http://www.doctordeluca.com/References/clozapine_cocaine.htm
1/2001


Medline search for 'clozapine' and 'cocaine' - 38 references with abstracts.

1
UI - 2
AU - Farren CK
AU - Hameedi FA
AU - Rosen MA
AU - Woods S
AU - Jatlow P
AU - Kosten TR
AD - Department of Psychiatry, Division of Substance Abuse, Yale University School of Medicine, New Haven, CT, USA
TI - Significant interaction between clozapine and cocaine in cocaine addicts [In Process Citation]
AB - Because clozapine may be prescribed to cocaine abusing patients with schizophrenia, we studied cocaine-clozapine interactions in a controlled setting. Eight male cocaine addicts underwent four oral challenges with ascending doses of clozapine (12.5, 25 and 50 mg) and placebo followed 2 h later by a 2-mg/kg dose of intranasal cocaine. Subjective and physiological responses, and serum cocaine levels were measured over a total 4-h period. Clozapine pretreatment increased cocaine levels during the study and significantly increased the peak serum cocaine levels in a dose dependent manner. In spite of this elevation in blood levels, clozapine pretreatment had a significant diminishing effect upon subjective responses to cocaine, including 'expected high', 'high' and 'rush', notably at the 50 mg dose. There was also a significant effect upon 'sleepiness', 'paranoia' and 'nervous'. Clozapine caused a significant near-syncopal episode in one subject in the study, requiring his removal from the study. Clozapine had no significant effect on baseline pulse rate and systolic blood pressure, but it attenuated the significant pressor effects of the single dose of intranasal cocaine. These data suggested a possible therapeutic role for clozapine in the treatment of cocaine addiction in humans, but also suggests caution due to the near-syncopal event and the increase in serum cocaine levels
MH - Clozapine
MH - Cocaine
MH - Human
MH - Male
MH - Schizophrenia
RP - NOT IN FILE
NT - UI - 20351347LA - EngDA - 20001116IS - 0376-8716SB - MCY - IRELANDJC - EBSAA - AUTHORRO - O:099
UR - PM:0010891628
SO - Drug Alcohol Depend 2000 May 1 ;59(2):153-163

2
UI - 4
AU - Millan MJ
AU - Brocco M
AU - Rivet JM
AU - Audinot V
AU - Newman-Tancredi A
AU - Maiofiss L
AU - Queriaux S
AU - Despaux N
AU - Peglion JL
AU - Dekeyne A
AD - Psychopharmacology Department, Institut de Recherches Servier, Centre de Recherches de Croissy, Paris, Croissy-sur-Seine, France
TI - S18327 (1-[2-[4-(6-fluoro-1, 2-benzisoxazol-3-yl)piperid-1-yl]ethyl]3- phenyl imidazolin-2-one), a novel, potential antipsychotic displaying marked antagonist properties at alpha(1)- and alpha(2)-adrenergic receptors: II. Functional profile and a multiparametric comparison with haloperidol, clozapine, and 11 other antipsychotic agents
AB - S18327 was dose-dependently active in several models of potential antipsychotic activity involving dopaminergic hyperactivity: inhibition of apomorphine-induced climbing in mice, of cocaine- and amphetamine- induced hyperlocomotion in rats, and of conditioned avoidance responses in rats. Furthermore, reflecting its high affinity at serotonin(2A) sites, S18327 potently blocked phencyclidine-induced locomotion and 1- [2, 5-dimethoxy-4-iodophenyl]-2-aminopropane-induced head-twitches in rats. In models of glutamatergic hypoactivity, S18327 blocked hyperlocomotion and spontaneous tail-flicks elicited by the N-methyl-D- aspartate antagonist dizocilpine. The actions of S18327, together with its binding profile at multiple monoaminergic receptors (15 parameters in total), were compared with those of clozapine, haloperidol, and 11 other antipsychotics by multiparametric analysis, and the resulting dendrogram positioned S18327 close to clozapine. Consistent with a clopazine-like profile, S18327 generalized to a clozapine discriminative stimulus and evoked latent inhibition in rats, blocked aggression in isolated mice, and displayed anxiolytic properties in the ultrasonic vocalization and Vogel procedures in rats. Relative to the above paradigms, only markedly (>20-fold) higher doses of S18327 were active in models predictive of potential extrapyramidal side effects: induction of catalepsy and prolactin secretion, and inhibition of methylphenidate-induced gnawing in rats. S18327 showed only modest affinity for histaminic and muscarinic receptors. Multiparametric analysis of these data distinguished S18327 from both haloperidol (high extrapyramidal potential) and clozapine (high histaminic and muscarinic affinity). In conclusion, S18327 displays a broad-based pattern of potential antipsychotic activity at doses appreciably lower than those eliciting extrapyramidal side effects. In this respect, S18327 closely resembles clozapine, but it is chemically distinct and displays weak affinity for histaminic and muscarinic receptors
MH - Adrenergic Antagonists
MH - Aggression
MH - Amphetamine
MH - Animal
MH - antagonists & inhibitors
MH - Antipsychotic Agents
MH - Apomorphine
MH - Avoidance Learning
MH - Clozapine
MH - Cocaine
MH - Comparative Study
MH - Dopamine
MH - Dopamine Antagonists
MH - Dose-Response Relationship,Drug
MH - drug effects
MH - Drug Interactions
MH - Extrapyramidal Tracts
MH - Haloperidol
MH - Imidazoles
MH - Isoxazoles
MH - Male
MH - Mice
MH - Pain Measurement
MH - pharmacology
MH - Prolactin
MH - Protein Binding
MH - Rats
MH - Rats,Wistar
MH - Receptors,Adrenergic,alpha-1
MH - Receptors,Adrenergic,alpha-2
MH - Receptors,Histamine
MH - Receptors,Muscarinic
RP - NOT IN FILE
NT - UI - 20072794LA - EngRN - 0 (Adrenergic Antagonists)RN - 0 (Antipsychotic Agents)RN - 0 (Dopamine Antagonists)RN - 0 (Imidazoles)RN - 0 (Isoxazoles)RN - 0 (Receptors, Adrenergic, alpha-1)RN - 0 (Receptors, Adrenergic, alpha-2)RN - 0 (Receptors, Histamine)RN - 0 (Receptors, Muscarinic)RN - 0 (S 18327)RN - 300-62-9 (Amphetamine)RN - 50-36-2 (Cocaine)RN - 52-86-8 (Haloperidol)RN - 5786-21-0 (Clozapine)RN - 58-00-4 (Apomorphine)PT - JOURNAL ARTICLEDA - 20000127IS - 0022-3565SB - MCY - UNITED STATESJC - JP3AA - AuthorEM - 200003
UR - PM:0010604931
SO - J Pharmacol Exp Ther 2000 Jan ;292(1):54-66

3
UI - 1
AU - Rasmussen T
AU - Sauerberg P
AU - Nielsen EB
AU - Swedberg MD
AU - Thomsen C
AU - Sheardown MJ
AU - Jeppesen L
AU - Calligaro DO
AU - DeLapp NW
AU - Whitesitt C
AU - Ward JS
AU - Shannon HE
AU - Bymaster FP
AU - Fink-Jensen A
AD - Health Care Discovery, Novo Nordisk A/S, Novo Nordisk Park, DK-2760, Malov, Denmark
TI - Muscarinic receptor agonists decrease cocaine self-administration rates in drug-naive mice [In Process Citation]
AB - (5R,6R)-6-(3-Propylthio-1,2,5-thiadiazol-4-yl)-1-azabicyclo[3.2. 1]octane (PTAC) is a selective muscarinic receptor ligand. The compound exhibits high affinity for central muscarinic receptors with partial agonist mode of action at muscarinic M(2) and M(4) and antagonist mode of action at muscarinic M(1), M(3) and M(5) receptor subtypes. The compound was earlier reported to exhibit functional dopamine receptor antagonism in rodents despite its lack of affinity for dopamine receptors. In the present study, we report that PTAC, as well as the muscarinic receptor agonists pilocarpine and oxotremorine, dose- dependently decreased rates of intravenous self-administration (fixed ratio 1) of the indirect dopamine receptor agonist cocaine in drug naive mice. Similar decreases in cocaine self-administration rates were obtained with the dopamine receptor antagonists olanzapine, clozapine, risperidone, fluphenazine and haloperidol. These findings suggest that compounds with partial muscarinic receptor agonist mode of action may be used in the medical treatment of cocaine abuse
MH - Clozapine
MH - Cocaine
MH - Dopamine
MH - Haloperidol
MH - Mice
MH - Self Administration
RP - NOT IN FILE
NT - UI - 20416190LA - EngDA - 20001014IS - 0014-2999SB - MCY - NETHERLANDSJC - EN6AA - AUTHORRO - O:099
UR - PM:0010958890
SO - Eur J Pharmacol 2000 Aug 25 ;402(3):241-246

4
UI - 3
AU - Zimmet SV
AU - Strous RD
AU - Burgess ES
AU - Kohnstamm S
AU - Green AI
AD - Commonwealth Research Center, Department of Psychiatry, Harvard Medical School, Boston, Massachusetts, USA
TI - Effects of clozapine on substance use in patients with schizophrenia and schizoaffective disorder: a retrospective survey
AB - Substance use disorders, particularly those involving alcohol, marijuana, and cocaine, are highly prevalent among patients with schizophrenia and contribute markedly to its overall morbidity. Unfortunately, standard (typical) antipsychotic medications do not seem to reduce substance use in patients with schizophrenia and may even increase it. Recently, however, a few anecdotal case reports and two previous small "N" surveys have found that clozapine, an atypical antipsychotic medication, seems to decrease substance use in patients treated with this drug for their psychoses. The authors report data from a retrospective survey of substance use in 58 patients treated with clozapine who had a history of comorbid schizophrenia (or schizoaffective disorder) and substance use disorder. Of these 58 patients, 43 were being treated with clozapine at the time of the survey; the remaining 15 patients had discontinued clozapine before the survey. The survey involved chart review and clinician interview to assess change in substance use and global clinical symptoms while receiving treatment with clozapine. More than 85% of the patients who were active substance users at the time of initiation of treatment with clozapine decreased their substance use over the course of clozapine administration. For patients who continued treatment with clozapine up to the present, the decrease in substance use was strongly correlated with a decrease in global clinical symptoms. Data from this retrospective survey further support the previous observations that clozapine reduces substance use among patients with schizophrenic disorders. Moreover, the data suggest the need for prospective controlled studies of the effects of clozapine on substance use in this population
MH - Adult
MH - Antipsychotic Agents
MH - blood
MH - Case Report
MH - Clozapine
MH - Cocaine
MH - Diagnosis,Dual (Psychiatry)
MH - drug therapy
MH - Female
MH - Human
MH - Male
MH - Medical Records
MH - Middle Age
MH - Pilot Projects
MH - Psychotic Disorders
MH - Retrospective Studies
MH - Schizophrenia
MH - Substance-Related Disorders
MH - Support,Non-U.S.Gov't
MH - Support,U.S.Gov't,P.H.S.
MH - therapeutic use
RP - NOT IN FILE
NT - UI - 20116916LA - EngRN - 0 (Antipsychotic Agents)RN - 5786-21-0 (Clozapine)PT - JOURNAL ARTICLEID - R01 MH99891/MH/NIMHID - RO1 MH52376/MH/NIMHDA - 20000315IS - 0271-0749SB - MCY - UNITED STATESJC - HUDAA - AuthorEM - 200005
UR - PM:0010653215
SO - J Clin Psychopharmacol 2000 Feb ;20(1):94-98

5
UI - 6
AU - O'Neill MF
AU - Shaw G
AD - Lilly Research Centre, Windlesham, Surrey, UK. oneill_michael_f@lilly.com
TI - Comparison of dopamine receptor antagonists on hyperlocomotion induced by cocaine, amphetamine, MK-801 and the dopamine D1 agonist C-APB in mice
AB - RATIONALE: Direct or indirect stimulation of dopamine receptors increases locomotor activity in mice. Determining the role played by D1 and D2 dopamine receptors in the mediation of this activity can be difficult due to the wide variety of experimental paradigms used to investigate these phenomena. OBJECTIVES: This study set out to compare the role of selective antagonism of dopamine D1 and D2 receptors on the hyperactivity induced by a range of stimulants. METHODS: Mice were habituated to perspex locomotor activity boxes (30 x 30 x 30 cm) and activity was measured via photobeam interrupts. RESULTS: Haloperidol and clozapine both reduced the hyperactivity induced by MK-801. Haloperidol did so only at a dose that also decreased spontaneous activity (0.1 mg/kg), whereas clozapine reduced MK-801-induced hyperactivity at a dose that had no effect on spontaneous activity (1.25 mg/kg). The D1 antagonist SCH23390 (0.01 mg/kg) reduced hyperlocomotion induced by amphetamine (2.5 mg/kg), cocaine (10 mg/kg) and C-APB (1.0 mg/kg) at doses that did not consistently alter spontaneous activity, whereas the selective D2 antagonist raclopride only attenuated the hyperlocomotion induced by amphetamine, cocaine and C-APB at doses in excess of the minimum dose required to attenuate spontaneous locomotor activity significantly. The latency to peak levels of hyperlocomotion induced by MK-801 (0.3 mg/kg) was delayed by SCH23390 (0.1 mg/kg) but peak levels of activity were not reduced. CONCLUSIONS: The results of the present study suggest that selective blockade of D1 receptors suppresses amphetamine and cocaine-induced hyperactivity in mice but not MK-801-induced locomotor activity
MH - Amphetamine
MH - Analysis of Variance
MH - Animal
MH - Benzazepines
MH - Clozapine
MH - Cocaine
MH - Comparative Study
MH - Dizocilpine Maleate
MH - Dopamine
MH - Dopamine Agonists
MH - Dopamine Antagonists
MH - Dopamine Uptake Inhibitors
MH - drug effects
MH - Drug Interactions
MH - Excitatory Amino Acid Antagonists
MH - Female
MH - Haloperidol
MH - Locomotion
MH - metabolism
MH - Mice
MH - pharmacology
MH - Receptors,Dopamine D1
RP - NOT IN FILE
NT - UI - 99424359LA - EngRN - 0 (Benzazepines)RN - 0 (Dopamine Agonists)RN - 0 (Dopamine Antagonists)RN - 0 (Dopamine Uptake Inhibitors)RN - 0 (Excitatory Amino Acid Antagonists)RN - 0 (Receptors, Dopamine D1)RN - 300-62-9 (Amphetamine)RN - 50-36-2 (Cocaine)RN - 77086-22-7 (Dizocilpine Maleate)RN - 80751-65-1 (SK&F 82958)PT - JOURNAL ARTICLEDA - 19991018IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199912
UR - PM:0010494572
SO - Psychopharmacology (Berl) 1999 Aug ;145(3):237-250

6
UI - 7
AU - Poncelet M
AU - Barnouin MC
AU - Breliere JC
AU - Le Fur G
AU - Soubrie P
AD - Sanofi Recherche, Montpellier, France. martine.poncelet@sanofi.com
TI - Blockade of cannabinoid (CB1) receptors by 141716 selectively antagonizes drug-induced reinstatement of exploratory behaviour in gerbils
AB - RATIONALE: A cannabinoid hypothesis of schizophrenia has been proposed according to which cognitive dysfunction could be associated with dysregulation of an endogenous cannabinoid system. OBJECTIVE: The present study investigated whether SR 141716, a selective CB1 receptor antagonist, was able to reduce the hyperactivity induced in gerbils by various stimulant drugs known to produce or exacerbate schizophrenic symptoms. METHODS: Cocaine, d-amphetamine, morphine, and Win 55212-2 were administered intraperitoneally (IP) either immediately before placing the animals in the test apparatus (non-habituated gerbils) or after a 2- to 3-h habituation period in the actimeter (habituated gerbils). SR 141716 was given IP 30 min before the injection of stimulant drugs. Horizontal activity was recorded every 10 min for 1 h in Digiscan activity monitor. RESULTS: SR 141716 (0.3-3 mg/kg) dose- dependently suppressed the enhanced locomotor activity induced by each stimulant drug in habituated gerbils, but not in non-habituated animals. Clozapine, an atypical antipsychotic compound, but not haloperidol, shared with SR 141716, the ability to differentially affect drug-induced hyperactivity in habituated versus non-habituated gerbils. CONCLUSION: The activation of cannabinoid systems is a required, permissive element in the ability of cocaine, d-amphetamine, morphine, and Win 55212-2 to reinstate behaviour, i.e., to override stimulus satiation
MH - Animal
MH - antagonists & inhibitors
MH - Antipsychotic Agents
MH - Cannabinoids
MH - Central Nervous System Stimulants
MH - Clozapine
MH - Cocaine
MH - drug effects
MH - Exploratory Behavior
MH - Gerbillinae
MH - Haloperidol
MH - Male
MH - Morphine
MH - Motor Activity
MH - Narcotics
MH - pharmacology
MH - Piperidines
MH - Pyrazoles
MH - Receptors,Drug
MH - Schizophrenia
RP - NOT IN FILE
NT - UI - 99320918LA - EngRN - 0 (cannabinoid receptor)RN - 0 (Antipsychotic Agents)RN - 0 (Cannabinoids)RN - 0 (Central Nervous System Stimulants)RN - 0 (Narcotics)RN - 0 (Piperidines)RN - 0 (Pyrazoles)RN - 0 (Receptors, Drug)RN - 158681-13-1 (SR 141716A)PT - JOURNAL ARTICLEDA - 19990817IS - 0033-3158SB - MCY - GERMANYJC - QGIAA - AuthorEM - 199910
UR - PM:0010394995
SO - Psychopharmacology (Berl) 1999 May ;144(2):144-150

7
UI - 8
AU - Ufer M
AU - Dadmarz M
AU - Vogel WH
AD - Department of Biochemistry and Molecular Pharmacology, Jefferson Medical College, Thomas Jefferson University, Philadelphia PA, USA
TI - Voluntary consumption of amphetamine, cocaine, ethanol and morphine by rats as influenced by a preceding period of forced drug intake and clozapine
AB - Forced nicotine intake was previously found to decrease a subsequent free choice selection, whereas clozapine (CL) caused a marked increase in its consumption. Here these findings are extended to ethanol, cocaine, morphine and amphetamine. Forced intake of ethanol, cocaine, morphine and amphetamine had no major effect on a subsequent voluntary intake. CL, a dopamine D4 antagonist, increased the voluntary consumption of amphetamine and morphine with no effects on ethanol or cocaine intake. Only for cocaine was it found that low-consuming rats increased but high-consuming rats decreased their voluntary cocaine intake by CL. Thus, forced drug exposure per se does not lead to subsequent enhancement of voluntary intake; CL exerts differential effects on intake of these drugs, and a specific dopaminergic set point may govern the voluntary intake of cocaine by individual rats
MH - administration & dosage
MH - Administration,Oral
MH - Amphetamine
MH - Animal
MH - Central Nervous System Depressants
MH - Clozapine
MH - Cocaine
MH - Comparative Study
MH - Dopamine
MH - Dopamine Agents
MH - Ethanol
MH - etiology
MH - Male
MH - Morphine
MH - Narcotics
MH - pharmacology
MH - Rats
MH - Rats,Sprague-Dawley
MH - Self Administration
MH - Substance-Related Disorders
RP - NOT IN FILE
NT - UI - 99263074LA - EngRN - 0 (Central Nervous System Depressants)RN - 0 (Dopamine Agents)RN - 0 (Narcotics)RN - 300-62-9 (Amphetamine)RN - 50-36-2 (Cocaine)RN - 57-27-2 (Morphine)RN - 5786-21-0 (Clozapine)RN - 64-17-5 (Ethanol)PT - JOURNAL ARTICLEDA - 19990622IS - 0031-7012SB - MCY - SWITZERLANDJC - P43AA - AuthorEM - 199908
UR - PM:0010325573
SO - Pharmacology 1999 Jun ;58(6):285-291

8
UI - 5
AU - van Campenhout N
AU - De Haes P
AU - Meert TF
AD - Janssen Research Foundation, Beerse, Belgium
TI - Inability of antipsychotics to antagonize the cueing properties of cocaine in rats
AB - In this study the possible antagonistic effects of five different antipsychotics on the discriminative stimulus properties of 10 mg/kg cocaine were evaluated by use of a two-lever food-reinforced drug discrimination procedure in rats. To do so, rats were treated with several doses of haloperidol, risperidone, seroquel, sertindole, and olanzapine, either at 60 or 120 min prior to testing. With all compounds tested, no substantial antagonism of the cocaine cue was observed. Only with haloperidol (maximum 60%), risperidone (maximal 20%), and olanzapine (maximal 20%) a partial antagonism without clearcut dose-response was observed. Clozapine, seroquel, and sertindole did not influence the discriminative stimulus properties of cocaine. These results indicate that antipsychotics with different pharmacological profiles are unable to antagonize more than partially the cueing properties of 10 mg/kg cocaine in rats, pointing to the unique underlying stimulus properties of this stimulant
MH - Animal
MH - antagonists & inhibitors
MH - Antipsychotic Agents
MH - Antipsychotic Agents,Butyrophenone
MH - Clozapine
MH - Cocaine
MH - Cues
MH - Discrimination (Psychology)
MH - Dopamine
MH - Dopamine Uptake Inhibitors
MH - drug effects
MH - Generalization,Stimulus
MH - Haloperidol
MH - Male
MH - pharmacology
MH - Rats
MH - Rats,Inbred Strains
RP - NOT IN FILE
NT - UI - 99443349LA - EngRN - 0 (Antipsychotic Agents)RN - 0 (Antipsychotic Agents, Butyrophenone)RN - 0 (Dopamine Uptake Inhibitors)RN - 50-36-2 (Cocaine)RN - 52-86-8 (Haloperidol)PT - JOURNAL ARTICLEDA - 19991220IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 200002
UR - PM:0010515326
SO - Pharmacol Biochem Behav 1999 Oct ;64(2):435-438

9
UI - 12
AU - Buckley PF
AD - Department of Psychiatry, Case Western Reserve University, and the Northcoast Behavioral Healthcare System, Cleveland, Ohio 44106, USA
TI - Substance abuse in schizophrenia: a review
AB - Approximately half of the patients who suffer from schizophrenia are also substance abusers at some time during their illness. The motivational drive toward abusive consumption is compounded in individuals with schizophrenia who turn toward substances with reinforcing properties to alleviate aspects of psychosis. This review examines the prevalence, etiology, and clinical effects of substance abuse (e.g., alcohol, nicotine, cocaine) among individuals with schizophrenia. Clearly, substance abuse persists despite and in spite of treatment with typical antipsychotics. The efficacy of newer generation antipsychotics in the reduction of substance abuse among the schizophrenic population has yet to be established, but clozapine has been shown to reduce alcohol, smoking, and cocaine use. Hence, clozapine is a therapeutic option for dually diagnosed patients because of its superior efficacy relative to conventional neuroleptics and its capacity to control substance abuse
MH - Antipsychotic Agents
MH - Clozapine
MH - Cocaine
MH - Comorbidity
MH - Cost-Benefit Analysis
MH - diagnosis
MH - Diagnosis,Dual (Psychiatry)
MH - Drug Monitoring
MH - drug therapy
MH - epidemiology
MH - Human
MH - pharmacology
MH - Precipitating Factors
MH - Prevalence
MH - Schizophrenia
MH - Substance-Related Disorders
MH - Support,Non-U.S.Gov't
MH - therapeutic use
RP - NOT IN FILE
NT - UI - 98200406LA - EngRN - 0 (Antipsychotic Agents)RN - 5786-21-0 (Clozapine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19980410IS - 0160-6689SB - MCY - UNITED STATESJC - HICAA - AuthorEM - 199806
UR - PM:0009541335
SO - J Clin Psychiatry 1998 ;59 Suppl 3():26-30

10
UI - 38
AU - Green AI
AU - Zimmet SV
AU - Strous RD
AU - Schildkraut JJ
TI - Clozapine for comorbid substance use disorder and schizophrenia: do patients with schizophrenia have a reward-deficiency syndrome that can beameliorated by clozapine?
AB - Alcohol and other drugs of abuse are commonly used by persons withschizophrenia and contribute to the overall morbidity of the disorder.Standard, or typical, antipsychotic drugs do not limit such substance useand may even render it more likely. However, preliminary data from ourgroup and others suggest that the atypical antipsychotic clozapine may decreasesubstance use in this population. While recognizing the likelihood thatsubstance use decreases negative symptoms (as well as extrapyramidalsymptoms) in persons with schizophrenia, we hypothesize that thebiological basis of substance use relates to a "reward-deficiency syndrome" secondaryto dysfunctional dopamine-mediated mesocorticolimbic neurons in theseindividuals. We further suggest that clozapine's beneficial effect inpatients with comorbid schizophrenia and substance use disorders mayrelate to its presumed ability to ameliorate the deficits in both themesocortical and mesolimbic dopaminergic neuronal projections through its variousactions on dopaminergic, serotonergic, and particularly noradrenergic neurons.
MH - Clozapine
MH - Schizophrenia
RP - NOT IN FILE
SO - J Clin Psychiatry 1998 ;59():26-30

11
UI - 10
AU - Millan MJ
AU - Schreiber R
AU - Dekeyne A
AU - Rivet JM
AU - Bervoets K
AU - Mavridis M
AU - Sebban C
AU - Maurel-Remy S
AU - Newman-Tancredi A
AU - Spedding M
AU - Muller O
AU - Lavielle G
AU - Brocco M
AD - Institut de Recherches Servier, Centre de Recherches de Croissy, Psychopharmacology Department, 125, Chemin de Ronde, 78290-Croissy-sur- Seine, Paris, France
TI - S 16924 ((R)-2-[1-[2-(2,3-dihydro-benzo[1,4] dioxin-5-yloxy)-ethyl]- pyrrolidin-3yl]-1-(4-fluoro-phenyl)-ethanone), a novel, potential antipsychotic with marked serotonin (5-HT)1A agonist properties: II. Functional profile in comparison to clozapine and haloperidol
AB - S 16924 antagonized locomotion provoked by dizocilpine and cocaine, reduced conditioned avoidance responses and blocked climbing elicited by apomorphine, models predictive of control of the positive symptoms of schizophrenia: its median inhibitory dose (ID)50 was 0.96 mg/kg, s.c. vs. 1.91 for clozapine and 0.05 for haloperidol. Rotation elicited in unilateral, substantia nigra-lesioned rats by the D1 agonist, SKF 38393, and by the D2 agonist, quinpirole, was blocked equipotently by S 16924 (0.8 and 1. 7) and clozapine (0.6 and 2.0), whereas haloperidol preferentially blocked quinpirole (0.02) vs. SKF 38393 (1.8). S 16924 more potently inhibited the head-twitches elicited by 1-(2, 5-dimethoxy- 4-iodophenyl)-2-aminopropane (DOI) and the locomotion provoked by phencyclidine than it inhibited the locomotion elicited by amphetamine (ID50s = 0.15 and 0.02 vs. 2.4). Clozapine showed a similar preference (0.04 and 0.07 vs. 8.6), but not haloperidol (0. 07 and 0.08 vs. 0.04). The discriminative stimulus (DS) properties of DOI were also blocked by S 16924 (ID50 = 0.17) and clozapine (0. 05) but not by haloperidol (>0.16). S 16924 fully (100%) generalized [effective dose (ED)50 = 0.7] to a clozapine DS and clozapine (0.23) fully generalized to a S 16924 DS whereas haloperidol (>/=0.08) only partially generalized (</=50%) to their DS in each case. Power spectra analysis of electroencephalograms from frontal cortex showed that both S 16924 (2.0) and clozapine (5.0) reinforced frequencies in the 7 to 8 Hz range whereas haloperidol (0.5) preferentially reinforced frequencies in the 10 to 14 Hz range. In a model of perturbation of cognitive-attentional function, significant latent inhibition was obtained with S 16924 (0.08) and clozapine (0.16), but not haloperidol (0.0063 and 0.04): higher doses of S 16924 (2.5), clozapine (5.0) and haloperidol (0.1) all blocked disruption of latent inhibition by amphetamine (1.5). Catalepsy was provoked by haloperidol (0.04-0.63) but not by S 16924 (>/=80.0) or clozapine (>/=80.0). Further, S 16924 (ID50 = 3.2) and clozapine (5.5) inhibited induction of catalepsy by haloperidol. This action of S 16924 was abolished by the 5-HT1A receptor antagonist, WAY 100,635 (0.16), which less markedly attenuated the anticataleptic action of clozapine. Further, although gnawing elicited by methylphenidate was inhibited by S 16924 (ID50 = 8.4), clozapine (19.6) and haloperidol (0.04), only the action of S 16924 was blocked by WAY 100,635 (0.16). Haloperidol potently (0.01-0.16, approximately 24-fold) increased prolactin levels whereas they were less markedly affected by S 16924 (2.5-40.0, 4-fold) and clozapine (10.0-40.0, 3-fold). Clozapine displayed high affinity at cloned, human, muscarinic (M1) and native, histamine (H1) receptors (Kis = 4.6 and 5.4 nM, respectively), whereas S 16924 (>1000 and 158) and haloperidol (>1000 and 453) displayed low affinity. In conclusion, S 16924 displays a profile of activity in diverse models of potential antipsychotic and extrapyramidal properties similar to that of clozapine and different to that of haloperidol. In particular, reflecting its partial agonist actions at 5-HT1A receptors, S 16924 inhibits rather than induces catalepsy in rats. However, in contrast to clozapine, S 16924 displays only low affinity for muscarinic and histaminic receptors
MH - Amphetamine
MH - Amphetamines
MH - Animal
MH - Antipsychotic Agents
MH - Apomorphine
MH - Attention
MH - blood
MH - Clozapine
MH - Cocaine
MH - Cognition
MH - Comparative Study
MH - Discrimination Learning
MH - drug effects
MH - Electroencephalography
MH - Haloperidol
MH - Human
MH - Male
MH - metabolism
MH - Mice
MH - Mice,Inbred ICR
MH - Motor Activity
MH - pharmacology
MH - Prolactin
MH - Pyrrolidines
MH - Rats
MH - Rats,Wistar
MH - Receptors,Serotonin
MH - Schizophrenia
MH - Serotonin
MH - Serotonin Agonists
RP - NOT IN FILE
NT - UI - 98404190LA - EngRN - 0 (Amphetamines)RN - 0 (Antipsychotic Agents)RN - 0 (Pyrrolidines)RN - 0 (Receptors, Serotonin)RN - 0 (S 16924)RN - 0 (Serotonin Agonists)RN - 112692-38-3 (serotonin 1A receptor)RN - 52-86-8 (Haloperidol)RN - 5786-21-0 (Clozapine)RN - 64584-34-5 (4-iodo-2,5-dimethoxyphenylisopropylamine)RN - 9002-62-4 (Prolactin)PT - JOURNAL ARTICLEDA - 19981008IS - 0022-3565SB - MCY - UNITED STATESJC - JP3AA - AuthorEM - 199812
UR - PM:0009732399
SO - J Pharmacol Exp Ther 1998 Sep ;286(3):1356-1373

12
UI - 11
AU - Wennig R
AU - Moeller MR
AU - Haguenoer JM
AU - Marocchi A
AU - Zoppi F
AU - Smith BL
AU - de la TR
AU - Carstensen CA
AU - Goerlach-Graw A
AU - Schaeffler J
AU - Leinberger R
AD - Laboratoire National de Sante, Centre Universitaire, Luxembourg
TI - Development and evaluation of immunochromatographic rapid tests for screening of cannabinoids, cocaine, and opiates in urine
AB - The test principle and the optimization of the reactive ingredients are described for the one-step dip and-read immunochromatographic FRONTLINE rapid tests for drugs-of-abuse testing in urine samples. In a multicenter evaluation the rapid tests were compared with FPIA and EMIT immunoassays. Discrepant results were further analyzed by gas chromatography-mass spectrometry methods. In the comparison of the cannabinoids rapid tests versus both immunoassays using clinical and forensic urine samples (399 versus FPIA and 755 versus EMIT), sensitivities and specificities were 97% or better for both comparisons. For cocaine, a sensitivity of 100% versus both routine technologies was obtained, whereas the specificity was reduced somewhat to 91% because of some cross-reactivity with metabolites of methadone and of clozapine. Specificity was very high for the cocaine rapid tests (98-100%) when applied to urine samples of persons not in a methadone maintenance program. Sensitivities and specificities for the opiates rapid tests were 99% or better at all sites when compared with the routine methods. In the screening of about 1200 clinical urine samples for cannabinoids, cocaine or opiates misuse only six samples would have stayed undetected by rapid test analyzes. These results show the FRONTLINE assays allow a reliable and immediate screening for drugs of abuse
MH - Cannabinoids
MH - Chromatography
MH - Clozapine
MH - Cocaine
MH - Comparative Study
MH - Cross Reactions
MH - Evaluation Studies
MH - Fluorescence Polarization Immunoassay
MH - Human
MH - Immunoenzyme Techniques
MH - Mass Fragmentography
MH - methods
MH - Narcotics
MH - Reagent Kits,Diagnostic
MH - Reproducibility of Results
MH - Sensitivity and Specificity
MH - Substance Abuse Detection
MH - Support,Non-U.S.Gov't
MH - urine
RP - NOT IN FILE
NT - UI - 98208628LA - EngRN - 0 (Cannabinoids)RN - 0 (Narcotics)RN - 0 (Reagent Kits, Diagnostic)RN - 50-36-2 (Cocaine)PT - JOURNAL ARTICLEPT - MULTICENTER STUDYDA - 19980515IS - 0146-4760SB - MCY - UNITED STATESJC - K4RAA - AuthorEM - 199807
UR - PM:0009547412
SO - J Anal Toxicol 1998 Mar ;22(2):148-155

13
UI - 9
AU - Wyatt RJ
AU - Karoum F
AU - Masserano J
AD - Neuropsychiatry Branch, Intramural Research Program, National Institute of Mental Health, Washington, DC 20032, USA. wyattr@dirpc.nimh.nih.gov
TI - Effects of antipsychotics, vitamin E, and MK-801 on dopamine dynamics in the rat brain following discontinuation of cocaine
AB - Cocaine, 10 mg/kg, I.P., twice daily, was given to rats for 1 week. At 1 and 4 weeks following discontinuation of cocaine, the initial rate of 3,4-dihydroxyphenylacetic acid (DOPAC) formation was assessed. The initial rate of DOPAC formation was found to be decreased in the frontal and cingulate cortices at 1 week, but was only decreased in the frontal cortex at 4 weeks. When administered in conjunction with cocaine, haloperidol, clozapine, and vitamin E, but not MK-801, were found to prevent cocaine's effects. In addition to the potential value these findings have for further understanding cocaine abuse, it is proposed that the alteration in dopamine metabolism produced by cocaine, and the ability of haloperidol, clozapine and vitamin E to decrease cocaine's effects, model some biochemical aspects of schizophrenia
MH - 3,4-Dihydroxyphenylacetic Acid
MH - Aged
MH - Animal
MH - Antipsychotic Agents
MH - Brain
MH - Clozapine
MH - Cocaine
MH - Cocaine-Related Disorders
MH - Dizocilpine Maleate
MH - Dopamine
MH - drug effects
MH - Haloperidol
MH - Human
MH - Male
MH - metabolism
MH - Neuroprotective Agents
MH - pharmacology
MH - Rats
MH - Rats,Sprague-Dawley
MH - Schizophrenia
MH - Time Factors
MH - Vitamin E
RP - NOT IN FILE
NT - UI - 99010961LA - EngRN - 0 (Antipsychotic Agents)RN - 0 (Neuroprotective Agents)RN - 1406-18-4 (Vitamin E)RN - 50-36-2 (Cocaine)RN - 51-61-6 (Dopamine)RN - 77086-22-7 (Dizocilpine Maleate)PT - JOURNAL ARTICLEDA - 19990225IS - 0165-1781SB - MCY - IRELANDJC - QC4AA - AuthorEM - 199904
UR - PM:0009796937
SO - Psychiatry Res 1998 Sep 21 ;80(3):213-225

14
UI - 15
AU - Rubinstein M
AU - Phillips TJ
AU - Bunzow JR
AU - Falzone TL
AU - Dziewczapolski G
AU - Zhang G
AU - Fang Y
AU - Larson JL
AU - McDougall JA
AU - Chester JA
AU - Saez C
AU - Pugsley TA
AU - Gershanik O
AU - Low MJ
AU - Grandy DK
AD - Instituto de Investigaciones en Ingenieria Genetica y Biologia Molecular, CONICET, and Depto. Quimica Biologica, FCEyN, Universidad de Buenos Aires, Argentina
TI - Mice lacking dopamine D4 receptors are supersensitive to ethanol, cocaine, and methamphetamine
AB - The human dopamine D4 receptor (D4R) has received considerable attention because of its high affinity for the atypical antipsychotic clozapine and the unusually polymorphic nature of its gene. To clarify the in vivo role of the D4R, we produced and analyzed mutant mice (D4R- /-) lacking this protein. Although less active in open field tests, D4R- /- mice outperformed wild-type mice on the rotarod and displayed locomotor supersensitivity to ethanol, cocaine, and methamphetamine. Biochemical analyses revealed that dopamine synthesis and its conversion to DOPAC were elevated in the dorsal striatum from D4R-/- mice. Based on these findings, we propose that the D4R modulates normal, coordinated and drug-stimulated motor behaviors as well as the activity of nigrostriatal dopamine neurons
MH - 3,4-Dihydroxyphenylacetic Acid
MH - Amino Acid Sequence
MH - analysis
MH - anatomy & histology
MH - Animal
MH - Antipsychotic Agents
MH - Attention
MH - Behavior,Animal
MH - Central Nervous System Depressants
MH - chemistry
MH - Clozapine
MH - Cocaine
MH - Corpus Striatum
MH - deficiency
MH - Dopamine
MH - Dopamine Agents
MH - drug effects
MH - Ethanol
MH - genetics
MH - Genotype
MH - Human
MH - Levodopa
MH - Locomotion
MH - Maternal Behavior
MH - metabolism
MH - Methamphetamine
MH - Mice
MH - Mice,Knockout
MH - Molecular Sequence Data
MH - Motor Activity
MH - Mutagenesis,Site-Directed
MH - Narcotics
MH - Nucleus Accumbens
MH - pharmacokinetics
MH - pharmacology
MH - physiology
MH - Receptors,Dopamine D2
MH - Sensitivity and Specificity
MH - Substantia Nigra
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 - Transcription,Genetic
RP - NOT IN FILE
NT - UI - 97462900LA - EngRN - 0 (Antipsychotic Agents)RN - 0 (Central Nervous System Depressants)RN - 0 (Dopamine Agents)RN - 0 (Levodopa)RN - 0 (Narcotics)RN - 0 (Receptors, Dopamine D2)RN - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)RN - 137750-34-6 (dopamine D4 receptor)RN - 50-36-2 (Cocaine)RN - 51-61-6 (Dopamine)RN - 537-46-2 (Methamphetamine)RN - 5786-21-0 (Clozapine)RN - 64-17-5 (Ethanol)PT - JOURNAL ARTICLEDA - 19971020IS - 0092-8674SB - MSB - XCY - UNITED STATESJC - CQ4AA - AuthorEM - 199712
UR - PM:0009323127
SO - Cell 1997 Sep 19 ;90(6):991-1001

15
UI - 14
AU - Skuza G
AU - Rogoz Z
AU - Wieczorek A
AD - Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland
TI - Neuropsychopharmacological profile of remoxipride in comparison with clozapine
AB - Central effects of remoxipride /(-)-(S)-3-bromo-N-[(1-ethyl-2- pyrrolidinyl)methyl]-2-6-dimethoxybenz amide hydrochloride, RPD/, one of newer antipsychotic drugs with high affinity to sigma sites was studied in comparison with clozapine (CLOZ), another atypical antipsychotic agent, devoid of such an activity. It has been found that RPD decreased the locomotor activity of naive rats, as well as hyperactivity induced by D-amphetamine and apomorphine. The drug antagonized stereotypy induced by both dopamine agonists as well as apomorphine-induced climbing in mice. RPD shortened the time of SKF 38393 (dopamine D1 receptor agonist)-induced grooming in rats. Moreover, it markedly decreased quinpirole (dopamine D2/3 receptor agonist)-induced hyperactivity of rats, and less potently inhibited stimulatory activity induced by cocaine and MK-801 (non-competitive NMDA receptor antagonist). The drug impaired retention of conditioned avoidance responses and induced catalepsy in rats, at relatively high doses though. The effects of CLOZ differed to some extent from those of RPD. The former did not antagonize the apomorphine-induced stereotypy and decreased that caused by D-amphetamine less potently than RPD did. Besides, it did not induce catalepsy, even at relatively high doses while its inhibitory activity towards apomorphine- and quinpirole- induced hyperactivity, as well as locomotor activity of naive rats were much less potent. The effects of RPD and CLOZ in other experimental models were comparable. The obtained results indicating many similarities between psychopharmacological profiles of RPD and CLOZ with some essential differences as well as an equivalence of RPD central effects and the activity of EMD 57445 (selective sigma ligand devoid of any effects at other receptors) permit a supposition that, beside dopamine receptors, the sigma receptors may also be of importance to the mechanism of action of RPD
MH - Animal
MH - Antipsychotic Agents
MH - Apomorphine
MH - Avoidance Learning
MH - Catalepsy
MH - chemically induced
MH - Clozapine
MH - Cocaine
MH - Comparative Study
MH - Dopamine
MH - Dopamine Agonists
MH - Dopamine Uptake Inhibitors
MH - drug effects
MH - Drug Interactions
MH - Excitatory Amino Acid Antagonists
MH - Grooming
MH - Mice
MH - Motor Activity
MH - pharmacology
MH - psychology
MH - Rats
MH - Rats,Wistar
MH - Remoxipride
MH - Stereotyped Behavior
MH - Support,Non-U.S.Gov't
RP - NOT IN FILE
NT - UI - 98093611LA - EngRN - 0 (Antipsychotic Agents)RN - 0 (Dopamine Agonists)RN - 0 (Dopamine Uptake Inhibitors)RN - 0 (Excitatory Amino Acid Antagonists)RN - 5786-21-0 (Clozapine)RN - 80125-14-0 (Remoxipride)PT - JOURNAL ARTICLEDA - 19980218IS - 1230-6002SB - MCY - POLANDJC - BT7AA - AuthorEM - 199804
UR - PM:0009431546
SO - Pol J Pharmacol 1997 Jan ;49(1):5-15

16
UI - 13
AU - Squires RF
AU - Saederup E
AD - Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York 10962, USA
TI - [New GABA-A receptor blockers: attempts to find more powerful clozapine- like selective GABA antagonists]
AB - Because clozapine and a number of other antipsychotic, as well as antidepressant drugs selectively block subsets of GABAA receptors, we have routinely screened 1100 compounds since 1983 for GABA antagonistic effects on 35S-TBPS binding, with a view to finding more potent clozapine-like selective GABAA receptor blockers. About 225 GABA antagonists were identified. Among compounds not previously published, four groups of tricyclic compounds (phenothiazines, phenoxazines, acridines and phenazines) contained GABAA receptor blockers, with acridines and oxidized phenothiazines in general being the most potent. Other active groups include cocaine derivatives, xanthines, indoles and phenethylamine derivatives. A large group of miscellaneous structures includes all known GABAA receptor blockers, as well as some antihistamines, antitussives, antimalarial/antiprotozoals, potential antidepressant, and a large non-therapeutic category consisting of diverse chemical structures. The amino steroid R5135 remains the most potent GABAA receptor blocker by far (EC50 = 5.7 nM, delta Bopt = 130%), and is non-aromatic. Pitrazepin, the next-most potent GABAA receptor blocker (EC50 = 360 nM), also fully reverses the inhibitory effect of 1 microM GABA on 35S-TBPS binding, but is 63-fold less potent than R5135. Appropriately positioned amidino groups, ring (aromatic) nitrogen, ether and keto groups can contribute to the potency of GABAA receptor blockade. Clozapine-like selective GABAA receptor blockers with EC50 values in the low nanomolar range remain to be identified. Such compounds may have potent antipsychotic effects
MH - antagonists & inhibitors
MH - Antipsychotic Agents
MH - classification
MH - Clozapine
MH - Cocaine
MH - English Abstract
MH - Gaba
MH - GABA Antagonists
MH - pharmacology
MH - Receptors,GABA-A
RP - NOT IN FILE
NT - UI - 98164316LA - RusRN - 0 (Antipsychotic Agents)RN - 0 (GABA Antagonists)RN - 0 (Receptors, GABA-A)RN - 5786-21-0 (Clozapine)PT - JOURNAL ARTICLEDA - 19980406IS - 0042-8809SB - MCY - RUSSIAJC - XIQAA - AuthorEM - 199806
UR - PM:0009503575
SO - Vopr Med Khim 1997 Nov ;43(6):576-583

17
UI - 19
AU - Hameedi FA
AU - Sernyak MJ
AU - Navui SA
AU - Kosten TR
TI - Near syncope associated with concomitant clozapine and cocaine use [letter]
MH - administration & dosage
MH - Administration,Intranasal
MH - Adult
MH - adverse effects
MH - Blood Pressure
MH - Case Report
MH - chemically induced
MH - Clozapine
MH - Cocaine
MH - complications
MH - drug effects
MH - Drug Interactions
MH - drug therapy
MH - Heart Rate
MH - Human
MH - Male
MH - Schizophrenia
MH - Substance-Related Disorders
MH - Syncope
RP - NOT IN FILE
NT - UI - 96354718LA - EngRN - 50-36-2 (Cocaine)RN - 5786-21-0 (Clozapine)PT - LETTERDA - 19960919IS - 0160-6689SB - MCY - UNITED STATESJC - HICEM - 199611
UR - PM:0008752022
SO - J Clin Psychiatry 1996 Aug ;57(8):371-372

18
UI - 17
AU - Howard JS
AD - Mental Health Unit, Southland Hospital, Invercargill, New Zealand
TI - Cocaine, Neuroleptics, and tardive dyskinesia as paleocortical escape
AB - Human orobuccolingual movement is reviewed in terms of stimulation and inhibition within the striatonigral pathways and its domination and control by motor area 4 and the inhibitory neocortex. Haloperidol, clozapine and cocaine are then compared in terms of the effects of each on the physiology and function within these areas under normal and certain pathological conditions. Theoretical models are then derived that formulate evidence that a unique, previously unreported, combination of two distinct neurological circumstances must occur simultaneously to satisfy the criteria for pathological orobuccolingual movement
MH - administration & dosage
MH - Adult
MH - adverse effects
MH - Animal
MH - Antipsychotic Agents
MH - Brain Mapping
MH - Case Report
MH - Cerebral Cortex
MH - Clozapine
MH - Cocaine
MH - Corpus Striatum
MH - Cranial Nerves
MH - Dopamine
MH - drug effects
MH - Dyskinesia,Drug-Induced
MH - Female
MH - Gaba
MH - Haloperidol
MH - Human
MH - innervation
MH - Masticatory Muscles
MH - Motor Neurons
MH - Neural Inhibition
MH - Neural Pathways
MH - Opioid-Related Disorders
MH - physiology
MH - physiopathology
MH - rehabilitation
MH - Schizophrenia
MH - Substance Withdrawal Syndrome
MH - Substantia Nigra
MH - Tongue
RP - NOT IN FILE
NT - UI - 97137425LA - EngRN - 0 (Antipsychotic Agents)RN - 50-36-2 (Cocaine)RN - 51-61-6 (Dopamine)RN - 52-86-8 (Haloperidol)RN - 56-12-2 (GABA)RN - 5786-21-0 (Clozapine)PT - JOURNAL ARTICLEPT - REVIEWPT - REVIEW, TUTORIALDA - 19970410IS - 1053-881XSB - MCY - UNITED STATESJC - AX0AA - AuthorEM - 199706
UR - PM:0008982762
SO - Integr Physiol Behav Sci 1996 Oct ;31(4):306-314

19
UI - 16
AU - Masserano JM
AU - Baker I
AU - Natsukari N
AU - Wyatt RJ
AD - National Institute of Mental Health, Neuropsychiatry Branch Neuroscience Center at Saint Elizabeths, Washington, DC, USA. masseraj@dirpc.nimh.nih.gov
TI - Chronic cocaine administration increases tyrosine hydroxylase activity in the ventral tegmental area through glutaminergic- and dopaminergic D2-receptor mechanisms
AB - Tyrosine hydroxylase activity was measured in the brain of rats treated chronically with saline or cocaine (10 mg/kg, 2 x day, for 7 days). Tyrosine hydroxylase activity was significantly increased in the ventral tegmental area 1, 6 and 12 weeks after the last treatment with cocaine. The increase in tyrosine hydroxylase activity at 6 weeks after the last cocaine injection was prevented by the prior administration of MK-801, haloperidol or clozapine but not by the D1 receptor antagonist, SCH-23390. SCH-23390 produced a significant increase in tyrosine hydroxylase activity when administered with saline. These data indicate that glutaminergic and dopaminergic D2-receptor mediated mechanisms are important in regulating the effect of cocaine on the ventral tegmental area
MH - Animal
MH - antagonists & inhibitors
MH - Clozapine
MH - Cocaine
MH - Dizocilpine Maleate
MH - Dopamine
MH - Dopamine Antagonists
MH - Dopamine Uptake Inhibitors
MH - drug effects
MH - enzymology
MH - Excitatory Amino Acid Antagonists
MH - Haloperidol
MH - Male
MH - metabolism
MH - pharmacology
MH - Rats
MH - Rats,Sprague-Dawley
MH - Receptors,Dopamine D1
MH - Receptors,Dopamine D2
MH - Receptors,Glutamate
MH - Sch-23390
MH - Tyrosine 3-Monooxygenase
MH - Ventral Tegmental Area
RP - NOT IN FILE
NT - UI - 97073351LA - EngRN - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)RN - 0 (Dopamine Antagonists)RN - 0 (Dopamine Uptake Inhibitors)RN - 0 (Excitatory Amino Acid Antagonists)RN - 0 (Receptors, Dopamine D1)RN - 0 (Receptors, Dopamine D2)RN - 0 (Receptors, Glutamate)RN - 50-36-2 (Cocaine)RN - 52-86-8 (Haloperidol)RN - 77086-22-7 (Dizocilpine Maleate)RN - 87075-17-0 (Sch-23390)PT - JOURNAL ARTICLEDA - 19970305IS - 0304-3940SB - MCY - IRELANDJC - N7NAA - AuthorEM - 199705
UR - PM:0008916075
SO - Neurosci Lett 1996 Oct 18 ;217(2-3):73-76

20
UI - 18
AU - McLean PG
AU - Coupar IM
AD - School of Pharmaceutical Biology and Pharmacology, Victorian College of Pharmacy, Monash University, Parkville, Victoria, Australia
TI - Characterisation of a postjunctional 5-ht7-like and a prejunctional 5- HT3 receptor mediating contraction of rat isolated jejunum
AB - The 5-HT (5-hydroxytryptamine)-induced contractile biphasic concentration-effect curve in rat isolated jejunum was investigated. The pEC50 values for the first and second phases were 8.0 and 6.1, respectively. The responses were insensitive to atropine (0.1 microM), ketanserin (2 microM), (-)-pindolol (5 microM), yohimbine (0.1 microM) and GR 113808 (1-[2-(methyl-sulphonylamino)ethyl]-4-piperidinylmethyl 1- methyl-1 H-indole-3-carboxylate, 1 microM) but susceptible to cocaine (10 microM). The low affinity phase was blocked by tetrodotoxin (1 microM), ondansetron (1 microM) and SR48968 (S)-N-methyl-N-[4-(4- acetylamino-4-phenyl piperidino)-2-(3,4-dichlorophenyl)butyl]benzamide, 0.1 microM). The high affinity phase was antagonised non-surmountably by fluoxetine (1 microM) methysergide (0.1 microM), spiperone (0.1 microM) and methiothepin (0.1 microM). Ritanserin (0.01-0.1 microM) and mesulergine (0.01-0.1 microM) acted as surmountable, competitive antagonists with pA2 values of 8.0 and 8.1, respectively. Clozapine (0.1 microM) was a surmountable antagonist with an apparent pA2 value of 8.0. The rank potency order of the 5-HT receptor agonists was 5-CT (5-carboxyamidotryptamine) > or = 5-HT = 5-methoxytryptamine > or = alpha-methyl-5-HT > > 8-OH-DPAT ((+/-)-2-dipropyl-amino-8-hydroxy- 1,2,3, 4-tetrahydronaphthalene) > dipropyl-5-CT > renzapride = sumatriptan. The responses to 5-HT and 5-CT were not potentiated by pargyline (10 and 100 microM). It is suggested that rat jejunum contains a neuronal 5-HT3 receptor facilitating neurokinin release and a contractile smooth muscle 5-HT receptor with a pharmacological operational profile similar to the cloned 5-ht7 receptor
MH - Animal
MH - Atropine
MH - Benzamides
MH - Clozapine
MH - Cocaine
MH - Dose-Response Relationship,Drug
MH - drug effects
MH - In Vitro
MH - Jejunum
MH - Male
MH - metabolism
MH - Methysergide
MH - Monoamine Oxidase Inhibitors
MH - Muscle Contraction
MH - Ondansetron
MH - pharmacology
MH - Piperidines
MH - Rats
MH - Rats,Wistar
MH - Receptors,Serotonin
MH - Serotonin
MH - Serotonin Antagonists
MH - Tetrodotoxin
RP - NOT IN FILE
NT - UI - 97049871LA - EngRN - 0 (Benzamides)RN - 0 (Monoamine Oxidase Inhibitors)RN - 0 (Piperidines)RN - 0 (Receptors, Serotonin)RN - 0 (Serotonin Antagonists)RN - 142001-63-6 (SR 48968)RN - 361-37-5 (Methysergide)RN - 4368-28-9 (Tetrodotoxin)RN - 50-67-9 (Serotonin)RN - 51-55-8 (Atropine)RN - 99614-02-5 (Ondansetron)PT - JOURNAL ARTICLEDA - 19970331IS - 0014-2999SB - MCY - NETHERLANDSJC - EN6AA - AuthorEM - 199706
UR - PM:0008894599
SO - Eur J Pharmacol 1996 Sep 26 ;312(2):215-225

21
UI - 20
AU - Robertson GS
AU - Jian M
AD - Department of Pharmacology, Faculty of Medicine, University of Ottawa, Ontario, Canada
TI - D1 and D2 dopamine receptors differentially increase Fos-like immunoreactivity in accumbal projections to the ventral pallidum and midbrain
AB - Alterations in dopaminergic neurotransmission have profound effects on neuronal expression of the putative activity marker, Fos, in both the dorsal and ventral striatum. Stimulants such as D-amphetamine and cocaine increase Fos-like immunoreactivity by enhancing the activation of D1 dopamine receptors. In contrast, neuroleptics such as haloperidol and raclopride increase Fos-like immunoreactivity by blocking striatal D2 dopamine receptors. In the dorsal striatum, D1 receptor stimulation elevates Fos-like immunoreactivity predominantly in neurons projecting to the midbrain (substantia nigra), whereas D2 receptor antagonism enhances Fos-like immunoreactivity principally in neurons projecting to the pallidum (globus pallidus). These findings are consistent with the proposal that D1 receptors are located chiefly on striatonigral neurons, whereas D2 receptors reside mainly on striatopallidal neurons. Since the nucleus accumbens (largest component of the ventral striatum) also sends projections to the midbrain (ventral tegmental area and substantia nigra) and pallidum (ventral pallidum), the present study utilized retrograde tract-tracing techniques to determine if there was a similar segregation of D1 agonist- and D2 antagonist-induced Fos-like immunoreactivity in these accumbal projections. In addition, we examined whether these relationships were the same in the core and shell regions of the nucleus accumbens. Like the dorsal striatum, D1 agonists (D-amphetamine and CY 208-243), but not D2 antagonists (haloperidol and clozapine), increased Fos-like immunoreactivity in accumbal neurons projecting to the midbrain (ventral tegmental area and substantia nigra). Also like the dorsal striatum, D2 antagonist-induced Fos-like immunoreactivity was located preferentially in accumbal neurons projecting to the pallidum (ventral pallidum). However, unlike the dorsal striatum, where the vast majority of neurons which display D1 agonist-induced Fos-like immunoreactivity project to the midbrain, nearly 50% of those neurons in the nucleus accumbens which were Fos- immunoreactive after D-amphetamine or CY 208-243 projected to the ventral pallidum. Thus, a similar number of accumbal neurons which expressed D1 agonist-induced Fos-like immunoreactivity were retrogradely labelled from the midbrain and ventral pallidum. Accumbal projections to the midbrain and ventral pallidum were retrogradely labelled with different retrograde tracers in order to determine the degree of collateralization between these pathways. Approximately 20% of retrogradely labelled neurons displayed both tracers, indicating that collateralization and damage to fibres of passage could not account for all of those cases in which D1 agonist-induced Fos-like immunoreactivity was detected in accumbal neurons projecting to the ventral pallidum.(ABSTRACT TRUNCATED AT 400 WORDS)
MH - Animal
MH - Clozapine
MH - Cocaine
MH - Dopamine
MH - Globus Pallidus
MH - Haloperidol
MH - Immunohistochemistry
MH - immunology
MH - Male
MH - Mesencephalon
MH - Nucleus Accumbens
MH - pharmacology
MH - physiology
MH - Proto-Oncogene Proteins c-fos
MH - Rats
MH - Rats,Wistar
MH - Receptors,Dopamine D1
MH - Receptors,Dopamine D2
MH - Substantia Nigra
MH - Support,Non-U.S.Gov't
MH - Ventral Tegmental Area
RP - NOT IN FILE
NT - UI - 95272888LA - EngRN - 0 (Proto-Oncogene Proteins c-fos)RN - 0 (Receptors, Dopamine D1)RN - 0 (Receptors, Dopamine D2)RN - 52-86-8 (Haloperidol)RN - 5786-21-0 (Clozapine)PT - JOURNAL ARTICLEDA - 19950621IS - 0306-4522SB - MCY - ENGLANDJC - NZRAA - AuthorEM - 199508
UR - PM:0007753373
SO - Neuroscience 1995 Feb ;64(4):1019-1034

22
UI - 22
AU - Gygi SP
AU - Gibb JW
AU - Hanson GR
AD - Department of Pharmacology and Toxicology, University of Utah, Salt Lake City
TI - Differential effects of antipsychotic and psychotomimetic drugs on neurotensin systems of discrete extrapyramidal and limbic regions
AB - The effects of two antipsychotic (dopamine antagonist) drugs, haloperidol and clozapine, and of two psychotomimetic (dopamine- releasing) drugs, methamphetamine and cocaine, on neurotensin (NT) concentrations in discrete regions of the caudate nucleus, nucleus accumbens and globus pallidus were examined. Multiple administrations of haloperidol (HA, 1 mg/kg), clozapine (20 mg/kg), methamphetamine (METH, 10 mg/kg) or cocaine (30 mg/kg) increased NT-like immunoreactivity (NTLI) in the whole striatum (caudate nucleus plus globus pallidus). The effects of combined HA and METH treatment on striatal NTLI were additive. In contrast, the effects of clozapine plus METH were not different from those caused by either drug alone. The caudate nucleus, nucleus accumbens and globus pallidus were dissected into nine areas based on anterior-posterior and medial-lateral position. Across the caudate areas, some differences in NTLI concentrations occurred when cocaine- and METH-treated groups were compared, even though whole striata in these groups did not differ significantly. The effects of the antipsychotic drugs in discrete caudate regions, alone or in combination with METH, confirmed the observations in the whole striata, although significant regional differences existed. There were also differential regional effects in the nucleus accumbens. Drug-induced changes in the NTLI content of the anterior nucleus accumbens were similar to those observed in the whole striatum, whereas NTLI changes in the posterior region of this structure often were opposite. Finally, NTLI concentrations in the globus pallidus were increased by Ha or METH treatment, but were not affected by clozapine or cocaine treatment. These findings suggest that NT systems throughout the entire striatum and nucleus accumbens do not respond in a homogeneous manner to these drugs which stimulate or block dopamine activity. The regional differences in NT responses may reflect different dopamine neurons which are affected differentially by dopamine-altering drugs

MH - Animal
MH - antagonists & inhibitors
MH - Antipsychotic Agents
MH - Caudate Nucleus
MH - Clozapine
MH - Cocaine
MH - Comparative Study
MH - Corpus Striatum
MH - Dopamine
MH - drug effects
MH - Extrapyramidal Tracts
MH - Globus Pallidus
MH - Hallucinogens
MH - Haloperidol
MH - immunology
MH - Limbic System
MH - Male
MH - metabolism
MH - Methamphetamine
MH - Neurotensin
MH - Nucleus Accumbens
MH - pharmacology
MH - Rats
MH - Rats,Sprague-Dawley
MH - Receptors,Dopamine D2
MH - Support,U.S.Gov't,P.H.S.
RP - NOT IN FILE
NT - UI - 94308940LA - EngRN - 0 (Antipsychotic Agents)RN - 0 (Hallucinogens)RN - 0 (Receptors, Dopamine D2)RN - 39379-15-2 (Neurotensin)RN - 50-36-2 (Cocaine)RN - 51-61-6 (Dopamine)RN - 52-86-8 (Haloperidol)RN - 537-46-2 (Methamphetamine)RN - 5786-21-0 (Clozapine)PT - JOURNAL ARTICLEID - DA00869/DA/NIDAID - DA00422/DA/NIDADA - 19940815IS - 0022-3565SB - MCY - UNITED STATESJC - JP3AA - AuthorEM - 199410
UR - PM:0007913495
SO - J Pharmacol Exp Ther 1994 Jul ;270(1):192-197

23
UI - 23
AU - Kosten TA
AU - Nestler EJ
AD - Division of Substance Abuse, Yale University School of Medicine, New Haven, CT 06519
TI - Clozapine attenuates cocaine conditioned place preference
AB - Clozapine, an atypical neuroleptic, has dopamine and serotonin antagonist actions that suggest its potential as a cocaine abuse pharmacotherapy. Yet, self-administration and discriminative stimulus studies in animals have reported both an enhancement and a partial blockade of cocaine's behavioral effects with clozapine. The present study examines further the effects of clozapine on cocaine conditioned place preference. Clozapine (10 mg/kg, s.c.) treatment significantly attenuated the development of cocaine (10 mg/kg, i.p.) conditioned place preference. These results, coupled with research that shows clozapine has limited extrapyramidal side effects, suggest that it should be considered as a pharmacotherapy for cocaine abuse
MH - Analysis of Variance
MH - Animal
MH - antagonists & inhibitors
MH - Clozapine
MH - Cocaine
MH - Conditioning,Classical
MH - Dopamine
MH - drug effects
MH - Male
MH - pharmacology
MH - Rats
MH - Rats,Sprague-Dawley
MH - Self Administration
MH - Serotonin
MH - Spatial Behavior
MH - Support,Non-U.S.Gov't
MH - Support,U.S.Gov't,P.H.S.
RP - NOT IN FILE
NT - UI - 94285696LA - EngRN - 50-36-2 (Cocaine)RN - 5786-21-0 (Clozapine)PT - JOURNAL ARTICLEID - P50-DA04060/DA/NIDADA - 19940725IS - 0024-3205SB - MSB - XCY - ENGLANDJC - L62AA - AuthorEM - 199409
UR - PM:0008015343
SO - Life Sci 1994 ;55(1):L9-14

24
UI - 21
AU - Yovell Y
AU - Opler LA
AD - Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York, New York
TI - Clozapine reverses cocaine craving in a treatment-resistant mentally ill chemical abuser: a case report and a hypothesis
MH - Adult
MH - Case Report
MH - Clozapine
MH - Cocaine
MH - Comorbidity
MH - diagnosis
MH - Diagnosis,Dual (Psychiatry)
MH - drug therapy
MH - Drug Therapy,Combination
MH - epidemiology
MH - Fluphenazine
MH - Human
MH - Lithium
MH - Male
MH - Psychotic Disorders
MH - Substance-Related Disorders
MH - therapeutic use
MH - Treatment Outcome
RP - NOT IN FILE
NT - UI - 95016582LA - EngRN - 50-36-2 (Cocaine)RN - 5786-21-0 (Clozapine)RN - 69-23-8 (Fluphenazine)RN - 7439-93-2 (Lithium)PT - JOURNAL ARTICLEDA - 19941026IS - 0022-3018SB - ASB - MCY - UNITED STATESJC - JAFEM - 199501
UR - PM:0007931211
SO - J Nerv Ment Dis 1994 Oct ;182(10):591-592

25
UI - 24
AU - French D
AU - Witkin JM
AD - Psychobiology Section, Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224
TI - Effects of the dopamine release inhibitor, CGS 10746B, on the locomotor stimulant and discriminative stimulus effects of cocaine and methamphetamine
AB - CGS 10746B or 5-(4-methyl-1 piperazinyl)-imadazo[2,1- b]1,3,5]benzothiadiazepine maleate is a clozapine analog that, unlike clozapine, produces decreases in neostriatal dopamine release without changing dopamine metabolism or occupying D2 receptors. CGS 10746B also blocks neuronal impulse flow. The ability of this atypical antipsychotic candidate to alter the discriminative stimulus effects induced by cocaine or methamphetamine in rats or the stimulation of locomotor activity in mice was evaluated. A range of doses of CGS 10746B was tested against maximally effective doses of the psychomotor stimulants. Although CGS 10746B completely blocked the locomotor stimulant effects of cocaine and methamphetamine, it also decreased spontaneous activity in mice over the same dose range. Rats were trained to discriminate 10 mg/kg cocaine or 1 mg/kg methamphetamine from saline. The discriminative stimulus effects of cocaine or methamphetamine were not blocked by CGS 10746B. Thus, in contrast to other potential atypical antipsychotic compounds (e.g., D1 receptor antagonists), CGS 10746B does not appear to produce selective blockade of these behavioral effects of psychomotor stimulant compounds
MH - Animal
MH - antagonists & inhibitors
MH - Clozapine
MH - Cocaine
MH - Discrimination (Psychology)
MH - Discrimination Learning
MH - Dopamine
MH - drug effects
MH - Male
MH - metabolism
MH - Methamphetamine
MH - Mice
MH - Motor Activity
MH - pharmacology
MH - Rats
MH - Rats,Sprague-Dawley
MH - Stimulation,Chemical
MH - Thiazepines
RP - NOT IN FILE
NT - UI - 94143395LA - EngRN - 0 (Thiazepines)RN - 50-36-2 (Cocaine)RN - 51-61-6 (Dopamine)RN - 537-46-2 (Methamphetamine)RN - 81382-52-7 (CGS 10746B)PT - JOURNAL ARTICLEDA - 19940315IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199405
UR - PM:0008309980
SO - Pharmacol Biochem Behav 1993 Dec ;46(4):989-993

26
UI - 25
AU - Sachs H
AU - Raff I
AD - Institute of Legal Medicine, University of Ulm, Germany
TI - Comparison of quantitative results of drugs in human hair by GC/MS
AB - Until the first determination of opiates in human hair by GC/MS in 1985, radioimmunological results of hair examinations met with opposition. Since then, further GC/MS methods have been developed that have led not only to considerably increased sensitivity, but can also be used in hair analysis for screening purposes and can detect substances for which RIA kits are not available. In the present study different extraction methods were used along with two GC/MS processes which back-up each other. These methods include the enzymatic dissolution of the hair, incubation with a buffer solution followed by a solid-phase extraction and incubation with methanol without a further extraction. The GC/MS examination for heroin, cocaine, hashish and selected pharmaceuticals was carried out after derivatization with pentafluoropropionic acid anhydride or pentafluoro-1-propanol. Because of the higher sensitivity and versatility of GC/MS, two GC/MS processes were used to confirm each other instead of backing-up radioimmunological measurements with GC/MS
MH - analysis
MH - chemistry
MH - Child
MH - Clozapine
MH - Cocaine
MH - Codeine
MH - Comparative Study
MH - Hair
MH - Human
MH - Mass Fragmentography
MH - methods
MH - Morphine
MH - Radioimmunoassay
MH - Street Drugs
MH - Substance Abuse Detection
RP - NOT IN FILE
NT - UI - 94186115LA - EngRN - 0 (Street Drugs)RN - 57-27-2 (Morphine)RN - 5786-21-0 (Clozapine)RN - 76-57-3 (Codeine)PT - JOURNAL ARTICLEDA - 19940428IS - 0379-0738SB - MCY - IRELANDJC - F49AA - AuthorEM - 199406
UR - PM:0008138222
SO - Forensic Sci Int 1993 Dec ;63(1-3):207-216

27
UI - 26
AU - Vanover KE
AU - Piercey MF
AU - Woolverton WL
AD - Drug Abuse Research Center, University of Chicago, Pritzker School of Medicine, Illinois
TI - Evaluation of the reinforcing and discriminative stimulus effects of cocaine in combination with (+)-AJ76 or clozapine
AB - Because self-administration and discrimination of a drug by animals correlate with its abuse and subjective effects in humans, interventions that modify the reinforcing and discriminative stimulus effects of the drug may be useful in the treatment of its abuse. The present study was designed to evaluate the effects of the putative dopamine autoreceptor antagonist (+)-AJ76 (AJ) or the atypical antipsychotic clozapine (CLZ) on the reinforcing and discriminative stimulus effects of cocaine in monkeys. One group of rhesus monkeys (n = 6) was allowed to self-administer cocaine (0.03 or 0.1 mg/kg/injection i.v. fixed-ratio 10, 2 hr/day). A second group of monkeys (n = 5) was trained to discriminate cocaine (0.2 or 0.4 mg/kg i.m., 10 min presession) from saline in a two lever, food-reinforced, drug discrimination paradigm. When behavior was stable, AJ or CLZ was administered i.m., 15 or 30 min presession. Intermediate doses of both compounds (1.0-3.0 mg/kg of AJ; 0.3-1.0 mg/kg of CLZ) increased cocaine self-administration, while responding remained evenly distributed over the session. A higher dose of CLZ decreased cocaine self-administration in an apparently nonspecific manner. When combined with saline, partial substitution for cocaine was seen in one of three monkeys with AJ and in none with CLZ. In combination with the training dose of cocaine in the discrimination experiment, both AJ and CLZ decreased drug appropriate responding by at least 50% in two of four monkeys, but had little or no effect in the other monkeys up to doses that completely suppressed lever pressing (6.4 mg/kg of AJ; 3.2 mg/kg of CLZ). Taken together, the present findings suggest that any blockade of the reinforcing and discriminative stimulus effects of cocaine by AJ and CLZ was, at best, partial. Furthermore, the stimulant effects of AJ observed in rats were not prominent in monkeys
MH - Animal
MH - antagonists & inhibitors
MH - Clozapine
MH - Cocaine
MH - Discrimination Learning
MH - Dopamine
MH - Dose-Response Relationship,Drug
MH - drug effects
MH - Female
MH - Human
MH - Macaca mulatta
MH - Male
MH - pharmacology
MH - Rats
MH - Receptors,Dopamine
MH - Reinforcement (Psychology)
MH - Self Administration
MH - Support,U.S.Gov't,P.H.S.
MH - Tetrahydronaphthalenes
RP - NOT IN FILE
NT - UI - 93360166LA - EngRN - 0 (Receptors, Dopamine)RN - 0 (Tetrahydronaphthalenes)RN - 50-36-2 (Cocaine)RN - 5786-21-0 (Clozapine)RN - 85379-09-5 (AJ 76)PT - JOURNAL ARTICLEID - DA-00250/DA/NIDAID - DA-00161/DA/NIDADA - 19930917IS - 0022-3565SB - MCY - UNITED STATESJC - JP3AA - AuthorEM - 199311
UR - PM:0008355207
SO - J Pharmacol Exp Ther 1993 Aug ;266(2):780-789

28
UI - 27
AU - Loh EA
AU - Fitch T
AU - Vickers G
AU - Roberts DC
AD - Department of Psychology, Carleton University, Ottawa, Ontario, Canada
TI - Clozapine increases breaking points on a progressive-ratio schedule reinforced by intravenous cocaine
AB - The effect of the atypical neuroleptic clozapine on cocaine self- administration reinforced on a progressive-ratio schedule in rats was examined. The rat's first response on a lever each day produced an IV infusion of cocaine (0.6 mg/injection) after which the requirements of the schedule escalated with each infusion until the frequency of responding on the lever fell below a criterion level. The final ratio completed was defined as the breaking point. Doses of 5 and 20 mg/kg clozapine produced either no effect or a nonspecific disruption in responding. Rats pretreated with 10 mg/kg clozapine responded to significantly higher breaking points, indicating an increased motivation to self-administer cocaine
MH - Animal
MH - Clozapine
MH - Cocaine
MH - Conditioning,Operant
MH - Dopamine
MH - drug effects
MH - Injections,Intravenous
MH - Male
MH - pharmacology
MH - physiology
MH - Rats
MH - Rats,Wistar
MH - Reinforcement Schedule
MH - Self Administration
MH - Serotonin
MH - Support,U.S.Gov't,P.H.S.
RP - NOT IN FILE
NT - UI - 93028665LA - EngRN - 50-36-2 (Cocaine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 5786-21-0 (Clozapine)PT - JOURNAL ARTICLEID - 271-90-7401DA - 19921118IS - 0091-3057SB - MCY - UNITED STATESJC - P3QAA - AuthorEM - 199301
UR - PM:0001409791
SO - Pharmacol Biochem Behav 1992 Jul ;42(3):559-562

29
UI - 28
AU - Velasco-Martin A
AU - Garcia JL
AU - Duenas A
AD - Department of Pharmacology, School of Medicine, University of Valladolid, Spain
TI - Effects of several neuroleptics, antidepressants and monoamine uptake blockers on ATPase activity and related oxygen uptake in rat brain in vitro
AB - An experimental trial was conducted to study the effects of phenoxybenzamine, cocaine, carbamazepine, loxapine, clozapine, clothiapine, thiothixene, droperidol, alprazolam, imipramine, maprotiline, dibenzepin, nomifensine, trazodone, mianserin, viloxazine, doxepin and amoxapine on photocolorimetrically rated ATPase activity and on related oxygen uptake, determined by manometrical means, within a concentration range of 0.1-0.001 mM. Phenoxybenzamine, clothiapine and maprotiline at 0.1 mM inhibited sodium-potassium ATPase activity and related QO2 by 30-40%. Loxapine, trazodone, amoxapine and alprazolam at 0.1 mM inhibited sodium-potassium ATPase activity by 25- 35%. Imipramine, nomifensine and droperidol at 0.1 mM inhibited QO2 by 20-35%. Cocaine, at all concentrations assayed, inhibited ouabain insensitive ATPase. The remaining drugs did not produce significant modifications
MH - Adenosinetriphosphatase
MH - Animal
MH - antagonists & inhibitors
MH - Antidepressive Agents
MH - Antipsychotic Agents
MH - Brain
MH - Clozapine
MH - Cocaine
MH - drug effects
MH - enzymology
MH - In Vitro
MH - Male
MH - metabolism
MH - Monoamine Oxidase Inhibitors
MH - Nomifensine
MH - Ouabain
MH - Oxygen Consumption
MH - pharmacology
MH - Rats
RP - NOT IN FILE
NT - UI - 90173495LA - EngRN - EC 3.6.1.3 (Adenosinetriphosphatase)RN - 0 (Antidepressive Agents)RN - 0 (Antipsychotic Agents)RN - 0 (Monoamine Oxidase Inhibitors)RN - 630-60-4 (Ouabain)PT - JOURNAL ARTICLEDA - 19900410IS - 0379-0355SB - MCY - SPAINJC - LZNAA - AuthorEM - 199006
UR - PM:0002576298
SO - Methods Find Exp Clin Pharmacol 1989 Dec ;11(12):737-741

30
UI - 29
AU - Drescher K
AU - Hetey L
AD - Institute of Pharmacology and Toxicology of Charite, Humboldt University, Berlin, GDR
TI - Influence of antipsychotics and serotonin antagonists on presynaptic receptors modulating the release of serotonin in synaptosomes of the nucleus accumbens of rats
AB - In the nucleus accumbens of rats the release of [3H]serotonin (5-HT) from superfused synaptosomes stimulated by 30 mM K+ was investigated. In the presence of 40 microM of the uptake inhibitor cocaine the release of [3H]5-HT was inhibited by 5-HT in a concentration-dependent manner (IC50 = 0.45 microM). The maximum inhibitory effect of 5-HT was 54% of controls. The inhibition of K+-stimulated release of [3H]5-HT induced by 5-HT was antagonized completely by methiothepine and clozapine, respectively, whereas methysergide had only a weak antagonizing effect in a concentration of 20 microM or less, haloperidol was ineffective. Furthermore, the synaptosomal K+- stimulated release of [3H]5-HT was also inhibited by dopamine (DA) in a concentration-dependent manner (IC50 = 0.1 microM). This inhibitory effect was antagonized by antipsychotic drugs, the rank order of antagonistic potencies was sulpiride greater than haloperidol greater than clozapine; methiothepine was ineffective. The experimental system (the K+-stimulated synaptosomal release of [3H]5-HT seems to be a suitable model for differentiating dopaminergic and/or serotonergic components of antipsychotics or other drugs on presynaptic receptors
MH - Animal
MH - antagonists & inhibitors
MH - Antipsychotic Agents
MH - Clozapine
MH - Cocaine
MH - Dopamine
MH - drug effects
MH - Haloperidol
MH - In Vitro
MH - Male
MH - metabolism
MH - Nucleus Accumbens
MH - pharmacology
MH - Rats
MH - Rats,Inbred Strains
MH - Receptors,Dopamine
MH - Receptors,Serotonin
MH - Septal Nuclei
MH - Serotonin
MH - Serotonin Antagonists
MH - Sulpiride
MH - Synaptosomes
RP - NOT IN FILE
NT - UI - 88175417LA - EngRN - 0 (Antipsychotic Agents)RN - 0 (Receptors, Dopamine)RN - 0 (Receptors, Serotonin)RN - 0 (Serotonin Antagonists)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)PT - JOURNAL ARTICLEDA - 19880422IS - 0028-3908SB - MCY - ENGLANDJC - NZBAA - AuthorEM - 198807
UR - PM:0002895429
SO - Neuropharmacology 1988 Jan ;27(1):31-36

31
UI - 30
AU - Dougan DF
AU - Duffield P
AU - Wade DN
TI - Modulation of dopamine receptors in the Tapes clam by dextroamphetamine and phenylethanolamine
AB - The mechanism underlying the modulation, by dextroamphetamine and compounds related to phenylethanolamine, of responses to dopamine and serotonin has been studied in the isolated ventricle and aortic bulb of the clam Tapes watlingi. Dextroamphetamine and phenylethanolamine but not cocaine and benztropine have the ability to unmask inhibitory responses to both dopamine and serotonin in the ventricle. Chlordimeform but not clozapine attenuates the inhibitory response to both dextroamphetamine and phenylethanolamine in concentrations which have little or no effect on the inhibitory response to dopamine in the ventricle. Phenylethanolamine, dextroamphetamine, phenylpropylolamine and p-chloro-phenylethanolamine but not octopamine or noradrenaline attenuate the contractile responses to both dopamine and serotonin in preparations of the quiescent aortic bulb. These data show that there are specific receptors for phenylethanolamine in the Tapes heart capable of modulating responses to dopamine and serotonin, and suggests that this biogenic phenethylamine can act as an environmental and physiological factor which may determine how the mollusc heart responds to dopamine
MH - Adenosine Monophosphate
MH - Amantadine
MH - Animal
MH - Benztropine
MH - Chlorphenamidine
MH - Clams
MH - Clozapine
MH - Cocaine
MH - Dextroamphetamine
MH - Dopamine
MH - drug effects
MH - Ethanolamines
MH - Heart Rate
MH - Myocardial Contraction
MH - pharmacology
MH - physiology
MH - Receptors,Dopamine
MH - Serotonin
MH - Support,Non-U.S.Gov't
MH - Tetrahydronaphthalenes
RP - NOT IN FILE
NT - UI - 87188878LA - EngRN - 0 (Ethanolamines)RN - 0 (Receptors, Dopamine)RN - 0 (Tetrahydronaphthalenes)RN - 122-98-5 (N-phenylethanolamine)RN - 2954-50-9 (2-aminotetralin)RN - 50-36-2 (Cocaine)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 51-64-9 (Dextroamphetamine)RN - 5786-21-0 (Clozapine)RN - 61-19-8 (Adenosine Monophosphate)RN - 6164-98-3 (Chlorphenamidine)RN - 768-94-5 (Amantadine)RN - 86-13-5 (Benztropine)PT - JOURNAL ARTICLEDA - 19870608IS - 0742-8413SB - MCY - ENGLANDJC - DNXAA - AuthorEM - 198708
UR - PM:0002882924
SO - Comp Biochem Physiol C 1987 ;86(2):317-324

32
UI - 32
AU - Bergman J
AU - Spealman RD
TI - Some behavioral effects of histamine H1 antagonists in squirrel monkeys
AB - Graded dose of the histamine H1 antagonists tripelennamine (0.1-3.0 mg/kg), promethazine (0.1-3.0 mg/kg), diphenhydramine (0.3-10.0 mg/kg) and chlorpheniramine (0.3-1.7 mg/kg) increased rates of nonsuppressed responding under a second-order schedule of food presentation to a maximum beyond which responding was increased less or decreased. In contrast, the H2 antagonist, cimetidine, had no effect or decreased responding at the highest doses studied (56.0-100.0 mg/kg). Intermediate doses of tripelennamine, diphenhydramine and promethazine also increased rates of food-maintained responding that were suppressed by electric shock. Maximal increases in rates of suppressed responding were comparable to those produced by effective doses of chlordiazepoxide (3.0-10.0 mg/kg). Under identical conditions, clozapine (0.1-1.0 mg/kg) increased responding to a lesser extent, and d-amphetamine (0.01-0.3 mg/kg) and cimetidine (3.0-100.0 mg/kg) either did not increase or, at the highest doses, only decreased rates of suppressed responding. Doses of tripelennamine and diphenhydramine that increased rates of nonsuppressed and suppressed responding also maintained self-administration in cocaine-trained squirrel monkeys under a second-order schedule of i.v. injection. Rates and patterns of responding maintained by tripelennamine and diphenhydramine were comparable to those maintained by cocaine and d-amphetamine under identical conditions. The results show that histamine H1 antagonists can have pronounced rate-increasing effects on nonsuppressed and suppressed behavior, and that they can serve as reinforcers in monkeys. These effects occur at doses that probably are greater than those required to saturate H1 sites of action in central nervous system and may not be mediated solely through histaminic mechanisms
MH - Animal
MH - Behavior,Animal
MH - Chlordiazepoxide
MH - Chlorpheniramine
MH - Cimetidine
MH - Clozapine
MH - Cocaine
MH - Conditioning,Operant
MH - Dextroamphetamine
MH - Diphenhydramine
MH - drug effects
MH - Electroshock
MH - Feeding Behavior
MH - Histamine H1 Antagonists
MH - Male
MH - pharmacology
MH - Promethazine
MH - Saimiri
MH - Self Administration
MH - Support,U.S.Gov't,P.H.S.
MH - Tripelennamine
RP - NOT IN FILE
NT - UI - 87011326LA - EngRN - 0 (Histamine H1 Antagonists)RN - 132-22-9 (Chlorpheniramine)RN - 50-36-2 (Cocaine)RN - 51-64-9 (Dextroamphetamine)RN - 51481-61-9 (Cimetidine)RN - 5786-21-0 (Clozapine)RN - 58-25-3 (Chlordiazepoxide)RN - 58-73-1 (Diphenhydramine)RN - 60-87-7 (Promethazine)RN - 91-81-6 (Tripelennamine)PT - JOURNAL ARTICLEID - DA03774/DA/NIDAID - DA00499/DA/NIDAID - DA02658/DA/NIDAID - +DA - 19861117IS - 0022-3565SB - MCY - UNITED STATESJC - JP3AA - AuthorEM - 198701
UR - PM:0002876090
SO - J Pharmacol Exp Ther 1986 Oct ;239(1):104-110

33
UI - 31
AU - Hetey L
AU - Drescher K
TI - Influence of antipsychotics on presynaptic receptors modulating the release of dopamine in synaptosomes of the nucleus accumbens of rats
AB - The release of preloaded [3H]dopamine (DA) from superfused synaptosomes stimulated by 30 mM K+ was investigated in the nucleus accumbens of rats. Under conditions preventing the uptake of DA (presence of 40 microM cocaine) release of [3H]DA was inhibited by DA and apomorphine in a concentration-dependent manner (IC50s 0.65 and 0.3 microM, respectively). The maximal inhibitory effects of DA, as well as of apomorphine, were about 50% of the controls. The DA-induced inhibition was antagonized by antipsychotics completely; the rank order of antagonistic potencies was haloperidol greater than clozapine greater than sulpiride; methiothepine was ineffective. Furthermore, the K+- stimulated release of [3H]DA was inhibited by serotonin in a concentration-dependent manner (IC50 = 0.9 microM). This inhibitory effect was antagonized by methiothepine with a high efficiency, by clozapine and methysergide with moderate efficiencies; haloperidol and sulpiride were ineffective. The experimental system demonstrated appears to be suitable for characterizing the DA- and serotonin- antagonistic potencies of antipsychotics and other drugs on presynaptic autoreceptors as well as receptors modulating release of DA in the nucleus accumbens
MH - Animal
MH - Antipsychotic Agents
MH - Apomorphine
MH - Clozapine
MH - Cocaine
MH - Dopamine
MH - drug effects
MH - Haloperidol
MH - In Vitro
MH - Male
MH - Nucleus Accumbens
MH - pharmacology
MH - physiology
MH - Potassium
MH - Psychotropic Drugs
MH - Rats
MH - Rats,Inbred Strains
MH - Receptors,Dopamine
MH - Septal Nuclei
MH - Serotonin
MH - Serotonin Antagonists
MH - Sulpiride
MH - Synaptosomes
RP - NOT IN FILE
NT - UI - 87065488LA - EngRN - 0 (Antipsychotic Agents)RN - 0 (Receptors, Dopamine)RN - 0 (Serotonin Antagonists)RN - 50-67-9 (Serotonin)RN - 51-61-6 (Dopamine)RN - 58-00-4 (Apomorphine)RN - 7440-09-7 (Potassium)PT - JOURNAL ARTICLEDA - 19870102IS - 0028-3908SB - MCY - ENGLANDJC - NZBAA - AuthorEM - 198703
UR - PM:0002878387
SO - Neuropharmacology 1986 Oct ;25(10):1103-1109

34
UI - 33
AU - Baud P
AU - Arbilla S
AU - Langer SZ
TI - Inhibition of the electrically evoked release of [3H]acetylcholine in rat striatal slices: an experimental model for drugs that enhance dopaminergic neurotransmission
AB - The activation by endogenous dopamine of the inhibitory 3,4- dihydroxyphenylethylamine (dopamine) receptors modulating the electrically evoked release of [3H]acetylcholine [( 3H]ACh) and [3H]dopamine in rat striatal slices is a function of the concentration of dopamine accumulated in the synaptic cleft during electrical stimulation. When the release of 3H-neurotransmitters was elicited with a 2-min period of stimulation at a frequency of 1 Hz, neither dopamine autoreceptors nor dopamine receptors modulating [3H]ACh were activated by endogenously released dopamine. On the other hand, exposure to (S)- sulpiride facilitated the release of [3H]dopamine and [3H]ACh elicited when the 2-min stimulation was carried out at a frequency of 3 Hz but this effect was not observed at a lower frequency of stimulation (1 Hz). In the presence of amphetamine the dopamine receptors modulating the electrically evoked release of [3H]ACh can be activated by endogenous dopamine even at the lower frequency of stimulation (1 Hz). Similar effects can be obtained if the neuronal uptake of dopamine is inhibited by cocaine or nomifensine. The inhibition by amphetamine of the release of [3H]ACh elicited by electrical stimulation at 1 Hz involves dopamine receptors and can be fully antagonized by clozapine, haloperidol, chlorpromazine, or pimozide. The stereoselectivity of this antagonism can be demonstrated with the optical enantiomers of sulpiride and butaclamol. This inhibitory effect of amphetamine on cholinergic neurotransmission appears to be the result of the stimulation of dopamine receptors of the D2 subtype, as they were resistant to blockade by the preferential D1 receptor antagonist SCH 23390.(ABSTRACT TRUNCATED AT 250 WORDS)
MH - Acetylcholine
MH - Amphetamine
MH - Animal
MH - Chlorpromazine
MH - Clozapine
MH - Cocaine
MH - Corpus Striatum
MH - Dopamine
MH - drug effects
MH - Electric Stimulation
MH - Haloperidol
MH - Male
MH - metabolism
MH - Nomifensine
MH - pharmacology
MH - physiology
MH - Rats
MH - Rats,Inbred Strains
MH - Receptors,Dopamine
MH - Sulpiride
MH - Synaptic Transmission
RP - NOT IN FILE
NT - UI - 85082047LA - EngRN - 0 (Receptors, Dopamine)RN - 15676-16-1 (Sulpiride)RN - 24526-64-5 (Nomifensine)RN - 300-62-9 (Amphetamine)RN - 50-36-2 (Cocaine)RN - 50-53-3 (Chlorpromazine)RN - 51-61-6 (Dopamine)RN - 51-84-3 (Acetylcholine)RN - 52-86-8 (Haloperidol)RN - 5786-21-0 (Clozapine)PT - JOURNAL ARTICLEDA - 19850221IS - 0022-3042SB - MCY - UNITED STATESJC - JAVAA - AuthorEM - 198504
UR - PM:0002981280
SO - J Neurochem 1985 Feb ;44(2):331-337

35
UI - 34
AU - Roberts DC
AU - Vickers G
TI - Atypical neuroleptics increase self-administration of cocaine: an evaluation of a behavioural screen for antipsychotic activity
AB - Several drugs have been shown to exert antipsychotic effects, yet they display an atypical profile with respect to standard neuroleptic drug screens. Low doses of traditional neuroleptics are known to increase self-administration of psychomotor stimulants; we sought to determine whether these atypical drugs would cause a comparable effect. Sulpiride, metoclopramide and thioridazine produced a dose-dependent increase in cocaine intake similar to that found for chlorpromazine, haloperidol, pimozide and flupenthixol. This effect was found to correlate (r = 0.94) with daily clinical dose. Clozapine, however, produced a dose-dependent decrease in cocaine intake. The advantages and disadvantages of using this measure as a screening procedure for neuroleptic drugs are discussed
MH - administration & dosage
MH - Animal
MH - Antipsychotic Agents
MH - Chlorpromazine
MH - Clozapine
MH - Cocaine
MH - Dopamine
MH - drug effects
MH - Drug Screening
MH - Haloperidol
MH - Male
MH - methods
MH - pharmacology
MH - Rats
MH - Rats,Inbred Strains
MH - Receptors,Dopamine
MH - Self Administration
MH - Sulpiride
MH - Support,Non-U.S.Gov't
RP - NOT IN FILE
NT - UI - 84119980LA - EngRN - 0 (Antipsychotic Agents)RN - 0 (Receptors, Dopamine)RN - 50-36-2 (Cocaine)RN - 5786-21-0 (Clozapine)PT - JOURNAL ARTICLEDA - 19840316IS - 0033-3158SB - MCY - GERMANY, WESTJC - QGIAA - AuthorEM - 198405
UR - PM:0006141584
SO - Psychopharmacology (Berl) 1984 ;82(1-2):135-139

36
UI - 35
AU - Petersen EN
TI - Pre- and postsynaptic alpha-adrenoceptor antagonism by neuroleptics in vivo
AB - Different types of neuroleptics were studied for pre- and postsynaptic alpha-adrenoceptor antagonism in pithed rats using the blood pressure effect of clonidine as a measure of postsynaptic alpha-adrenoceptor activation and the depression of the heart rate response to electrical stimulation as a measure of presynaptic alpha-adrenoceptor activation. Yohimbine (0.1 mg/kg) was more active at pre- than postsynaptic alpha- adrenoceptors while the reverse was found with prazosin (0.02-5 mg/kg). Phentolamine (1-5 mg/kg) on the other hand was very active at both receptors. Cocaine 1-5 mg/kg had no effect on these responses indicating that noradrenaline uptake inhibition presumably does not interfere with the revaluation of the alpha-adrenoceptor antagonistic effect of the neuroleptics. Melperone, haloperidol, thioridazine and flupenthixol (0.15 mg/kg) were more selective antagonists at postsynaptic alpha-adrenoceptors than prazosin. Clozapine, chlorprothixene showed preferential presynaptic (0.15 mg/kg) were antagonists at both types of receptors. Chlorprothixene showed preferential presynaptic alpha-antagonism of high potency. Chlorprothixene was the only neuroleptic drug which like phentolamine (1-5 mg/kg) gave complete presynaptic alpha-antagonism. These results indicate widely different selectivity of neuroleptics for pre- and postsynaptic alpha-adrenoceptors on peripheral sympathetic nerves. It is suggested that neuroleptics with presynaptic alpha-adrenoceptor antagonism may enhance the activity of Beta-adrenergic systems indirectly both in peripheral organs like the heart, and within the central nervous system
MH - Adrenergic alpha-Antagonists
MH - Animal
MH - Antipsychotic Agents
MH - blood
MH - Blood Pressure
MH - Clonidine
MH - Clozapine
MH - Cocaine
MH - drug effects
MH - Haloperidol
MH - Heart Rate
MH - pharmacology
MH - Phentolamine
MH - Prazosin
MH - Rats
MH - Receptors,Adrenergic
MH - Receptors,Adrenergic,alpha
MH - Receptors,Adrenergic,beta
RP - NOT IN FILE
NT - UI - 81236694LA - EngRN - 0 (Adrenergic alpha-Antagonists)RN - 0 (Antipsychotic Agents)RN - 0 (Receptors, Adrenergic)RN - 0 (Receptors, Adrenergic, alpha)RN - 0 (Receptors, Adrenergic, beta)RN - 19216-56-9 (Prazosin)RN - 4205-90-7 (Clonidine)RN - 50-36-2 (Cocaine)RN - 50-60-2 (Phentolamine)PT - JOURNAL ARTICLEDA - 19810925IS - 0014-2999SB - MCY - NETHERLANDSJC - EN6AA - AuthorEM - 198111
UR - PM:0006113964
SO - Eur J Pharmacol 1981 Feb 19 ;69(4):399-405

37
UI - 36
AU - Gross G
AU - Schumann HJ
TI - Enhancement of noradrenaline release from rat cerebral cortex by neuroleptic drugs
AB - The effect of different neuroleptic drugs (levomepromazine, haloperidol, thioridazine, clozapine and sulpiride) on (-)-3H- noradrenaline uptake and release by parieto-occipital slices of the rat cerebral cortex was investigated. 1. All neuroleptic drugs tested increased the 3H-efflux from electrically stimulated cortical slices preincubated in (-)-3H-noradrenaline already at 1 microM, clozapine was the most potent compound followed by haloperidol, thioridazine, levomepromazine and sulpiride. The enhanced 3H-efflux due to field stimulation was found at concentrations, which did not increase the basal 3H-efflux. Only haloperidol raised the basal 3H-efflux at 1 microM. 2. All neuroleptic drugs failed to inhibit (-)-3H-noradrenaline (10(-7) M) accumulation by cortical slices at 1 microM. Sulpiride was inactive in concentrations up to 100 microM. Clozapine again proved to be most potent at 10-100 microM. 3. Clozapine was able to enhance the stimulated transmitter overflow when noradrenaline uptake was already blocked by cocaine thus indicating a different mode of action. 4. Clozapine and levomepromazine antagonized the presynaptic alpha- adrenergic effect of clonidine. 5. The antidepressant drug amitriptyline increased the transmitter efflux at the same concentrations and to a similar extent as neuroleptic agents. It is concluded that neuroleptics enhance the stimulation induced noradrenaline release mainly by acting on presynaptic alpha- adrenoceptors. The effect of clozapine, however, includes a noradrenaline uptake inhibition. These findings may explain the increased noradrenaline turnover produced by neuroleptic drugs and the weak antidepressant action of low potent neuroleptics as well
MH - Amitriptyline
MH - Animal
MH - Antipsychotic Agents
MH - Cerebral Cortex
MH - Clozapine
MH - Cocaine
MH - Haloperidol
MH - In Vitro
MH - Male
MH - metabolism
MH - Norepinephrine
MH - pharmacology
MH - Promazine
MH - Rats
MH - Stimulation,Chemical
MH - Sulpiride
MH - Support,Non-U.S.Gov't
RP - NOT IN FILE
NT - UI - 81148891LA - EngRN - 0 (Antipsychotic Agents)RN - 50-36-2 (Cocaine)RN - 50-48-6 (Amitriptyline)RN - 51-41-2 (Norepinephrine)RN - 5786-21-0 (Clozapine)RN - 58-40-2 (Promazine)PT - JOURNAL ARTICLEDA - 19810513IS - 0028-1298SB - MCY - GERMANY, WESTJC - NTQAA - AuthorEM - 198107
UR - PM:0006111028
SO - Naunyn Schmiedebergs Arch Pharmacol 1980 ;315(2):103-109

38
UI - 37
AU - Kilbey MM
AU - Ellinwood EH
TI - Discriminative stimulus properties of psychomotor stimulants in the cat
AB - Cats were trained to choose between two levels or an operant chamber using interoceptive cues provided by d-amphetamine or saline as the discriminative stimuli. Following training, stimulus generalization was observed to additional doses of d-amphetamine and cocaine. but not to morphine. Clozapine blocked the generalization of the drug discrimination response to d-amphetamine, but had no effect on generalization to cocaine. These data indicate that discriminative stimulus properties of psychomotor stimulants, previously described in rats, are similar in cats
MH - Animal
MH - Cats
MH - Central Nervous System Stimulants
MH - Clozapine
MH - Cocaine
MH - Dextroamphetamine
MH - Discrimination (Psychology)
MH - drug effects
MH - Feeding Behavior
MH - Female
MH - Male
MH - Morphine
MH - pharmacology
MH - Rats
MH - Reinforcement Schedule
MH - Support,U.S.Gov't,P.H.S.
RP - NOT IN FILE
NT - UI - 79247496LA - EngPT - JOURNAL ARTICLEDA - 19791024SB - MCY - GERMANY, WESTJC - QGIAA - AuthorEM - 197912
UR - PM:0000038476
SO - Psychopharmacology (Berl) 1979 May 25 ;63(2):151-153

Alexander DeLuca, M.D., FASAM.
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Revised: March 13, 2001.