Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A previously healthy 33-year-old patient developed a schizophrenia-like psychosis of 5 weeks' duration after inhalation of hashish contaminated with phencyclidine (PCP). The literature is reviewed and the epidemiology, clinical features, therapy and neuropharmacology of phencyclidine intoxication are discussed.
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PMID:[Phencyclidine (PCP): a psychotomimetic drug. Case report and review of literature]. 663 38

Phencyclidine (PCP) is a widely abused drug inducing a psychosis relieved by such dopamine antagonists as the neuroleptics. In the current study we compared two neuroleptics which act at different dopamine receptor sites. Haloperidol, a DA-2 receptor antagonist, and chlorpromazine, a DA-1 antagonist, were used to treat a total of 20 patients who experienced a phencyclidine psychosis. Ten patients each received two doses of one or the other neuroleptic on an alternating basis. Haloperidol 5 mg i.m. was shown to be superior to chlorpromazine 50 mg i.m. in relieving all signs of psychosis. The authors hypothesize that the DA-2 receptor is site-specific for PCP.
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PMID:Comparison of haloperidol and chlorpromazine in the treatment of phencyclidine psychosis. 672 21

The scientific literature on PCP (phencyclidine) was reviewed with a view to determining whether or not current knowledge coincides with the picture of PCP presented by the popular media. The media portray PCP as an insidious drug whose use has reached almost epidemic proportions among American youth. Serious adverse reactions, including psychosis and violent behavior, are seen as common if not inevitable consequences of use. The literature indicates that this picture of PCP is not justified. Both the prevalence of use and the relative frequency of severe adverse effects appear to have been overstated by the media.
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PMID:The PCP epidemic: a critical review. 675 54

Rats were treated with d-amphetamine sulfate (5 and 10 mg/kg i.p.) and phencyclidine (PCP) (5 mg/kg i.p.) twice per day. After 21 days, [3H]spiroperidol binding in striatum was reduced by all treatments; receptor number (Bmax) and not affinity (KD) was affected. These results suggest that the psychotic effect of PCP may, like those of amphetamine, involve changes in dopamine receptors.
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PMID:Chronic phencyclidine, like amphetamine, produces a decrease in [3H]spiroperidol binding in rat striatum. 706 31

Phencyclidine (PCP), a widely abused drug currently, has multiple pharmacological actions, including psychotomimetic [1], anesthetic [2], sympathomimetic [2], anticholinergic [3-7], and dopaminergic [8-10]. Similarly, PCP intoxication in man can present with diverse symptoms: schizophrenia-like delusions and hallucinations; mania; violence, dyskinetic, catatonic, or stereotyped movements; hypertension; and coma [11, 12]. There is general agreement that the treatment of PCP intoxication includes support of vital functions and acidification of the urine [13]. However, there is no known specific antidote for PCP toxicity. Although diazepam [13], haloperidol [14, 15], and chlorpromazine [16] have been reported to improve the agitation and psychotic symptoms caused by PCP, the therapeutic efficacy of these agents has rarely been documented with objective clinical measures. Recently we found that intramuscular physostigmine and haloperidol [17, 18] improved several symptoms of acute PCP intoxication as measured by the Brief Psychiatric Rating Scale (BPRS) [19].
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PMID:Phencyclidine intoxication: assessment of possible antidotes. 713 17

Routine blood samples of 145 consecutive patients seen in the Los Angeles County Psychiatric Hospital Emergency Room during a 48-hour weekday period in June 1979 were examined for phencyclidine (PCP) using a sensitive and specific gas capillary gas chromatographic nitrogen detector (GC2-N) method. Of these 145 samples 63 (43.4%) were positive and PCP levels ranged 0.34 to 142.9 nanograms/ml (mean 14.6 ng/ml +/- 3.4 S.E.M.). An analysis of the records of these 63 patients revealed a wide variety of psychotic clinical pictures resembling mania, depression or schizophrenia with relatively few of the supposedly characteristic manifestations of PCP intoxication. Each of the 63 patients had at least one manifestation of toxic psychosis and/or acute delirium, in addition to the florid symptoms characteristic of functional states. PCP measurement, pharmacokinetics and the possible relationships of this intoxication to the psychiatric manifestations are discussed.
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PMID:The urban epidemic of phencyclidine (PCP) use: clinical and laboratory evidence from a public psychiatric hospital emergency service. 721 23

Phencyclidine (PCP) is a popular illicit drug often misrepresented as some other hallucinogenic substance and distributed in widely varying dosage forms and strengths. Users of hallucinogenic drugs may present with unintentional PCP overdoses. Toxicological laboratory analyses are essential to establish the diagnosis. In nine admitted overdose patients, the consciousness level ranged from alert to comatose on presentation, and all showed a prolonged recovery phase with agitation and toxic psychosis. Severe behavior disorder, paranoid ideation, and amnesia for the entire period of in-hospital stay are characteristic. In very high dose patients, shallow respiratory excursions and periods of apnoea and cyanosis coincided with generalized extensor spasm and spasm of neck muscles. Excessive bronchial secretions, gross ataxia, opisthotonic posturing, and grimacing occur. PCP toxic psychosis should be considered in drug-abusing patients presenting with schizophrenic-like symptoms, psychosis, or other bizarre behavior, whether or not they admit to taking PCP.
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PMID:Phencyclidine ingestion: drug abuse and psychosis. 728 52

The influence of cholecystokinin (CCK), bilaterally injected into the rostral nucleus accumbens, on the EEG and behavioural effects induced by phencyclidine (PCP) has been studied in rats. CCK (10 ng) significantly inhibited PCP-induced EEG effects (increase of spectral power with respect to pre-drug tracing; increase of relative power distribution in the slowest frequency bands), and behavioural effects (circling and ataxia). The inhibitory effects of CCK were completely antagonized by 1 ng PD 135-158, a selective CCKB receptor antagonist, but not by lorglumide (1 microgram), a selective CCKA receptor antagonist. Since the effects induced by PCP in rodents have been proposed to be an experimental correlate of the psychotic symptoms it induces in humans, these results indicate that CCK may act as a neuroleptic. They also suggest that CCKB receptors located in the rostral nucleus accumbens may be involved in the neuroleptic-like activity of CCK.
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PMID:The stimulation of cholecystokinin receptors in the rostral nucleus accumbens significantly antagonizes the EEG and behavioural effects induced by phencyclidine in rats. 748 May 47

In this study, we investigated whether risperidone, a serotonin-S2A (5-HT2A)/dopamine-D2 (D2)-receptor antagonist, inhibits phencyclidine (PCP)-induced stereotyped behaviors in comparison with haloperidol and ritanserin. Moreover, we also attempted to investigate the effects of these antipsychotics on the contents of dopamine, serotonin (5-HT) and their metabolites in rat striatum and frontal cortex. In rats, PCP (5 mg/kg, i.p.) caused hyperlocomotion and stereotyped behaviors, including sniffing, head-weaving, backpedalling and turning. Both resperidone (0.8-2.4 mg/kg, p.o.) and haloperidol (0.3-1.0 mg/kg, p.o.) inhibited these behaviors, except for backpedalling, in a dose-dependent manner. PCP (10 mg/kg, i.p.) produced hyperlocomotion and stereotyped behaviors, including rearing, sniffing head-twitch, backpedalling and turning. Risperidone (0.8-2.4 mg/kg, p.o.) inhibited both hyperlocomotion and PCP-induced behaviors, except for backpedalling, while ritanserin (3-10 mg/kg, p.o.) inhibited only the head-twitch. These results suggest that risperidone may have an antipsychotic effect on schizophrenia as well as PCP psychosis in humans by exerting a mixed 5-HT2A/D2 antagonism. Neurochemically, the increasing effects of risperidone on the content of DOPAC and the ratio of DOPAC to dopamine in the striatum were lower than those of haloperidol. These findings may support the view that the extrapyramidal side effects of risperidone are lower than those of haloperidol in clinical situations.
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PMID:Effects of risperidone on phencyclidine-induced behaviors: comparison with haloperidol and ritanserin. 753 32

Phencyclidine (PCP), in a dose of 15 mg/kg, produced delayed cognitive dysfunction (at 24 h) in rats subjected to water maze tasks. At 24 h after PCP administration, ataxia, hyperlocomotion and stereotyped behavior were not induced. NE-100, N,N-dipropyl-2-[4-methoxy-3-(2-phenylethoxy)phenyl]-enthylamine monohydrochloride, a selective and potent sigma receptor ligand, was administered orally 10 min after PCP administration or 15 min before the first trial (24 h after PCP administration). In both cases, NE-100 dose-dependently attenuated the delayed cognitive dysfunction induced by PCP. As these findings show that ingestion of PCP led to delayed cognitive dysfunction similar to the cognitive signs of psychosis seen in humans, NE-100 is being further studied for possible treatment of subjects with schizophrenia.
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PMID:Effect of NE-100, a novel sigma receptor ligand, on phencyclidine- induced delayed cognitive dysfunction in rats. 760 28


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