM - 199309

UR  - PM:0008099337

SO  - Forensic Sci Int 1993 Apr ;59(1):63-70

 

195

UI  - 193

AU  - Robinson TE

AU  - Castaneda E

AU  - Whishaw IQ

AD  - Department of Psychology, University of Michigan, Ann Arbor 48109

TI  - Effects of cortical serotonin depletion induced by 3,4- methylenedioxymethamphetamine (MDMA) on behavior, before and after additional cholinergic blockade

AB  - Repeated treatment with high doses of 3,4-methylenedioxymethamphetamine (MDMA; "ecstasy") produces a long-lasting depletion of brain serotonin, presumably because of the degeneration of serotonin axon terminals. However, very little is known about the long-term behavioral consequences of MDMA neurotoxicity. The experiments reported here were designed to evaluate the effects of MDMA neurotoxicity on a number of behavioral tests known to be sensitive to neocortical and hippocampal damage. Also, the effect of additional cholinergic blockade in MDMA- pretreated rats was evaluated because loss of both the serotonergic and cholinergic inputs to the cortex produces a functional decortication and a behavioral syndrome reminiscent of human global dementia. Partial depletion of neocortical serotonin (72.6%) did not produce deficits on a variety of behavioral tests, including a place navigation learning- set task, skilled forelimb use, or the ability to make complex judgements regarding the stimulus properties of food in a foraging situation, and neither did additional cholinergic blockade. MDMA- pretreated rats had a mild impairment in rapidly developing an efficient search strategy in the place navigation task, but once the goal was located, MDMA pretreated rats performed at control levels and showed no deficits in memory for spatial location. It is concluded that the extent of serotonergic denervation produced by MDMA is not sufficient to produce marked and lasting behavioral deficits, possibly because of neurocompensatory changes in the remaining serotonin terminals

MH  - Animal

MH  - Atropine

MH  - pharmacology

MH  - Behavior,Animal

MH  - drug effects

MH  - Male

MH  - Prosencephalon

MH  - physiology

MH  - Random Allocation

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 93143831LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-55-8 (Atropine)PT - JOURNAL ARTICLEID - 4294DA - 19930226IS - 0893-133XSB - MCY - UNITED STATESJC - ADQAA - AuthorEM - 199305

UR  - PM:0008093836

SO  - Neuropsychopharmacology 1993 Jan ;8(1):77-85

 

196

UI  - 213

AU  - Campkin NT

AU  - Davies UM

TI  - Another death from Ecstacy [letter; comment]

MH  - Adolescence

MH  - Case Report

MH  - Death,Sudden

MH  - etiology

MH  - Designer Drugs

MH  - poisoning

MH  - Human

MH  - Male

MH  - Substance-Related Disorders

MH  - complications

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 92194250LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - COMMENTPT - LETTERDA - 19920423IS - 0141-0768SB - MCY - ENGLANDJC - JX1EM - 199206RO - M:LC1

UR  - PM:0001347789

SO  - J R Soc Med 1992 Jan ;85(1):61

 

197

UI  - 197

AU  - Glennon RA

AU  - Higgs R

AD  - Department of Medicinal Chemistry, School of Pharmacy, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0581

TI  - Investigation of MDMA-related agents in rats trained to discriminate MDMA from saline

AB  - To determine whether metabolite-related analogs of N-methyl-1-(3,4- methylenedioxyphenyl)-2-aminopropane (MDMA) produce stimulus effects similar to those of the parent compound, and to determine the structural requirements associated with the MDMA stimulus, several MDMA analogs were examined in tests of stimulus generalization using rats trained to discriminate 1.5 mg/kg MDMA from saline. Although several of the analogs produced up to 50-60% MDMA-appropriate responding, none [with the exception of N-methyl-1-(4-methoxyphenyl)-2-aminopropane (PMMA)] resulted in stimulus generalization. The partial generalization, coupled with the possible reduced ability of certain of the agents to penetrate the blood-brain barrier relative to MDMA, suggests that these agents are not behaviorally inactive. PMMA, although not a metabolite of MDMA, is closely related in chemical structure to MDMA and its metabolites; PMMA produces > 80% MDMA- appropriate responding and is approximately three times more potent (ED50 = 0.2 mg/kg) than MDMA itself (ED50 = 0.76 mg/kg). PMMA is a newer scheduled substance with an as yet unknown mechanism of action; however, on the basis of the stimulus generalization observed PMMA may share some behavioral and mechanistic similarity with MDMA. These results also indicate that an intact methylenedioxy ring, such as that found in MDMA but absent in PMMA, is not a prerequisite for MDMA-like activity and further support the notion that ring-opened MDMA metabolites may produce effects that contribute to the actions of MDMA

MH  - Animal

MH  - Discrimination (Psychology)

MH  - drug effects

MH  - Male

MH  - Methamphetamine

MH  - pharmacology

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 93079274LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 537-46-2 (Methamphetamine)PT - JOURNAL ARTICLEID - DA 01642/DA/NIDADA - 19921230IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199303

UR  - PM:0001360162

SO  - Pharmacol Biochem Behav 1992 Nov ;43(3):759-763

 

198

UI  - 204

AU  - Grob CS

AU  - Bravo GL

AU  - Walsh RN

AU  - Liester MB

AD  - Department of Psychiatry, University of California, Irvine Medical Center, Orange 92668

TI  - The MDMA-neurotoxicity controversy: implications for clinical research with novel psychoactive drugs

MH  - Animal

MH  - Combined Modality Therapy

MH  - Designer Drugs

MH  - adverse effects

MH  - therapeutic use

MH  - Human

MH  - Mental Disorders

MH  - therapy

MH  - Nervous System

MH  - drug effects

MH  - Nervous System Diseases

MH  - chemically induced

MH  - Psychotherapy

MH  - Research Design

MH  - standards

MH  - Serotonin

MH  - physiology

MH  - Substance-Related Disorders

MH  - etiology

MH  - psychology

MH  - Synaptic Transmission

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 92277070LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEDA - 19920702IS - 0022-3018SB - ASB - MCY - UNITED STATESJC - JAFEM - 199209

UR  - PM:0001350614

SO  - J Nerv Ment Dis 1992 Jun ;180(6):355-356

 

199

UI  - 211

AU  - Kehne JH

AU  - McCloskey TC

AU  - Taylor VL

AU  - Black CK

AU  - Fadayel GM

AU  - Schmidt CJ

AD  - Marion Merrell Dow Research Institute, Cincinnati, Ohio

TI  - Effects of the serotonin releasers 3,4-methylenedioxymethamphetamine (MDMA), 4-chloroamphetamine (PCA) and fenfluramine on acoustic and tactile startle reflexes in rats

AB  - The substituted amphetamines 4-chloroamphetamine (PCA), 3,4- methylenedioxymethamphetamine (MDMA) and fenfluramine (FEN) share the common neurochemical action of acutely releasing central serotonin (5- HT), and yet their behavioral effects are quite different. The present study evaluated the effects of these compounds on acoustic and tactile startle reflexes. PCA and MDMA were qualitatively similar in producing dose-related increases in acoustic and tactile startle reflexes that were slow in onset, but sustained throughout the 3.5-hr test session. Changes in motor activity did not account for the observed excitation of startle. In marked contrast to MDMA and PCA, FEN did not alter tactile startle and tended to depress acoustic startle. The excitatory effect of 20 mg/kg of MDMA was prevented by the 5-HT uptake blockers MDL 27,777A and fluoxetine. MDMA excitation was not affected by a dose of the dopamine antagonist haloperidol that attenuated the startle- enhancing effect of d-amphetamine. MDMA excitation was greatly attenuated by a general depletion of central 5-HT produced by prior intraventricular injection of the 5-HT neurotoxin 5,7- dihydroxytryptamine. PCA and MDMA excitations of startle were attenuated in rats specifically depleted of spinal 5-HT or in rats with radio frequency lesions of the dorsal raphe nucleus. Thus, PCA and MDMA have similar prolonged excitatory effects on startle reflexes that are mediated by ascending (dorsal raphe) and descending (spinal) pathways, whereas FEN differs in its lack of excitation of startle. Differences in the neurochemical properties of these compounds or their patterns of 5-HT release may underlie their different behavioral profiles

MH  - p-Chloroamphetamine

MH  - pharmacology

MH  - Animal

MH  - Dose-Response Relationship,Drug

MH  - Fenfluramine

MH  - Fluoxetine

MH  - Indenes

MH  - Male

MH  - N-Methylaspartate

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Reflex,Acoustic

MH  - drug effects

MH  - Serotonin

MH  - physiology

MH  - secretion

MH  - Startle Reaction

MH  - Touch

MH  - 5,7-Dihydroxytryptamine

RP  - NOT IN FILE

NT  - UI - 92113946LA - EngRN - 0 (Indenes)RN - 130835-44-8 (MDL 27777)RN - 31363-74-3 (5,7-Dihydroxytryptamine)RN - 458-24-2 (Fenfluramine)RN - 50-67-9 (Serotonin)RN - 54910-89-3 (Fluoxetine)RN - 6384-92-5 (N-Methylaspartate)RN - 64-12-0 (p-Chloroamphetamine)PT - JOURNAL ARTICLEDA - 19920218IS - 0022-3565SB - MCY - UNITED STATESJC - JP3AA - AuthorEM - 199204

UR  - PM:0001731054

SO  - J Pharmacol Exp Ther 1992 Jan ;260(1):78-89

 

200

UI  - 212

AU  - Krystal JH

AU  - Price LH

AU  - Opsahl C

AU  - Ricaurte GA

AU  - Heninger GR

AD  - Psychiatry Service, Yale University School of Medicine, West Haven VA Medical Center, Connecticut 06516

TI  - Chronic 3,4-methylenedioxymethamphetamine (MDMA) use: effects on mood and neuropsychological function?

AB  - 3,4-Methylenedioxymethamphetamine (MDMA; "ecstasy") is a selective serotonin (5-HT) neurotoxin in animals. There is now preliminary evidence in humans of 5-HT deficits associated with extensive use of MDMA. In order to begin to describe the cognitive and mood effects of chronic MDMA use, nine individuals with extensive MDMA use histories were studied. Despite the absence of memory deficits on clinical examination, a pattern of mild-to-moderate impairment was observed on both the Initial and Delayed Paragraph Tests of the Wechsler Memory Scale; eight of the subjects had at least mild impairment on at least one test in the neuropsychological battery. Despite previously reported suggestive evidence of 5-HT deficit in this group, none reported depressed mood or met clinical criteria for an affective disorder at the time of testing. These preliminary findings raise concern about possible detrimental effects of MDMA use on neuropsychological function for future systematic study and they highlight important issues regarding the effects of 5-HT deficits on cognitive function and mood regulation

MH  - Adult

MH  - Cognition Disorders

MH  - diagnosis

MH  - etiology

MH  - physiopathology

MH  - Depressive Disorder

MH  - Female

MH  - Human

MH  - Male

MH  - Middle Age

MH  - Neuropsychological Tests

MH  - Serotonin

MH  - physiology

MH  - Substance-Related Disorders

MH  - complications

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,Non-P.H.S.

MH  - Support,U.S.Gov't,P.H.S.

MH  - Wechsler Scales

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 93035167LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEID - MH-00579/MH/NIMHID - MH-36229/MH/NIMHID - MH-25642/MH/NIMHID - +DA - 19921105IS - 0095-2990SB - MCY - UNITED STATESJC - 3GWAA - AuthorEM - 199301

UR  - PM:0001357957

SO  - Am J Drug Alcohol Abuse 1992  ;18(3):331-341

 

201

UI  - 207

AU  - Kumagai Y

AU  - Schmitz DA

AU  - Cho AK

AD  - Department of Pharmacology, UCLA School of Medicine 90024

TI  - Aromatic hydroxylation of methylenedioxybenzene (MDB) and methylenedioxymethamphetamine (MDMA) by rabbit liver microsomes

AB  - 1. Metabolites formed during incubation of methylenedioxybenzene (MDB) and methylenedioxymethamphetamine (MDMA) with rabbit liver microsomes were examined by h.p.l.c.-electrochemical detection and g.l.c.-mass spectrometry. 2. The trifluoroacetyl derivative of metabolite M-1, obtained from MDB, had a molecular ion at m/z 234 and was identified as 3,4-methylenedioxy-6-hydroxybenzene (sesamol) by comparison with authentic material. 3. The trifluoroacetyl derivative of metabolite M- 2, obtained from MDMA, exhibited a molecular ion at m/z 401. Experiments with the deuterium substituted variants of MDMA indicated that the product was hydroxylated on the aromatic ring. 4. The formation of these hydroxylated metabolites required NADPH and was inhibited by carbon monoxide, indicating the possible participation of cytochrome P-450. Phenobarbital (PB) induction caused a marked enhancement of MDP hydroxylase activity whereas MDMA hydroxylation was not affected. 5. The aromatic hydroxylation of MDB and MDMA was also observed in a reconstituted system with cytochrome P-450 isozyme IIB4

MH  - Animal

MH  - Carbon Monoxide

MH  - pharmacology

MH  - Chromatography,High Pressure Liquid

MH  - Cytochrome P-450

MH  - antagonists & inhibitors

MH  - metabolism

MH  - Dioxoles

MH  - Hydroxylases

MH  - Hydroxylation

MH  - Male

MH  - Microsomes,Liver

MH  - drug effects

MH  - Models,Biological

MH  - Nadp

MH  - Phenols

MH  - Potentiometry

MH  - Rabbits

MH  - Spectrum Analysis,Mass

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,Non-P.H.S.

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 92397557LA - EngRN - EC 1.14. (Hydroxylases)RN - 0 (Dioxoles)RN - 0 (Phenols)RN - 274-09-9 (1,3-benzodioxole)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 53-59-8 (NADP)RN - 533-31-3 (sesamol)RN - 630-08-0 (Carbon Monoxide)RN - 9035-51-2 (Cytochrome P-450)PT - JOURNAL ARTICLEID - DA 04206/DA/NIDADA - 19921015IS - 0049-8254SB - MCY - ENGLANDJC - XQUAA - AuthorEM - 199212

UR  - PM:0001523860

SO  - Xenobiotica 1992 Apr ;22(4):395-403

 

202

UI  - 205

AU  - Lehmann J

AU  - DeSouza EB

AU  - Culp S

AU  - Zaczek R

AD  - Department of Mental Health Services, Hahnemann University, Philadelphia, Pennsylvania 19102-1192

TI  - Regional distribution to recovery of 5-HT levels after administration of "atrophins" MDMA and D,L-fenfluramine. Stereospecificity and comparison with 5,7-dihydroxytryptamine

MH  - Animal

MH  - Atrophy

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - pathology

MH  - Cerebral Ventricles

MH  - physiology

MH  - Comparative Study

MH  - Designer Drugs

MH  - toxicity

MH  - Dopamine

MH  - Fenfluramine

MH  - administration & dosage

MH  - Homovanillic Acid

MH  - Hydroxyindoleacetic Acid

MH  - Injections,Intraventricular

MH  - Male

MH  - Norepinephrine

MH  - Organ Specificity

MH  - Piperidines

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Serotonin

MH  - Stereoisomerism

MH  - 3,4-Dihydroxyphenylacetic Acid

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - 5,7-Dihydroxytryptamine

RP  - NOT IN FILE

NT  - UI - 92344212LA - EngRN - 0 (Designer Drugs)RN - 0 (Piperidines)RN - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)RN - 306-08-1 (Homovanillic Acid)RN - 31363-74-3 (5,7-Dihydroxytryptamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 458-24-2 (Fenfluramine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-41-2 (Norepinephrine)RN - 51-61-6 (Dopamine)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 61869-08-7 (Paroxetine)PT - JOURNAL ARTICLEDA - 19920821IS - 0077-8923SB - MSB - XCY - UNITED STATESJC - 5NMEM - 199210

UR  - PM:0001379013

SO  - Ann N Y Acad Sci 1992 May 11 ;648():291-295

 

203

UI  - 198

AU  - Lim HK

AU  - Zeng S

AU  - Chei DM

AU  - Foltz RL

AD  - Department of Pharmacology and Toxicology, University of Utah, Salt Lake City 84108

TI  - Comparative investigation of disposition of 3,4- (methylenedioxy)methamphetamine (MDMA) in the rat and the mouse by a capillary gas chromatography-mass spectrometry assay based on perfluorotributylamine-enhanced ammonia positive ion chemical ionization

AB  - A gas chromatography-mass spectrometry assay based on perfluorotributylamine-enhanced ammonia positive ion chemical ionization has been developed for MDMA and three of its primary metabolites in biological specimens; the assay is linear from 2 to 1000 ng ml-1. Quantitatively, more of an administered dose of 10 mg kg-1 MDMA was excreted by the mouse (72%) than by the rat (35%); most in both species was excreted in urine and within 24 h. The difference in per cent excretion is entirely due to proportionally greater excretion of the parent drug by the mouse. 4-Hydroxy-3-methoxymethamphetamine (HMM) is the major urinary metabolite in both species. HMM and another primary metabolite, 4-hydroxy-3-methoxyamphetamine (HMA), were excreted mainly as glucuronide and sulphate conjugates (> 85%)

MH  - Ammonia

MH  - Animal

MH  - Comparative Study

MH  - Dopamine

MH  - analogs & derivatives

MH  - analysis

MH  - pharmacokinetics

MH  - Fluorocarbons

MH  - Male

MH  - Mass Fragmentography

MH  - Methamphetamine

MH  - Mice

MH  - Mice,Inbred Strains

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Species Specificity

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 93160323LA - EngRN - 0 (Fluorocarbons)RN - 117652-28-5 (4-hydroxy-3-methoxymethamphetamine)RN - 13026-44-3 (3-O-methyl-alpha-methyldopamine)RN - 311-89-7 (perfluorotributylamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 51-61-6 (Dopamine)RN - 537-46-2 (Methamphetamine)RN - 7664-41-7 (Ammonia)RN - 82801-81-8 (3,4-methylenedioxyethamphetamine)PT - JOURNAL ARTICLEID - RO1 DA 05860/DA/NIDADA - 19930316IS - 0731-7085SB - MCY - ENGLANDJC - A2CAA - AuthorEM - 199305RO - M:RMK

UR  - PM:0001363061

SO  - J Pharm Biomed Anal 1992 Sep ;10(9):657-665

 

204

UI  - 196

AU  - McCann UD

AU  - Ricaurte GA

AD  - Department of Behavioral Biology, Walter Reed Army Institute of Research, Washington, DC

TI  - MDMA ("ecstasy") and panic disorder: induction by a single dose

MH  - Administration,Oral

MH  - Adult

MH  - Alprazolam

MH  - therapeutic use

MH  - Anxiety Disorders

MH  - chemically induced

MH  - drug therapy

MH  - psychology

MH  - Arousal

MH  - drug effects

MH  - Case Report

MH  - Designer Drugs

MH  - administration & dosage

MH  - adverse effects

MH  - Dose-Response Relationship,Drug

MH  - Human

MH  - Imipramine

MH  - Male

MH  - Panic

MH  - Panic Disorder

MH  - Recurrence

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 93104329LA - EngRN - 0 (Designer Drugs)RN - 28981-97-7 (Alprazolam)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-49-7 (Imipramine)PT - JOURNAL ARTICLEID - DA 05938/DA/NIDADA - 19930127IS - 0006-3223SB - MCY - UNITED STATESJC - A3SEM - 199303

UR  - PM:0001361366

SO  - Biol Psychiatry 1992 Nov 15 ;32(10):950-953

 

205

UI  - 210

AU  - McGuire P

AU  - Fahy T

TI  - Flashbacks following MDMA [letter; comment]

MH  - Designer Drugs

MH  - adverse effects

MH  - Hallucinations

MH  - chemically induced

MH  - Human

MH  - Paranoid Disorders

MH  - Psychoses,Substance-Induced

MH  - etiology

MH  - Substance-Related Disorders

MH  - complications

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 92173851LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - COMMENTPT - LETTERDA - 19920406IS - 0007-1250SB - MCY - ENGLANDJC - B1KEM - 199206RO - M:LC2

UR  - PM:0001347241

SO  - Br J Psychiatry 1992 Feb ;160():276

 

206

UI  - 203

AU  - Pallanti S

AU  - Mazzi D

AD  - Department of Neurology and Psychiatry, Florence University Medical School, Italy

TI  - MDMA (Ecstasy) precipitation of panic disorder

AB  - The authors describe three patients whose panic disorder began during recreational use of MDMA (Ecstasy) and was subsequently complicated by agoraphobic avoidance that continued autonomously after cessation of the drug. Their panic disorder responded well to serotoninergic antidepressant drugs. Theoretical and practical implications are discussed

MH  - Adult

MH  - Agoraphobia

MH  - chemically induced

MH  - drug therapy

MH  - psychology

MH  - Alcohol Drinking

MH  - adverse effects

MH  - Amitriptyline

MH  - therapeutic use

MH  - Arousal

MH  - drug effects

MH  - Case Report

MH  - Fluvoxamine

MH  - Human

MH  - Male

MH  - Panic Disorder

MH  - Recurrence

MH  - Substance Withdrawal Syndrome

MH  - Tranylcypromine

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 93003854LA - EngRN - 155-09-9 (Tranylcypromine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-48-6 (Amitriptyline)RN - 54739-18-3 (Fluvoxamine)PT - JOURNAL ARTICLEDA - 19921120IS - 0006-3223SB - MCY - UNITED STATESJC - A3SAA - AuthorEM - 199301

UR  - PM:0001356491

SO  - Biol Psychiatry 1992 Jul 1 ;32(1):91-95

 

207

UI  - 214

AU  - Paris JM

AU  - Cunningham KA

AD  - Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston 77550

TI  - Lack of serotonin neurotoxicity after intraraphe microinjection of (+)- 3,4-methylenedioxymethamphetamine (MDMA)

AB  - Systemic administration of 3,4-methylenedioxymethamphetamine (MDMA) produces depletions of serotonin (5-HT) and its primary metabolite, 5- hydroxyindoleacetic acid (5-HIAA), decreases 5-HT reuptake sites and diminishes tryptophan hydroxylase activity in various forebrain regions. MDMA has been shown to be neurotoxic to the fine fibers originating from dorsal raphe (DR) 5-HT neurons but not the beaded fibers from the median raphe (MR) nucleus. In the present experiment, MDMA was microinjected directly into the DR or MR to determine whether differential neurotoxicity developed in the DR versus MR fiber systems as measured by 5-HT levels and immunocytochemistry. Two weeks following stereotaxic injection with either vehicle or (+)MDMA (50 micrograms base in 2 microliters) into the DR or MR, rat brains were assayed for 5- HT and catecholamine content or 5-HT immunocytochemistry. HPLC analysis revealed no significant changes in monoamine or metabolite concentrations in the hippocampus and striatum of rats administered intra-DR or -MR (+)MDMA. Raphe sections stained for 5-HT also did not reveal any apparent neurotoxicity. A single cerebral injection of (+)MDMA does not produce neurotoxicity to 5-HT neuronal systems originating in the raphe, although neurotoxicity of multiple MDMA injections into these raphe nuclei cannot be ruled out

MH  - Animal

MH  - Immunoenzyme Techniques

MH  - Male

MH  - Microinjections

MH  - Raphe Nuclei

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Serotonin

MH  - metabolism

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - toxicity

RP  - NOT IN FILE

NT  - UI - 92173998LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEID - DA05708/DA/NIDAID - DA05381/DA/NIDADA - 19920409IS - 0361-9230SB - MCY - UNITED STATESJC - B5MAA - AuthorEM - 199206

UR  - PM:0001347247

SO  - Brain Res Bull 1992 Jan ;28(1):115-119

 

208

UI  - 201

AU  - Paulus MP

AU  - Geyer MA

AD  - Department of Psychiatry, School of Medicine, University of California, San Diego, La Jolla 92093-0804

TI  - The effects of MDMA and other methylenedioxy-substituted phenylalkylamines on the structure of rat locomotor activity

AB  - The effects of acute subcutaneous injections of methylenedioxy- substituted phenylalkylamines in rats were tested in an unconditioned motor behavior paradigm using the Behavioral Pattern Monitor (BPM). Based on a previously developed scaling hypothesis and the associated temporal and spatial scaling exponents (alpha and d), the effects of racemic and S(+) 3,4-methylenedioxyamphetamine (MDA), racemic, S(+) and R(-) 3,4-methylenedioxymethamphetamine (MDMA), racemic N-methyl-1-(1,3- benzodioxol-5yl)-2-butanamine (MBDB), racemic N-ethyl-3,4- methylenedioxyamphetamine (MDEA), 2,5-dimethoxy-4-iodoamphetamine, and methamphetamine were characterized using the d-alpha plane. Three distinct dose-response patterns were observed. 1) S(+) and (+/-)MDA had pronounced dose-dependent effects on the structure of motor behavior, which were characterized by long-straight path movements and minimal changes in the amount of motor behavior. 2) (+/-)MDMA and (+/-)MBDB dose-dependently changed patterns of movements towards long-straight paths together with dose-dependent increases in the amount of motor activity. 3) S(+)MDMA and (+/-)MDEA produced dose-related increases in the amount of motor activity with minimal changes of the movement patterns in the BPM. Comparisons with the existing drug discrimination, operant, and biochemical literature on these compounds lead to the conclusion that the observed effects in the d-alpha plane do not simply reflect the different effects of these compounds as dopamine or serotonin (5-HT) releasers or reuptake inhibitors and do not parallel their different abilities to exhibit hallucinogen-like effects. Instead, indirect 5-HT1 effects appear to contribute substantially to the differential changes in the amount and structure of motor behavior induced by the phenylalkylamines. This conclusion may provide an encouraging rationale to develop postsynaptically effective "entactogens," a potential new drug category as adjunctive psychotherapeutics

MH  - Animal

MH  - Isomerism

MH  - Male

MH  - Mathematics

MH  - Models,Neurological

MH  - Motor Activity

MH  - drug effects

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Structure-Activity Relationship

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - pharmacology

RP  - NOT IN FILE

NT  - UI - 92398744LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEID - DA06325/DA/NIDAID - DA02925/DA/NIDAID - MH00188/MH/NIMHDA - 19921016IS - 0893-133XSB - MCY - UNITED STATESJC - ADQAA - AuthorEM - 199212

UR  - PM:0001355968

SO  - Neuropsychopharmacology 1992 Aug ;7(1):15-31

 

209

UI  - 200

AU  - Rezvani AH

AU  - Garges PL

AU  - Miller DB

AU  - Gordon CJ

AD  - Skipper Bowles Center for Alcohol Studies, University of North Carolina School of Medicine, Chapel Hill 27514

TI  - Attenuation of alcohol consumption by MDMA (ecstasy) in two strains of alcohol-preferring rats

AB  - Alcohol preference and manifestation of alcoholism are thought by many to be associated with serotonin (5-HT) dysfunction in the brain. Thus, experiments were performed to determine the effect of acute and subchronic administration of (+/-) 3,4-methylenedioxymethamphetamine (MDMA), an amphetamine analog that stimulates 5-HT release, on alcohol preference in two strains of alcohol-preferring rats, the Fawn-Hooded (FH) and alcohol-preferring (P) rats. Rats were individually housed and provided free access to a solution of 10% ethanol, food, and water. Ethanol, food, and water intakes were measured daily. After establishing a stable baseline for ethanol and water intake, each rat was injected SC with a dose of 5.0 mg/kg MDMA or an equal volume of saline for 1 or 3 consecutive days. Body temperature was recorded immediately before and 120, 240, and 360 min after MDMA treatment. Ethanol, food, and water intake were measured for the preceding 24 h. Further, to determine the effect of MDMA on alcohol metabolism rats were injected with 5.0 mg/kg MDMA or saline and 15 min later with 2.5 g/kg alcohol. Then, blood alcohol levels were determined at 1, 3, and 5 h after alcohol administration. Our results show that a single administration of 5.0 mg/kg MDMA significantly decreased ethanol intake in both FH and P rats and increased water intake. Subchronic administration of 5.0 mg/kg MDMA for 3 consecutive days significantly attenuated alcohol intake in both strains but only increased water intake in P rats. Administration of MDMA induced hyper- and hypothermia in FH and P rats, respectively. This drug failed to exert any significant effect on the pharmacokinetics of alcohol, indicating a central effect.(ABSTRACT TRUNCATED AT 250 WORDS)

MH  - Alcohol Drinking

MH  - genetics

MH  - psychology

MH  - Animal

MH  - Body Temperature

MH  - drug effects

MH  - Drinking Behavior

MH  - Eating

MH  - Male

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Serotonin

MH  - physiology

MH  - Species Specificity

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - pharmacology

RP  - NOT IN FILE

NT  - UI - 93028667LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEID - P50-AA07611/AA/NIAAADA - 19921102IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199301

UR  - PM:0001357675

SO  - Pharmacol Biochem Behav 1992 Sep ;43(1):103-110

 

210

UI  - 206

AU  - Ricaurte GA

AU  - Martello AL

AU  - Katz JL

AU  - Martello MB

AD  - Department of Neurology, Francis Scott Key Medical Center, Johns Hopkins University School of Medicine, Baltimore, Maryland

TI  - Lasting effects of (+-)-3,4-methylenedioxymethamphetamine (MDMA) on central serotonergic neurons in nonhuman primates: neurochemical observations

AB  - The purpose of this study was to assess the duration of (+-)-3,4- methylenedioxymethamphetamine's (MDMA's) effects on serotonin containing neurons in nonhuman primates. Fifteen squirrel monkeys were used: three served as controls, 12 received MDMA s.c. at a dose of 5 mg/kg twice daily for 4 consecutive days. Two weeks, 10 weeks, 8 months and 18 months after drug treatment, groups (n = 3) of MDMA-treated monkeys, along with controls, were examined for regional brain content of serotonin and 5-hydroxyindoleacetic acid, and for the number of [3H] paroxetine-labeled serotonin uptake sites. Two weeks after MDMA treatment, monkeys showed profound reductions in all three serotonergic presynaptic markers. By 10 weeks, there was evidence of partial recovery in some brain regions (e.g., hippocampus, caudate nucleus, frontal cortex). However, by 18 months, it was evident that recovery did not continue, as serotonergic deficits returned to the level of severity observed 2 weeks after MDMA treatment. This was the case in all brain regions examined except the thalamus and hypothalamus. In the thalamus, the level of serotonin increased to 63% of control, whereas that of 5-hydroxyindoleacetic acid recovered completely. In the hypothalamus, concentrations of serotonin and 5-hydroxyindoleacetic acid were 140 and 187% of control, respectively. These results suggest that MDMA produces lasting effects on serotonergic neurons in nonhuman primates, with most brain regions showing evidence of persistent denervation and some showing signs of reinnervation (thalamus) or possibly even hyperinnervation (hypothalamus). The morphological and functional correlates of these enduring neurochemical changes in the MDMA-treated primate remain to be delineated

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - Cell Membrane

MH  - Chromatography,High Pressure Liquid

MH  - Dopamine

MH  - chemistry

MH  - Female

MH  - Hydroxyindoleacetic Acid

MH  - Injections,Subcutaneous

MH  - Male

MH  - Neurons

MH  - Norepinephrine

MH  - Piperidines

MH  - Saimiri

MH  - Serotonin

MH  - Serotonin Antagonists

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Dihydroxyphenylacetic Acid

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - administration & dosage

MH  - pharmacology

RP  - NOT IN FILE

NT  - UI - 92251642LA - EngRN - 0 (Piperidines)RN - 0 (Serotonin Antagonists)RN - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-41-2 (Norepinephrine)RN - 51-61-6 (Dopamine)RN - 54-16-0 (Hydroxyindoleacetic Acid)RN - 61869-08-7 (Paroxetine)PT - JOURNAL ARTICLEID - DA 05707/DA/NIDADA - 19920605IS - 0022-3565SB - MCY - UNITED STATESJC - JP3AA - AuthorEM - 199208

UR  - PM:0001374470

SO  - J Pharmacol Exp Ther 1992 May ;261(2):616-622

 

211

UI  - 209

AU  - Rudnick G

AU  - Wall SC

AD  - Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06510

TI  - The molecular mechanism of "ecstasy" [3,4-methylenedioxy- methamphetamine (MDMA)]: serotonin transporters are targets for MDMA- induced serotonin release

AB  - MDMA ("ecstasy") has been widely reported as a drug of abuse and as a neurotoxin. This report describes the mechanism of MDMA action at serotonin transporters from plasma membranes and secretory vesicles. MDMA stimulates serotonin efflux from both types of membrane vesicle. In plasma membrane vesicles isolated from human platelets, MDMA inhibits serotonin transport and [3H]imipramine binding by direct interaction with the Na(+)-dependent serotonin transporter. MDMA stimulates radiolabel efflux from plasma membrane vesicles preloaded with [3H]serotonin in a stereo-specific, Na(+)-dependent, and imipramine-sensitive manner characteristic of transporter-mediated exchange. In membrane vesicles isolated from bovine adrenal chromaffin granules, which contain the vesicular biogenic amine transporter, MDMA inhibits ATP-dependent [3H]serotonin accumulation and stimulates efflux of previously accumulated [3H]serotonin. Stimulation of vesicular [3H]serotonin efflux is due to dissipation of the transmembrane pH difference generated by ATP hydrolysis and to direct interaction with the vesicular amine transporter

MH  - Animal

MH  - Biological Transport

MH  - drug effects

MH  - Blood Platelets

MH  - Cattle

MH  - Cell Membrane

MH  - metabolism

MH  - Cell-Free System

MH  - Chromaffin Granules

MH  - Designer Drugs

MH  - pharmacology

MH  - Human

MH  - Hydrogen-Ion Concentration

MH  - Imipramine

MH  - In Vitro

MH  - Potassium

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 92179273LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-49-7 (Imipramine)RN - 50-67-9 (Serotonin)RN - 7440-09-7 (Potassium)PT - JOURNAL ARTICLEDA - 19920407IS - 0027-8424SB - MSB - XCY - UNITED STATESJC - PV3AA - AuthorEM - 199206

UR  - PM:0001347426

SO  - Proc Natl Acad Sci U S A 1992 Mar 1 ;89(5):1817-1821

 

212

UI  - 199

AU  - Scheffel U

AU  - Lever JR

AU  - Stathis M

AU  - Ricaurte GA

AD  - Department of Radiology, Johns Hopkins Medical Institutions, Baltimore, MD 21205

TI  - Repeated administration of MDMA causes transient down-regulation of serotonin 5-HT2 receptors

AB  - The present study examined short- and long-term effects of MDMA (3,4- methylene-dioxymethamphetamine) on serotonin (5-HT2 and 5-HT1c) receptors in the brain of the rat. N1-Methyl-2-[125I]lysergic acid diethylamide ([125I]MIL) was used to label these receptors in vitro and in vivo. The usefulness of [125I]MIL for in vivo detection of changes in 5-HT2 receptors was confirmed in preliminary experiments in which rats were treated chronically with mianserin (5 mg/kg, once daily for 10 days). Decreases in specific in vivo binding of [125I]MIL, after treatment with mianserin were found to be of the same magnitude as those determined by others, using in vitro methods. The MDMA (8 doses; 5-20 mg/kg each) was administered to rats over a period of 4 days. At various times after administration of the last dose of MDMA, the binding of [125I]MIL was measured. Acutely, treatment with MDMA (20 mg/kg) reduced specific in vivo binding of [125I]MIL in all regions of brain studied. For example, in the frontal cortex, specific binding of [125I]MIL was decreased by 80% at 6 hr and by 62% at 24 hr, after cessation of treatment with MDMA. Twenty-one days after administration of MDMA however, the number of binding sites for [125I]MIL was back to control levels. Reductions in in vivo binding of [125I]MIL in frontal cortex were dependent on the dose of MDMA injected and were associated with decreases in the number of binding sites for [125I]MIL (Bmax values) in tissue homogenates of the same area. Autoradiographic studies of MDMA-treated rats confirmed the decreased density of 5-HT2 receptors and also suggested that the 5-HT1c receptor of the choroid plexus was not affected. These results indicate that repeated administration of MDMA caused transient down-regulation of 5-HT2 receptors in the brain of the rat. Further, they demonstrated that [125I]MIL is a suitable radioligand for labeling 5-HT2 receptors, both in vitro and in vivo. Once labeled with an appropriate radionuclide for SPECT (single photon emission computed tomography) or PET (positron emission tomography), MIL should prove useful for monitoring changes in the density of serotonin receptors in the living mammalian brain

MH  - Animal

MH  - Autoradiography

MH  - Brain

MH  - anatomy & histology

MH  - Brain Chemistry

MH  - drug effects

MH  - Down-Regulation (Physiology)

MH  - Half-Life

MH  - Iodine Radioisotopes

MH  - diagnostic use

MH  - Kinetics

MH  - Lysergic Acid Diethylamide

MH  - analogs & derivatives

MH  - metabolism

MH  - pharmacology

MH  - Male

MH  - Rats

MH  - Rats,Sprague-Dawley

MH  - Receptors,Serotonin

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 93063718LA - EngRN - 0 (Iodine Radioisotopes)RN - 0 (Receptors, Serotonin)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-37-3 (Lysergic Acid Diethylamide)RN - 97165-34-9 (N(1)-methyl-2-iodo-lysergic acid diethylamide)PT - JOURNAL ARTICLEID - DA 06309/DA/NIDAID - CA-32845/CA/NCIID - ES 03819/ES/NIEHSDA - 19921127IS - 0028-3908SB - MCY - ENGLANDJC - NZBAA - AuthorEM - 199302

UR  - PM:0001359444

SO  - Neuropharmacology 1992 Sep ;31(9):881-893

 

213

UI  - 208

AU  - Screaton GR

AU  - Singer M

AU  - Cairns HS

AU  - Thrasher A

AU  - Sarner M

AU  - Cohen SL

TI  - Hyperpyrexia and rhabdomyolysis after MDMA ("ecstasy") abuse [letter; comment]

MH  - Adult

MH  - Case Report

MH  - Fever

MH  - chemically induced

MH  - Human

MH  - Male

MH  - Rhabdomyolysis

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - adverse effects

RP  - NOT IN FILE

NT  - UI - 92177911LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - COMMENTPT - LETTERDA - 19920409IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199206RO - M:LC1

UR  - PM:0001347361

SO  - Lancet 1992 Mar 14 ;339(8794):677-678

 

214

UI  - 202

AU  - Solowij N

AU  - Hall W

AU  - Lee N

AD  - National Drug and Alcohol Research Centre, University of New South Wales, Kensington, Australia

TI  - Recreational MDMA use in Sydney: a profile of 'Ecstacy' users and their experiences with the drug

AB  - 'Ecstasy' (3,4-methylenedioxymethamphetamine or MDMA) is a recreational drug that is gaining popularity world wide. There is a paucity of research regarding the ways in which Ecstasy is used and the nature of its effects. A 'snowball' peer network technique was used to recruit 100 users who completed anonymous questionnaires. The research revealed that Ecstasy is primarily used by infrequent recreational drug users for 'fun' at dance parties and social gatherings. The primary reported effects of Ecstasy were a 'positive mood state' and feelings of intimacy and closeness to others. The secondary effects of Ecstasy were the stimulant effects of energy and activation, and the psychedelic effects of insight and perceptual and sensual enhancement. Ecstasy was reported to share the properties of both amphetamines and hallucinogens in the nature of its side effects and residual effects which were no more severe than those of the latter two classes of drug. It appeared Ecstasy was not conductive to regular and frequent use, because tolerance was reported to develop to the positive effects of Ecstasy, while negative effects increased with use. Although few problems associated with the recreational use of Ecstasy have surfaced to date, animal research has shown it to be neurotoxic to serotonergic nerve terminals. Caution must be observed until further research can determine the level of hazard in humans

MH  - Adolescence

MH  - Adult

MH  - Arousal

MH  - drug effects

MH  - Australia

MH  - Designer Drugs

MH  - Euphoria

MH  - Female

MH  - Human

MH  - Male

MH  - Middle Age

MH  - Pilot Projects

MH  - Substance-Related Disorders

MH  - psychology

MH  - Support,Non-U.S.Gov't

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - adverse effects

RP  - NOT IN FILE

NT  - UI - 92379418LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19921001IS - 0952-0481CY - ENGLANDJC - BJDAA - AuthorEM - 199212

UR  - PM:0001354992

SO  - Br J Addict 1992 Aug ;87(8):1161-1172

 

215

UI  - 219

AU  - Battaglia G

AU  - Sharkey J

AU  - Kuhar MJ

AU  - de Souza EB

AD  - Neuroscience Branch, National Institute on Drug Abuse, Baltimore, Maryland 21224

TI  - Neuroanatomic specificity and time course of alterations in rat brain serotonergic pathways induced by MDMA (3,4- methylenedioxymethamphetamine): assessment using quantitative autoradiography

AB  - The widely abused "designer" drug MDMA (3,4- methylenedioxymethamphetamine) has been shown to cause marked and long- lasting changes in brain serotonergic systems. The present study uses quantitative in vitro autoradiography of 3H-paroxetine labeled 5-HT uptake sites to assess the time-dependent effects of MDMA on 5-HT neurons in specific neuroanatomic loci. Following treatment with MDMA (20 mg/kg, b.i.d. for 4 days), marked decreases in 5-HT uptake sites were observed in a number of brain regions known to receive projections of 5-HT neurons. These regions included cerebral cortex, caudate nucleus, hippocampus, nucleus accumbens, olfactory tubercle, superior and inferior colliculi, geniculate nuclei, and most thalamic nuclei. In contrast, other areas such as the septal nuclei and some thalamic nuclei which also receive 5-HT projections were not substantially affected by this drug. In most regions, decreases in 5-HT uptake sites occurred within 24 hours of the last dose of MDMA and persisted at the 2 week time point. Some regions such as dorsal striatum exhibited a time-dependent reduction with greater reductions occurring at 2 weeks rather than immediately following the MDMA treatment regimen. The density of 5-HT uptake sites in other regions such as endopiriform nucleus and substantia nigra at the 2 week versus 18 hour time point indicated some degree of region-specific recovery. Regions which demonstrated no significant reduction in 5-HT uptake sites included the dorsal and median raphe nuclei, ventral tegmental area, central grey, interpeduncular nucleus, locus coerulus, pontine reticular formation and cerebellum. Likewise, regions containing 5-HT axons of passage (e.g., indusium griseum and lateral hypothalamus) appeared to be insensitive to the neurotoxic effects of MDMA on 5-HT neurons. Furthermore, the neurotoxic effects of MDMA showed specificity in that the catecholamine neurons labeled by 3H-mazindol were unaffected by the treatment regimen. These data indicate that the preferential degeneration of serotonergic neurons by MDMA is mediated primarily at 5- HT terminal regions, whereas regions containing 5-HT perikarya and axons of passage remain relatively unaffected. In addition, the observed time-dependent reductions and recovery of 5-HT uptake sites which were detected within 2 weeks of the treatment regimen in certain brain regions suggest region-specific differences in recovery of 5-HT systems from MDMA-induced lesion

MH  - Animal

MH  - Autoradiography

MH  - Brain

MH  - anatomy & histology

MH  - drug effects

MH  - metabolism

MH  - Dopamine

MH  - pharmacokinetics

MH  - Male

MH  - Mazindol

MH  - Neural Pathways

MH  - Norepinephrine

MH  - Piperidines

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Reference Values

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

MH  - Time Factors

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - pharmacology

RP  - NOT IN FILE

NT  - UI - 92023035LA - EngRN - 0 (Piperidines)RN - 22232-71-9 (Mazindol)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-41-2 (Norepinephrine)RN - 51-61-6 (Dopamine)RN - 61869-08-7 (Paroxetine)RN - 82801-81-8 (3,4-methylenedioxyethamphetamine)PT - JOURNAL ARTICLEDA - 19911114IS - 0887-4476SB - MCY - UNITED STATESJC - VFLAA - AuthorEM - 199201

UR  - PM:0001681594

SO  - Synapse 1991 Aug ;8(4):249-260

 

216

UI  - 217

AU  - Bilsky EJ

AU  - Hubbell CL

AU  - Delconte JD

AU  - Reid LD

AD  - Department of Psychology, Rensselaer Polytechnic Institute, Troy, NY 12180

TI  - MDMA produces a conditioned place preference and elicits ejaculation in male rats: a modulatory role for the endogenous opioids

AB  - Methylenedioxymethamphetamine (MDMA) can produce a conditioned place preference (CPP) among rats. The ability of MDMA to produce a CPP was assessed while some rats were under the influence of naltrexone, 56 mg/kg, given 4 h before conditioning. Naltrexone attenuated MDMA's ability to produce a CPP without completely blocking MDMA's effects. Having noticed previously the production of seminal plugs by rats receiving MDMA, the presence of seminal plugs was recorded across the 8 days of conditioning. Roughly half of the rats receiving 6.3 mg/kg of MDMA left plugs during the conditioning period, while over two-thirds of those receiving a combination of MDMA and naltrexone left plugs. A second study, assessing further doses of MDMA, tabulated the drug's effects on the production of seminal plugs across 3 h. Besides eliciting ejaculation, MDMA also led to increased urination and defecation and a loss of body weight. These results support suggestions that the endogenous opioids modulate the reinforcing properties of stimulant drugs and affect male sexuality

MH  - Animal

MH  - Conditioning,Operant

MH  - drug effects

MH  - Defecation

MH  - Ejaculation

MH  - Endorphins

MH  - physiology

MH  - Male

MH  - Naltrexone

MH  - pharmacology

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Serotonin Antagonists

MH  - Support,U.S.Gov't,P.H.S.

MH  - Tropanes

MH  - Urination

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 92213027LA - EngRN - 0 (Endorphins)RN - 0 (Serotonin Antagonists)RN - 0 (Tropanes)RN - 16590-41-3 (Naltrexone)RN - 40796-97-2 (bemesetron)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEID - DA04440/DA/NIDADA - 19920504IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199207

UR  - PM:0001687169

SO  - Pharmacol Biochem Behav 1991 Oct ;40(2):443-447

 

217

UI  - 223

AU  - Bilsky EJ

AU  - Reid LD

AD  - Department of Psychology, Rensselaer Polytechnic Institute, Troy, NY 12180

TI  - MDL72222, a serotonin 5-HT3 receptor antagonist, blocks MDMA's ability to establish a conditioned place preference

AB  - Methylenedioxymethamphetamine (MDMA) has previously been shown to produce a positive conditioned place preference (CPP) among rats. Here the effects of doses of a specific 5-HT3 antagonist, MDL72222, on MDMA's ability to produce a CPP were assessed. A dose of MDL72222 (0.03 mg/kg) blocked the establishment of a MDMA CPP. These results support the suggestions that compounds affecting the 5-HT3 receptor may be of particular interest in studying the pharmacology of self-administered drugs

MH  - Animal

MH  - Conditioning,Operant

MH  - drug effects

MH  - Male

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Receptors,Serotonin

MH  - antagonists & inhibitors

MH  - Serotonin Antagonists

MH  - pharmacology

MH  - Support,U.S.Gov't,P.H.S.

MH  - Tropanes

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 92052470LA - EngRN - 0 (Receptors, Serotonin)RN - 0 (Serotonin Antagonists)RN - 0 (Tropanes)RN - 40796-97-2 (bemesetron)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEID - DA 04440/DA/NIDADA - 19911126IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199202

UR  - PM:0001682951

SO  - Pharmacol Biochem Behav 1991 Jun ;39(2):509-512

 

218

UI  - 224

AU  - Chadwick IS

AU  - Curry PD

AU  - Linsley A

AU  - Freemont AJ

AU  - Doran B

AD  - Department of Anaesthetics, Manchester Royal Infirmary

TI  - Ecstasy, 3-4 methylenedioxymethamphetamine (MDMA), a fatality associated with coagulopathy and hyperthermia [see comments]

MH  - Adolescence

MH  - Case Report

MH  - Designer Drugs

MH  - poisoning

MH  - Disseminated Intravascular Coagulation

MH  - chemically induced

MH  - mortality

MH  - Female

MH  - Fever

MH  - Human

MH  - Substance-Related Disorders

MH  - complications

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 91287077LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19910806IS - 0141-0768SB - MCY - ENGLANDJC - JX1EM - 199110RO - M:LC1

UR  - PM:0001676424

SO  - J R Soc Med 1991 Jun ;84(6):371

 

219

UI  - 220

AU  - Dornan WA

AU  - Katz JL

AU  - Ricaurte GA

AD  - Department of Psychology, Illinois Wesleyan University, Bloomington 61702

TI  - The effects of repeated administration of MDMA on the expression of sexual behavior in the male rat

AB  - 3,4-Methylenedioxymethamphetamine (MDMA, "Ecstasy") is a potent neurotoxin which preferentially produces 5-HT nerve terminal degeneration in the CNS in both rodents and primates. Timely research on the behavioral effects of acute and long term treatment of MDMA is critical due to the neuropathological effects of MDMA and its abuse liability. Presently, there are no published reports that have systematically examined the effects of acute or chronic treatment of MDMA on animal sexual behavior. Accordingly, the effects of repeated systemic administration of MDMA on a variety of parameters of male sexual behavior in sexually vigorous male rats were studied. Treatment consisted of subcutaneous injections of MDMA (40 mg/kg) or saline (1 ml/kg) every 12 hours for 4 consecutive days. In addition, neurochemical assessments of brain 5-HT and 5-HIAA depletion following repeated MDMA treatment were also conducted using reverse phase liquid chromatography. The results of this study revealed that repeated systemic administration of MDMA to sexually vigorous male rats produced a transient disruption of the expression of male copulatory behavior. In addition, in MDMA-treated males that did display copulatory behavior, both the ejaculation latency and postejaculatory interval were dramatically lengthened when compared to saline injected controls. Surprisingly, one week after the first behavioral test, copulatory behavior in MDMA treated rats appeared unaffected despite a marked depletion of 5-HT and 5-HIAA content in the striatum, and hippocampus

MH  - Animal

MH  - Brain Chemistry

MH  - drug effects

MH  - Corpus Striatum

MH  - metabolism

MH  - Ejaculation

MH  - Hippocampus

MH  - Hydroxyindoleacetic Acid

MH  - Male

MH  - Motor Activity

MH  - Rats

MH  - Serotonin

MH  - Sex Behavior,Animal

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - pharmacology

RP  - NOT IN FILE

NT  - UI - 92150486LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - JOURNAL ARTICLEDA - 19920319IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199205

UR  - PM:0001723802

SO  - Pharmacol Biochem Behav 1991 Jul ;39(3):813-816

 

220

UI  - 218

AU  - Gan BK

AU  - Baugh D

AU  - Liu RH

AU  - Walia AS

AD  - Department of Criminal Justice, University of Alabama, Birmingham

TI  - Simultaneous analysis of amphetamine, methamphetamine, and 3, 4- methylenedioxymethamphetamine (MDMA) in urine samples by solid-phase extraction, derivatization, and gas chromatography/mass spectrometry

AB  - A rapid and effective solid-phase extraction procedure using Bond Elute Certify bonded silica sorbent cartridges was adopted to extract amphetamine, methamphetamine, and 3,4-methylenedioxymethamphetamine (MDMA or Ecstasy) from urine samples. The extract was derivatized with trichloroacetic anhydride prior to gas chromatography/mass spectrometry (GC/MS) analysis with selected ion monitoring of the following ions: 190, 91, 188; 204, 91, 202; 162, 135, 202; 194, 123; and 211, 209 for the derivatized amphetamine, methamphetamine, MDMA, d5-amphetamine, and d9-methamphetamine, respectively. The first of the ions listed for each compound was used for quantitation. The compound d5-amphetamine was used as the internal standard for amphetamine, and d9-methamphetamine was used for methamphetamine and MDMA. Results showed a higher than 65% recovery and a reproducibility with less than a 5% coefficient of variation. When a sample size of 2 mL was used, the lowest detectable concentration was about 50 ng/mL, and a near-perfect fit can be obtained (within the 250 to 4000-ng/mL concentration range studied) using a second-order polynomial model

MH  - Amphetamine

MH  - urine

MH  - Calibration

MH  - Human

MH  - Mass Fragmentography

MH  - Methamphetamine

MH  - Predictive Value of Tests

MH  - Reproducibility of Results

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 92065160LA - EngRN - 300-62-9 (Amphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 537-46-2 (Methamphetamine)PT - JOURNAL ARTICLEDA - 19920102IS - 0022-1198SB - MCY - UNITED STATESJC - I5ZAA - AuthorEM - 199203

UR  - PM:0001955829

SO  - J Forensic Sci 1991 Sep ;36(5):1331-1341

 

221

UI  - 221

AU  - Gough B

AU  - Ali SF

AU  - Slikker W

AU  - Holson RR

AD  - Division of Reproductive and Developmental Toxicology National Center for Toxicological Research, Jefferson, AR 72079

TI  - Acute effects of 3,4-methylenedioxymethamphetamine (MDMA) on monoamines in rat caudate

AB  - Extracellular levels of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA) and serotonin (5-HT) were assayed in the caudate of freely moving rats using microdialysis and high performance liquid chromatography with electrochemical detection (HPLC-EC) to detect changes in their release. Dialysates were assayed at 20-minute intervals for four hours after an intraperitoneal (IP) injection of MDMA (10 mg/kg). In a separate study to determine MDMA effects on total caudate levels of the above neurochemicals, animals were injected IP with MDMA (10 mg/kg) and then sacrificed at 20, 60, 120 and 180 minutes after treatment. Brains were quickly removed, and caudate nuclei were dissected for neurochemical analysis using HPLC-EC. MDMA elicited an amphetamine-like increase in DA release, followed by an increase in DA content. DOPAC and HVA were both reduced in homogenate. 5-HT release was also increased, followed by a drop in caudate homogenate levels by three hours. DA extracellular content was 686% of control at 80 minutes; caudate homogenate levels were 122% at 120 minutes. 5-HT extracellular release was 123% at 20 minutes, then decreased thereafter. It is concluded that the acute effect of MDMA on caudate is at least as great on the DA as it is on the 5-HT system

MH  - Animal

MH  - Biogenic Monoamines

MH  - metabolism

MH  - Caudate Nucleus

MH  - drug effects

MH  - Chromatography,High Pressure Liquid

MH  - Dialysis

MH  - Dopamine

MH  - Electrochemistry

MH  - Female

MH  - Homovanillic Acid

MH  - Hydroxyindoleacetic Acid

MH  - In Vitro

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Serotonin

MH  - 3,4-Dihydroxyphenylacetic Acid

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - pharmacology

RP  - NOT IN FILE

NT  - UI - 92150452LA - EngRN - 0 (Biogenic Monoamines)RN - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)RN - 306-08-1 (Homovanillic Acid)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - JOURNAL ARTICLEDA - 19920319IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199205

UR  - PM:0001723797

SO  - Pharmacol Biochem Behav 1991 Jul ;39(3):619-623

 

222

UI  - 215

AU  - Johnson MP

AU  - Huang XM

AU  - Nichols DE

AD  - Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, IN 47907

TI  - Serotonin neurotoxicity in rats after combined treatment with a dopaminergic agent followed by a nonneurotoxic 3,4- methylenedioxymethamphetamine (MDMA) analogue

AB  - There is increasing evidence linking dopamine (DA) to the long-term serotonergic (5-HT) neurotoxic effects of certain substituted amphetamines such as 3,4-methylenedioxymethamphetamine (MDMA). The present study was undertaken to examine the importance of DA metabolism, uptake inhibition and release in the long-term effects of these drugs by combining various dopaminergic agents with an analogue of MDMA that had low neurotoxic liability, namely 5,6-methylenedioxy-2- aminoindan (MDAI). Monoamine and metabolite levels and the number of 5- HT uptake sites (using [3H]paroxetine binding) were determined 3 hours or 1 week after treatments. Combining the monoamine oxidase inhibitors, clorgyline (MAOA selective) or deprenyl (MAOB selective) with MDAI did not result in any long-term reductions of serotonergic markers. Similarly, combining the DA uptake inhibitor GBR-12909 with MDAI did not result in any long-term changes in monoamine levels at 1 week. In contrast, a single pretreatment of posttreatment with the nonvesicular DA releaser S-amphetamine and MDAI resulted in small but significant long-term changes in monoamine levels. More importantly, if a subacute dosing regimen (every 12 hours for 4 days) was utilized, the combination of S-amphetamine with MDAI resulted in a marked long-term decrease in the levels of cortical, hippocampal and striatal 5-HT, 5- HIAA and the number of 5-HT uptake sites. The results are discussed in terms of the significance of DA and especially nonvesicular DA release in the long-term effects of MDMA-like drugs

MH  - Amphetamine

MH  - administration & dosage

MH  - toxicity

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - Dopamine

MH  - Dopamine Agents

MH  - Homovanillic Acid

MH  - Hydroxyindoleacetic Acid

MH  - Indans

MH  - Rats

MH  - Serotonin

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Dihydroxyphenylacetic Acid

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 92279339LA - EngRN - 0 (Dopamine Agents)RN - 0 (Indans)RN - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)RN - 132741-81-2 (5,6-methylenedioxy-2-aminoindan)RN - 300-62-9 (Amphetamine)RN - 306-08-1 (Homovanillic Acid)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - JOURNAL ARTICLEID - DA-04758/DA/NIDADA - 19920630IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199209

UR  - PM:0001726189

SO  - Pharmacol Biochem Behav 1991 Dec ;40(4):915-922

 

223

UI  - 226

AU  - Johnson MP

AU  - Frescas SP

AU  - Oberlender R

AU  - Nichols DE

AD  - Department of Medicinal Chemistry and Pharmacognosy, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, Indiana 47907

TI  - Synthesis and pharmacological examination of 1-(3-methoxy-4- methylphenyl)-2-aminopropane and 5-methoxy-6-methyl-2-aminoindan: similarities to 3,4-(methylenedioxy)methamphetamine (MDMA)

AB  - The racemate and the enantiomers of 1-(3-methoxy-4-methyphenyl)-2- aminopropane (6) and racemic 5-methoxy-6-methyl-2-aminoindan (11) were tested for stimulus generalization in the two-lever drug-discrimination paradigm. Both 6 and 11 were found to substitute with high potency in 3,4-(methylenedioxy)methamphetamine (1) and (S)-1-(1,3-benzodioxol-5- yl)-2-(methylamino)butane (2) trained rats. In the latter assay, both enantiomers of 6 had identical potencies, but their dose-response curves were not parallel. Racemic 6, but not 11, partially substituted for LSD. Racemic 6 and 11 did not substitute in (S)-amphetamine-trained rats. All of the test compounds were potent inhibitors of [3H]-5-HT uptake into synaptosomes in vitro, with the S enantiomer of 6 being most active. Rat brain monoamine levels were unaltered 1 week following a single high dose (10 or 20 mg/kg, sc) of 6 or 11, or two weeks following a subacute dosing regimen (20 mg/kg, sc, twice a day for 4 days). In addition, radioligand-binding parameters in rat brain homogenate with the 5-HT uptake inhibitor [3H]paroxetine were unchanged after subacute dosing with either racemic 6 or 11. The results indicate that compounds 6 and 11 have animal behavioral pharmacology similar to the methylenedioxy compounds 1 and 2, but that they do not induce the serotonin neurotoxicity that has been observed for the latter two drugs

MH  - Animal

MH  - Behavior,Animal

MH  - drug effects

MH  - Brain

MH  - metabolism

MH  - chemistry

MH  - Dose-Response Relationship,Drug

MH  - Indans

MH  - chemical synthesis

MH  - pharmacology

MH  - Male

MH  - Phenethylamines

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Serotonin Antagonists

MH  - Stereoisomerism

MH  - Structure-Activity Relationship

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 91237660LA - EngRN - 0 (Indans)RN - 0 (Phenethylamines)RN - 0 (Serotonin Antagonists)RN - 132980-16-6 (5-methoxy-6-methyl-2-aminoindan)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 87179-33-7 (1-(3-methoxy-4-methylphenyl)-2-aminopropane)PT - JOURNAL ARTICLEID - DA-04758/DA/NIDADA - 19910626IS - 0022-2623SB - MSB - XCY - UNITED STATESJC - J0FAA - AuthorEM - 199108

UR  - PM:0001674539

SO  - J Med Chem 1991 May ;34(5):1662-1668

 

224

UI  - 227

AU  - McGuire P

AU  - Fahy T

AD  - Maudsley Hospital, London

TI  - Chronic paranoid psychosis after misuse of MDMA ("ecstasy") [see comments]

MH  - Adult

MH  - Case Report

MH  - Designer Drugs

MH  - Human

MH  - Male

MH  - Paranoid Disorders

MH  - chemically induced

MH  - Substance-Related Disorders

MH  - psychology

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 91215310LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19910605IS - 0959-8138SB - ASB - MSB - XCY - ENGLANDJC - BMJEM - 199108RO - M:LC1

UR  - PM:0001673631

SO  - BMJ 1991 Mar 23 ;302(6778):697

 

225

UI  - 230

AU  - Noggle FT

AU  - Clark CR

AU  - Andurkar S

AU  - DeRuiter J

AD  - Alabama Department of Forensic Sciences, Auburn 36830

TI  - Methods for the analysis of 1-(3,4-methylenedioxyphenyl)-2-butanamine and N-methyl-1-(3,4-methylenedioxyphenyl)-2-propanamine (MDMA)

AB  - The infrared and mass spectra of N-methyl-1-(3,4-methylenedioxyphenyl)- 2-propanamine (MDMA) and 1-(3,4-methylenedioxyphenyl)-2-butanamine are quite similar. These two compounds differ only in the position of substitution of a single methyl group. MDMA is a controlled street drug known as Ecstasy, while the isomeric butanamine is a member of a new class of potential psychotherapeutic agents called entactogens. These two compounds produce similar mass spectral fragmentation patterns including a common base peak at m/z 58. Reversed-phase liquid chromatographic (RPLC) methods consisting of a C18 stationary phase and an aqueous scidic mobile phase were used to separate these two compounds. Thus, LC methods can be used to differentiate MDMA from the isomeric butanamine for forensic analysis

MH  - Chromatography,Liquid

MH  - instrumentation

MH  - methods

MH  - Forensic Medicine

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - analysis

RP  - NOT IN FILE

NT  - UI - 91286405LA - EngRN - 107447-03-0 (1-(3,4-methylenedioxyphenyl)-2-butanamine)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19910802IS - 0021-9665SB - MCY - UNITED STATESJC - HQMAA - AuthorEM - 199110

UR  - PM:0001676403

SO  - J Chromatogr Sci 1991 Mar ;29(3):103-106

 

226

UI  - 233

AU  - Pan HS

AU  - Wang RY

AD  - Department of Psychiatry and Behavioral Science, State University of New York, Stony Brook 11794

TI  - MDMA: further evidence that its action in the medial prefrontal cortex is mediated by the serotonergic system

AB  - Systemically administered (+/-)-MDMA (3,4- methylenedioxymethamphetamine, 'Ecstasy') suppressed the firing rates of the majority of neurons in the medial prefrontal cortex (mPFc). The responses of mPFc cells to (+/-)-MDMA is mimicked by (+)-MDMA but not (- )-MDMA. Furthermore, pretreatment with fluoxetine (a specific 5-HT uptake blocker) but not GBR 12909 (a specific dopamine uptake blocker) prevented the suppressant action of MDMA. These data support the notion that the 5-HT system mediates (+/-)-MDMA's action

MH  - Animal

MH  - Cerebral Cortex

MH  - drug effects

MH  - Electrophysiology

MH  - Fluoxetine

MH  - pharmacology

MH  - Male

MH  - Neurotransmitter Uptake Inhibitors

MH  - Piperazines

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Receptors,Serotonin

MH  - antagonists & inhibitors

MH  - Serotonin

MH  - physiology

MH  - Serotonin Antagonists

MH  - Stereoisomerism

MH  - Stereotaxic Techniques

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 91274820LA - EngRN - 0 (Neurotransmitter Uptake Inhibitors)RN - 0 (Piperazines)RN - 0 (Receptors, Serotonin)RN - 0 (Serotonin Antagonists)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54910-89-3 (Fluoxetine)RN - 67469-78-7 (GBR 12909)PT - JOURNAL ARTICLEID - MH-41440/MH/NIMHID - MH-00378/MH/NIMHDA - 19910731IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199110

UR  - PM:0001675911

SO  - Brain Res 1991 Jan 25 ;539(2):332-336

 

227

UI  - 228

AU  - Pan HS

AU  - Wang RY

AD  - Department of Psychiatry and Behavioral Science, State University of New York, Stony Brook 11794

TI  - The action of (+/-)-MDMA on medial prefrontal cortical neurons is mediated through the serotonergic system

AB  - The mechanism of action of systemically administered (+/-)-MDMA (3,4- methylenedioxymethamphetamine) on spontaneously active neurons in the medial prefrontal cortex (mPFc) of chloral hydrate anesthetized rats was examined using standard single unit extracellular recording techniques. Intravenously administered MDMA dose-dependently decreased the firing rates of the majority of mPFc neurons in control rats. In contrast, in rats that were pretreated with p-chlorophenylalanine (PCPA), which depletes the brain serotonin (5-hydroxytryptamine, 5-HT) content by inhibiting tryptophan hydroxylase, the rate-limiting enzyme in the synthesis of 5-HT, MDMA was largely ineffective in inhibiting the firing of mPFc cells. In PCPA-treated animals, the administration of 5-hydroxytryptophan (5-HTP), which presumably restored the brain 5- HT content, but not L-DOPA, reinstated MDMA's inhibitory action in PCPA- treated rats. In rats that were pretreated with alpha-methyl-p-tyrosine (AMPT), which depletes the brain dopamine (DA) content by inhibiting tyrosine hydroxylase, the rate-limiting enzyme in the synthesis of DA, MDMA inhibited the firing of all of the mPFc cells. MDMA's effect on mPFc neurons was reversed by 5-HT receptor antagonists such as granisetron and metergoline. These results strongly suggest that MDMA exerts its action on mPFc cells indirectly by releasing endogenous 5-HT

MH  - Analysis of Variance

MH  - Animal

MH  - Cerebral Cortex

MH  - drug effects

MH  - physiology

MH  - Designer Drugs

MH  - pharmacology

MH  - Dopamine

MH  - Electrophysiology

MH  - methods

MH  - Fenclonine

MH  - Levodopa

MH  - Male

MH  - Methyltyrosines

MH  - Neurons

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Reference Values

MH  - Serotonin

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - 5-Hydroxytryptophan

RP  - NOT IN FILE

NT  - UI - 91274945LA - EngRN - 0 (Designer Drugs)RN - 0 (Levodopa)RN - 0 (Methyltyrosines)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 56-69-9 (5-Hydroxytryptophan)RN - 658-48-0 (alpha-Methyltyrosine)RN - 7424-00-2 (Fenclonine)PT - JOURNAL ARTICLEID - MH-41440/MH/NIMHID - MH-00378/MH/NIMHDA - 19910801IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199110

UR  - PM:0001675924

SO  - Brain Res 1991 Mar 8 ;543(1):56-60

 

228

UI  - 234

AU  - Paris JM

AU  - Cunningham KA

AD  - Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston 77550

TI  - Lack of neurotoxicity after intra-raphe micro-injections of MDMA ("ecstasy")

MH  - Animal

MH  - Brain Chemistry

MH  - drug effects

MH  - Catecholamines

MH  - metabolism

MH  - Chromatography,High Pressure Liquid

MH  - Hydroxyindoleacetic Acid

MH  - Immunohistochemistry

MH  - Indoles

MH  - Male

MH  - Microinjections

MH  - Nervous System Diseases

MH  - chemically induced

MH  - physiopathology

MH  - Raphe Nuclei

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - administration & dosage

MH  - toxicity

RP  - NOT IN FILE

NT  - UI - 91342798LA - EngRN - 0 (Catecholamines)RN - 0 (Indoles)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - JOURNAL ARTICLEID - DA 05708/DA/NIDADA - 19910920IS - 1046-9516SB - MCY - UNITED STATESJC - NRMEM - 199111

UR  - PM:0001715034

SO  - NIDA Res Monogr 1991  ;105():333-334

 

229

UI  - 237

AU  - Park WK

AU  - Azmitia EC

AD  - Department of Biology, New York University, New York 10003

TI  - 5-HT, MDMA (ecstasy), and nimodipine effects on 45Ca-uptake into rat brain synaptosomes

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - ultrastructure

MH  - Calcium

MH  - Calcium Radioisotopes

MH  - Nimodipine

MH  - pharmacology

MH  - Rats

MH  - Serotonin

MH  - Synaptosomes

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 92074766LA - EngRN - 0 (Calcium Radioisotopes)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 66085-59-4 (Nimodipine)RN - 7440-70-2 (Calcium)PT - JOURNAL ARTICLEDA - 19920109IS - 0077-8923SB - MSB - XCY - UNITED STATESJC - 5NMEM - 199203

UR  - PM:0001683755

SO  - Ann N Y Acad Sci 1991  ;635():438-440

 

230

UI  - 232

AU  - Prat A

AU  - Montero M

AU  - Reig R

AU  - Sanz P

AD  - Departamento de Salud Publica y Legislacion Sanitaria, Facultad de Medicina, Universidad de Barcelona

TI  - [MDMA ("ecstasy"): a currently used drug in Spain]

MH  - chemistry

MH  - Designer Drugs

MH  - Human

MH  - Spain

MH  - epidemiology

MH  - Substance-Related Disorders

MH  - diagnosis

MH  - therapy

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 91252551LA - SpaRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19910709IS - 0014-2565CY - SPAINJC - RNLEM - 199109

UR  - PM:0001675014

SO  - Rev Clin Esp 1991 Feb ;188(2):106-108

 

231

UI  - 236

AU  - Rattray M

AD  - UMDS Division of Biochemistry, University of London, U.K

TI  - Ecstasy: towards an understanding of the biochemical basis of the actions of MDMA

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - Designer Drugs

MH  - pharmacology

MH  - Human

MH  - Molecular Structure

MH  - Neurons

MH  - Receptors,Neurotransmitter

MH  - physiology

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - adverse effects

MH  - chemistry

MH  - toxicity

RP  - NOT IN FILE

NT  - UI - 92137182LA - EngRN - 0 (Designer Drugs)RN - 0 (Receptors, Neurotransmitter)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19920306IS - 0071-1365SB - MCY - ENGLANDJC - EMGEM - 199205

UR  - PM:0001685707

SO  - Essays Biochem 1991  ;26():77-87

 

232

UI  - 229

AU  - Schechter MD

AD  - Department of Pharmacology, Northeastern Ohio Universities College of Medicine, Rootstown 44272

TI  - Effect of MDMA neurotoxicity upon its conditioned place preference and discrimination

AB  - Experiments were conducted to investigate the functional consequences of a neurotoxic regimen of MDMA administration upon two behaviors, conditioned place preference and drug discrimination. Rats were trained to discriminate 1.5 mg/kg MDMA from its vehicle and their discriminative performance was shown to be dose-responsive. Subsequently, MDMA was observed to produce a conditioned place preference as three conditioning sessions with 1.5 mg/kg MDMA paired with the nonpreferred chamber increased the time the rats spent in the chamber paired with MDMA. Administration of a proportedly neurotoxic dose (20 mg/kg subcutaneous) of MDMA, twice-a-day for four days, did not affect this conditioned place preference when it was redetermined at a time of maximal neurochemical compromise. In contrast, sensitivity to 1.0 mg/kg MDMA in the drug discrimination task was shown to be significantly decreased after the neurotoxic regimen. Results are discussed in light of MDMA effects upon both central serotonergic and dopaminergic neurons

MH  - Animal

MH  - Choice Behavior

MH  - drug effects

MH  - Conditioning,Classical

MH  - Designer Drugs

MH  - toxicity

MH  - Discrimination Learning

MH  - Dose-Response Relationship,Drug

MH  - Male

MH  - Nervous System

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Sodium Chloride

MH  - pharmacology

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 91296923LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 7647-14-5 (Sodium Chloride)PT - JOURNAL ARTICLEID - 04801DA - 19910813IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199110

UR  - PM:0001676847

SO  - Pharmacol Biochem Behav 1991 Mar ;38(3):539-544

 

233

UI  - 216

AU  - Schifano F

TI  - Chronic atypical psychosis associated with MDMA ("ecstasy") abuse [letter] [see comments]

MH  - Adult

MH  - Case Report

MH  - Chronic Disease

MH  - Human

MH  - Male

MH  - Psychoses,Substance-Induced

MH  - etiology

MH  - Substance-Related Disorders

MH  - complications

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 92047999LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - LETTERDA - 19911219IS - 0140-6736SB - ASB - MSB - XCY - ENGLANDJC - L0SEM - 199202RO - M:LC1RO - M:LC1

UR  - PM:0001682711

SO  - Lancet 1991 Nov 23 ;338(8778):1335

 

234

UI  - 235

AU  - St Omer VE

AU  - Ali SF

AU  - Holson RR

AU  - Duhart HM

AU  - Scalzo FM

AU  - Slikker W

AD  - Department of Veterinary Biomedical Sciences, College of Veterinary Medicine, University of Missouri, Columbia 65211

TI  - Behavioral and neurochemical effects of prenatal methylenedioxymethamphetamine (MDMA) exposure in rats

AB  - MDMA is a hallucinogenic drug that is used by the general public as a recreational drug of abuse. The neurobehavioral consequences of prenatal MDMA exposure are unknown. Groups of pregnant rats were gavaged with 0, 2.5, or 10 mg/kg MDMA during gestation on alternate gestational days 6-18. Gestational duration, litter size, neonatal birth weights and physical appearance at birth were unaffected by MDMA treatments. Pregnancy weight gain was significantly reduced by MDMA treatment. Progeny growth, maturational parameters (eye opening and incisor eruption times), surface righting reflex, swimming performance, forelimb grip strength, milk-induced behaviors, passive avoidance behavior, figure-8 maze activity over 48 hours, the density of brain serotonin (5-HT) uptake sites, and brain 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels were unaffected by MDMA treatments. Olfactory discrimination on postnatal days (PND) 9-11 was enhanced in both male and female MDMA-treated progeny, while negative geotaxis (PND 7-10) was delayed in female pups. In contrast to progeny, MDMA caused dose- dependent decreases in 5-HT and 5-HIAA levels in discrete brain areas of the dam. It is concluded that prenatal exposure to MDMA at the levels used here produces only subtle behavioral alterations in developing rats. The dam is more at risk for MDMA-induced 5-HT depletion than is the conceptus

MH  - Animal

MH  - Behavior,Animal

MH  - drug effects

MH  - Brain

MH  - metabolism

MH  - Designer Drugs

MH  - toxicity

MH  - Female

MH  - Hydroxyindoleacetic Acid

MH  - Male

MH  - Maternal-Fetal Exchange

MH  - Pregnancy

MH  - Rats

MH  - Serotonin

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,Non-P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 91260555LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54-16-0 (Hydroxyindoleacetic Acid)PT - JOURNAL ARTICLEDA - 19910715IS - 0892-0362SB - MCY - UNITED STATESJC - NATAA - AuthorEM - 199109

UR  - PM:0001710762

SO  - Neurotoxicol Teratol 1991 Jan ;13(1):13-20

 

235

UI  - 231

AU  - Steele TD

AU  - Brewster WK

AU  - Johnson MP

AU  - Nichols DE

AU  - Yim GK

AD  - Department of Pharmacology and Toxicology, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, IN 47907

TI  - Assessment of the role of alpha-methylepinine in the neurotoxicity of MDMA

AB  - To assess the potential involvement of metabolism of 3,4- methylenedioxymethamphetamine (MDMA) to the catechol alpha- methylepinine in producing serotonergic neurotoxicity, we attempted to correlate aspects of this reaction with the neurotoxicity profile of MDMA. In contrast to the stereoselectivity of S-(+)-MDMA in causing persistent declines in rat brain 5-hydroxyindole levels, no stereochemical component to the metabolic reaction was apparent. Rat liver microsomes generated a significantly greater amount of alpha- methylepinine than did mouse microsomes, but similar amounts of metabolite were produced by brain microsomes from the two species. Formation of alpha-methylepinine by hepatic, but not brain, microsomes was inhibited by SKF 525A and induced by phenobarbital, possibly indicating a tissue specificity in cytochrome P-450-dependent metabolism of MDMA. To directly assess whether alpha-methylepine is a likely mediator of MDMA neurotoxicity, the compound was administered intracerebroventricularly. No persistent declines in biogenic amines or their metabolites were observed one week following treatment. These data suggest that alpha-methylepinine alone is not responsible for the neurotoxic effects of MDMA

MH  - Animal

MH  - Biogenic Amines

MH  - metabolism

MH  - Brain Chemistry

MH  - drug effects

MH  - Chromatography,High Pressure Liquid

MH  - Cytochrome P-450

MH  - Deoxyepinephrine

MH  - analogs & derivatives

MH  - administration & dosage

MH  - toxicity

MH  - Electrochemistry

MH  - Injections,Intraventricular

MH  - Male

MH  - Mice

MH  - Microsomes,Liver

MH  - enzymology

MH  - Nervous System Diseases

MH  - chemically induced

MH  - physiopathology

MH  - Phenobarbital

MH  - pharmacology

MH  - Proadifen

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Species Specificity

MH  - 3,4-Methylenedioxyamphetamine

RP  - NOT IN FILE

NT  - UI - 91279806LA - EngRN - 15398-87-5 (alpha-methylepinine)RN - 302-33-0 (Proadifen)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-06-6 (Phenobarbital)RN - 501-15-5 (Deoxyepinephrine)RN - 9035-51-2 (Cytochrome P-450)PT - JOURNAL ARTICLEDA - 19910731IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199110

UR  - PM:0001676172

SO  - Pharmacol Biochem Behav 1991 Feb ;38(2):345-351

 

236

UI  - 222

AU  - Watson L

AU  - Beck J

AD  - Institute for Scientific Analysis, San Francisco, California 94123

TI  - New age seekers: MDMA use as an adjunct to spiritual pursuit

AB  - The use of MDMA as an adjunct to spiritual pursuit among New Ager seekers is examined. These study respondents indicated that social worlds greatly influenced which qualities of the MDMA experience were most pursued and valued. In contrast to recreationally oriented respondents, who saw minimal long-term benefits accruing from MDMA use, New Agers typically believed that carefully planned experiences possessed significant potential for lasting spiritual and/or therapeutic value. While many New Agers eschew the use of alcohol and other drugs, these respondents were generally impressed with MDMA. Nevertheless, they differed in their motivations for use and their perceptions of its influence in their lives: some employed MDMA as a sacramental adjunct for following specific spiritual paths; others viewed it as aiding their spiritual growth in more general ways. Because the approaches to and motivations for using MDMA differ so markedly for New Agers and recreationally oriented users, the importance of social worlds and context in studying drug-using behavior is underscored

MH  - Adult

MH  - Aged

MH  - Case Report

MH  - Female

MH  - Human

MH  - Male

MH  - Middle Age

MH  - Motivation

MH  - Philosophy

MH  - Spiritualism

MH  - psychology

MH  - Substance-Related Disorders

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 92130025LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEDA - 19920305IS - 0279-1072SB - MCY - UNITED STATESJC - JLPAA - AuthorEM - 199205

UR  - PM:0001685513

SO  - J Psychoactive Drugs 1991 Jul ;23(3):261-270

 

237

UI  - 225

AU  - Winstock AR

TI  - Chronic paranoid psychosis after misuse of MDMA [letter; comment]

MH  - Adult

MH  - Designer Drugs

MH  - Female

MH  - Human

MH  - Male

MH  - Paranoid Disorders

MH  - chemically induced

MH  - Psychoses,Substance-Induced

MH  - etiology

MH  - Substance-Related Disorders

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 91255744LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - COMMENTPT - LETTERDA - 19910712IS - 0959-8138SB - ASB - MSB - XCY - ENGLANDJC - BMJEM - 199109RO - M:LC1

UR  - PM:0001675133

SO  - BMJ 1991 May 11 ;302(6785):1150-1151

 

238

UI  - 242

AU  - Azmitia EC

AU  - Murphy RB

AU  - Whitaker-Azmitia PM

AD  - Department of Biology, New York University, NY 10003

TI  - MDMA (ecstasy) effects on cultured serotonergic neurons: evidence for Ca2(+)-dependent toxicity linked to release

AB  - Animal studies have established a correlation between release of 5- hydroxytryptamine (5-HT) and the long-term reduction of 5-HT (toxicity) by 3,4-methylenedioxymethamphetamine (MDMA) with the S(+) enantiomer being more active than the R(-). Using a microculture system of fetal raphe neurons, the enantiomers of MDMA were tested to determine if a similar difference in potency existed. The results showed that the development of the uptake capacity of [3H]5-HT in 4-day cultures was half-maximally inhibited by a single application at time of plating of 5 X 10(-6) M S(+)-MDMA and 5 X 10(-5) M R(-)-MDMA. In order to determine if the Ca2(+)-independent release (chemically induced through the transporter protein and inhibited by reuptake blockers) or the Ca2(+)-dependent release (K(+)-induced and inhibited by presynaptic receptors) contributed to the toxicity, fluoxetine and D1 and alpha 2 agonists were studied. The results showed that both forms of release were involved in the loss of [3H]5-HT uptake capacity, with the direct MDMA-induced Ca2(+)-independent (fluoxetine-sensitive) release being the first step. Evidence from binding studies indicates that MDMA has a micromolar affinity for the 5-HT2 receptor, and our studies in culture showed that ketanserin, a specific 5-HT2 antagonist, was effective at attenuating the effects of S(+)-MDMA on the development of the [3H]5-HT uptake capacity by the cultured raphe neurons. The 5-HT2 receptor is linked to increased intracellular Ca2+ through a second messenger phosphatidylinositol (PI)-hydrolysis mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

MH  - Amphetamines

MH  - pharmacology

MH  - Animal

MH  - Calcium

MH  - physiology

MH  - Cells,Cultured

MH  - Embryo

MH  - Fluoxetine

MH  - Ketanserin

MH  - Raphe Nuclei

MH  - cytology

MH  - drug effects

MH  - metabolism

MH  - Rats

MH  - Serotonin

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 90213216LA - EngRN - 0 (Amphetamines)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 54910-89-3 (Fluoxetine)RN - 74050-98-9 (Ketanserin)RN - 7440-70-2 (Calcium)PT - JOURNAL ARTICLEID - 271-87-8144DA - 19900521IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199007

UR  - PM:0001969761

SO  - Brain Res 1990 Feb 26 ;510(1):97-103

 

239

UI  - 244

AU  - de Souza EB

AU  - Battaglia G

AU  - Insel TR

AD  - Laboratory of Neurobiology, National Institute on Drug Abuse, Baltimore, Maryland 21224

TI  - Neurotoxic effect of MDMA on brain serotonin neurons: evidence from neurochemical and radioligand binding studies

AB  - In summary, the data from both neurochemical and neuroanatomical studies demonstrate widespread and long-lasting degeneration of serotonin neurons in brain without any major or consistent effects on catecholamine neurons following in vivo administration of MDMA in both rats and rhesus monkeys. A detailed examination of the parameters involved in the neurotoxic and neurodegenerative effects of MDMA on brain serotonin neurons indicate that the severity of the lesion is dependent on the dose of drug administered with the drug being more potent in rhesus monkeys than in rats. Furthermore, the neurodegenerative effects of the drug are long-lasting (up to one year) with respect to neuronal regeneration (i.e. recovery of serotonin uptake sites) while functional recovery may be permanently impaired since serotonin content remains markedly (40-50%) below levels in age- matched controls for as long as one year after drug administration. The neurochemical and autoradiographic data suggest that there are some regional differences and morphological specificity to the neurodegenerative effects of MDMA as demonstrated by greater reductions in serotonin uptake sites in brain regions containing primarily terminals while regions containing axons of passage and cell bodies are relatively unaffected

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - pathology

MH  - Designer Drugs

MH  - toxicity

MH  - Dopamine

MH  - Neurons

MH  - Neurotoxins

MH  - Serotonin

MH  - Species Specificity

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 91069165LA - EngRN - 0 (Designer Drugs)RN - 0 (Neurotoxins)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19910114IS - 0077-8923SB - MSB - XCY - UNITED STATESJC - 5NMAA - AuthorEM - 199103

UR  - PM:0001979218

SO  - Ann N Y Acad Sci 1990  ;600():682-697

 

240

UI  - 249

AU  - Gibb JW

AU  - Johnson M

AU  - Stone D

AU  - Hanson GR

AD  - Department of Pharmacology and Toxicology, University of Utah, Salt Lake City 84112

TI  - MDMA: historical perspectives

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - pathology

MH  - physiology

MH  - Designer Drugs

MH  - Tryptophan Hydroxylase

MH  - metabolism

MH  - Tyrosine 3-Monooxygenase

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - pharmacology

MH  - toxicity

RP  - NOT IN FILE

NT  - UI - 91069159LA - EngRN - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)RN - EC 1.14.16.4 (Tryptophan Hydroxylase)RN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19910114IS - 0077-8923SB - MSB - XCY - UNITED STATESJC - 5NMEM - 199103

UR  - PM:0001979213

SO  - Ann N Y Acad Sci 1990  ;600():601-611

 

241

UI  - 241

AU  - Grob C

AU  - Bravo G

AU  - Walsh R

TI  - Second thoughts on 3,4-methylenedioxymethamphetamine (MDMA) neurotoxicity [letter; comment]

MH  - Amphetamines

MH  - toxicity

MH  - Animal

MH  - Clinical Trials

MH  - Designer Drugs

MH  - Human

MH  - Mental Disorders

MH  - drug therapy

MH  - Nervous System Diseases

MH  - chemically induced

MH  - Rats

MH  - Research Design

MH  - standards

MH  - Substance-Related Disorders

MH  - complications

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - therapeutic use

RP  - NOT IN FILE

NT  - UI - 90165652LA - EngRN - 0 (Amphetamines)RN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - CLINICAL TRIALPT - COMMENTPT - LETTERDA - 19900326IS - 0003-990XSB - ASB - MCY - UNITED STATESJC - 72CEM - 199005RO - M:LC1

UR  - PM:0001968330

SO  - Arch Gen Psychiatry 1990 Mar ;47(3):288-289

 

242

UI  - 239

AU  - Kunsman GW

AU  - Manno JE

AU  - Cockerham KR

AU  - Manno BR

AD  - Department of Pharmacology, Louisiana State University Medical Center, Shreveport 71130

TI  - Application of the Syva EMIT and Abbott TDx amphetamine immunoassays to the detection of 3,4-methylene-dioxymethamphetamine (MDMA) and 3,4- methylene-dioxyethamphetamine (MDEA) in urine

AB  - MDMA and MDEA are hallucinogenic analogs of amphetamine. The need for laboratory monitoring of these substances has developed as a result of their increased recreational use. Since the Abbott TDx and Syva EMIT- d.a.u. immunoassays are commonly used tests for urine monitoring of drugs-of-abuse, the amphetamine assay of each manufacturer was assessed to determine the degree of cross-reactivity with MDMA and MDEA. Cross- reactivity was evaluated using a series of

MH  - Amphetamines

MH  - urine

MH  - Chemistry,Analytical

MH  - Cross Reactions

MH  - Dose-Response Relationship,Drug

MH  - False Negative Reactions

MH  - Fluorescence Polarization

MH  - methods

MH  - Human

MH  - Immunoenzyme Techniques

MH  - Mass Fragmentography

MH  - Reproducibility of Results

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 90325713LA - EngRN - 0 (Amphetamines)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 82801-81-8 (3,4-methylenedioxyethamphetamine)PT - JOURNAL ARTICLEDA - 19900830IS - 0146-4760SB - MCY - UNITED STATESJC - K4RAA - AuthorEM - 199011

UR  - PM:0001973747

SO  - J Anal Toxicol 1990 May ;14(3):149-153

 

243

UI  - 250

AU  - McKenna DJ

AU  - Peroutka SJ

AD  - Department of Neurology, Stanford University School of Medicine, California 94305

TI  - Neurochemistry and neurotoxicity of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy")

MH  - Amphetamines

MH  - toxicity

MH  - Animal

MH  - Brain

MH  - drug effects

MH  - metabolism

MH  - pathology

MH  - Designer Drugs

MH  - Receptors,Cell Surface

MH  - Serotonin

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - pharmacology

RP  - NOT IN FILE

NT  - UI - 90079439LA - EngRN - 0 (Amphetamines)RN - 0 (Designer Drugs)RN - 0 (Receptors, Cell Surface)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW LITERATUREDA - 19900119IS - 0022-3042SB - MCY - UNITED STATESJC - JAVEM - 199003

UR  - PM:0001967141

SO  - J Neurochem 1990 Jan ;54(1):14-22

 

244

UI  - 246

AU  - Molliver ME

AU  - Berger UV

AU  - Mamounas LA

AU  - Molliver DC

AU  - O'Hearn E

AU  - Wilson MA

AD  - Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

TI  - Neurotoxicity of MDMA and related compounds: anatomic studies

AB  - The cytotoxic effects of amphetamine derivatives were studied by immunocytochemistry to identify the cellular compartments affected by these drugs, to obtain morphologic evidence of neuronal degeneration, and to assess the potential for regeneration. The substituted amphetamines, MDA, MDMA, PCA, and fenfluramine, all release serotonin and cause acute depletion of 5-HT from most axon terminals in forebrain. (1) Unequivocal signs of axon degeneration were seen at 36- 48 hour survivals: 5-HT axons exhibited increased caliber, huge, swollen varicosities, fragmentation, and dilated proximal axon stumps. (2) Fine 5-HT axon terminals were persistently lost after drug administration, while beaded axons and raphe cell bodies were spared. These two types of 5-HT axons, which arise from separate raphe nuclei and form distinct ascending projections, are differentially vulnerable to psychotropic drugs. (3) From 2-8 months after treatment, there was progressive serotonergic re-innervation of neocortex along a fronto- occipital gradient. Longitudinal 5-HT axons grew into layers I and VI from rostral to caudal, before sprouting into middle cortical layers; this bilaminar pattern of growth simulates perinatal development of 5- HT innervation. This study demonstrates differential vulnerability of 5- HT projections, evidence for axonal degeneration, and sprouting of 5-HT axons leading to re-innervation of forebrain. While the sprouting axons are anatomically similar to the type that was damaged, it is not known whether a normal pattern of innervation is re-established

MH  - Animal

MH  - Brain

MH  - anatomy & histology

MH  - drug effects

MH  - pathology

MH  - Neurotoxins

MH  - toxicity

MH  - Structure-Activity Relationship

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 91069162LA - EngRN - 0 (Neurotoxins)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALID - DA04431/DA/NIDAID - NS15199/NS/NINDSID - NS21011/NS/NINDSDA - 19910114IS - 0077-8923SB - MSB - XCY - UNITED STATESJC - 5NMAA - AuthorEM - 199103

UR  - PM:0001979216

SO  - Ann N Y Acad Sci 1990  ;600():649-661

 

245

UI  - 243

AU  - Nash JF

AD  - Department of Psychiatry, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106-5000

TI  - Ketanserin pretreatment attenuates MDMA-induced dopamine release in the striatum as measured by in vivo microdialysis

AB  - Systemic administration of the amphetamine analogue, 3,4- methylenedioxymethamphetamine (MDMA) produced a dose-dependent increase in the extracellular concentration of dopamine (DA) in the striatum as measured by in vivo microdialysis in awake, freely-moving rats. The extracellular concentration of the DA metabolite, 3,4- dihydroxyphenylacetic acid (DOPAC), was significantly decreased in dialysate samples following the administration of MDMA (10 and 20 mg/kg, i.p.). The serotonin-2 (5-HT2) antagonist ketanserin (3 mg/kg, i.p.) had no effect on the extracellular concentration of DA or DOPAC in the striatum of vehicle- treated rats. The administration of ketanserin (3 mg/kg) 1 hr prior to MDMA (20 mg/kg) significantly attenuated the

MH  - Animal

MH  - Corpus Striatum

MH  - drug effects

MH  - secretion

MH  - Dialysis

MH  - Dopamine

MH  - Ketanserin

MH  - pharmacology

MH  - Male

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Receptors,Serotonin

MH  - Support,Non-U.S.Gov't

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Dihydroxyphenylacetic Acid

MH  - analysis

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 91087710LA - EngRN - 0 (Receptors, Serotonin)RN - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 51-61-6 (Dopamine)RN - 74050-98-9 (Ketanserin)PT - JOURNAL ARTICLEID - MH 41684/MH/NIMHDA - 19910207IS - 0024-3205SB - MSB - XCY - ENGLANDJC - L62AA - AuthorEM - 199104

UR  - PM:0001979830

SO  - Life Sci 1990  ;47(26):2401-2408

 

246

UI  - 248

AU  - Nichols DE

AU  - Oberlender R

AD  - Department of Medicinal Chemistry and Pharmacognosy, School of Pharmacy and Pharmacal Sciences, Purdue University, West Lafayette, Indiana 47907

TI  - Structure-activity relationships of MDMA and related compounds: a new class of psychoactive drugs?

MH  - Animal

MH  - Conditioning,Operant

MH  - drug effects

MH  - Discrimination (Psychology)

MH  - Male

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Structure-Activity Relationship

MH  - Support,U.S.Gov't,P.H.S.

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

MH  - pharmacology

RP  - NOT IN FILE

NT  - UI - 91069160LA - EngRN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)PT - JOURNAL ARTICLEID - 5 RO1 DA 04578/DA/NIDADA - 19910114IS - 0077-8923SB - MSB - XCY - UNITED STATESJC - 5NMEM - 199103

UR  - PM:0001979214

SO  - Ann N Y Acad Sci 1990  ;600():613-623

 

247

UI  - 238

AU  - Piercey MF

AU  - Lum JT

AU  - Palmer JR

AD  - CNS Research, Upjohn Company, Kalamazoo, MI 49001

TI  - Effects of MDMA ('ecstasy') on firing rates of serotonergic, dopaminergic, and noradrenergic neurons in the rat

AB  - 3,4-Methylenedioxymethamphetamine (MDMA), a non-hallucinogenic drug of abuse, potently depressed firing rates of a subpopulation of serotonin neurons in the dorsal and median raphe. High neurotoxic doses depressed those serotonin neurons unresponsive to low doses. Noradrenaline neurons in the locus coeruleus were also depressed by moderate doses. Dopamine neurons were unaffected. It is concluded that MDMA's unique psychological effects are mediated through a subpopulation of serotonergic and noradrenergic neurons, presumably through effects on release mechanisms

MH  - Action Potentials

MH  - drug effects

MH  - Animal

MH  - Designer Drugs

MH  - pharmacology

MH  - Dopamine

MH  - physiology

MH  - Electrodes,Implanted

MH  - Male

MH  - Neurons

MH  - Norepinephrine

MH  - Rats

MH  - Rats,Inbred Strains

MH  - Serotonin

MH  - 3,4-Methylenedioxyamphetamine

MH  - analogs & derivatives

RP  - NOT IN FILE

NT  - UI - 91077728LA - EngRN - 0 (Designer Drugs)RN - 42542-10-9 (N-Methyl-3,4-methylenedioxyamphetamine)RN - 4764-17-4 (3,4-Methylenedioxyamphetamine)RN - 50-67-9 (Serotonin)RN - 51-41-2 (Norepinephrine)RN - 51-61-6 (Dopamine)PT - JOURNAL ARTICLEDA - 19910131IS - 0006-8993SB - MCY - NETHERLANDSJC - B5LAA - AuthorEM - 199104

UR  - PM:0001979517

SO  - Brain Res 1990 Sep 3 ;526(2):203-206

 

248

UI  - 251

AU  - Ricaurte GA

AU  - Finnegan KT

AU  - Irwin I

AU  - Langston JW

AD  - Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

TI  - Aminergic metabolites in cerebrospinal fluid of humans previously exposed to MDMA: preliminary observations

MH  - Adult

MH  - Biogenic Amines

MH  - cerebrospinal fluid

MH  - Designer Drugs

MH  - pharmacology

MH  - Female

MH  - Homovanillic Acid

M