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)

Phencyclidine use has been noted to produce a psychosis of several week's duration in a small fraction of users. Descriptions of the premorbid personalities of those who became psychotic resemble descriptions of LSD and marijuana users who experienced prolonged psychiatric difficulty. In addition, the psychosis produced can often be recognized as a "hallucinogen" psychosis. Certain features of the phencyclidine psychosis, namely the neurologic abnormalities, dose-related severity of symptoms, and regularity of the length of illness, are not noted with other psychedelic drugs, leading to the conclusion that PCP psychosis is a drug effect rather than a brief functional psychosis precipitated by the disintegrating PCP experience. However, the infrequent occurrence of psychosis in the (apparently) large exposed population still suggests that this is a combination of drug effect and vulnerable, pathologic personality.
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PMID:Psychiatric sequelae of phencyclidine abuse. 1 Jan 26

In 15 patients hospitalized with phencyclidine (PCP) psychosis, several measures of psychopathology were examined in relationship to urine PCP levels, duration of hospitalization and mode of intoxication. Duration of hospitalization was found to be significantly shorter for smokers than for ingesters of PCP. Impaired ability to estimate 30 seconds duration was found to correlate significantly with a higher urine PCP level and a longer hospitalization. No other measure of psychopathology was found to correlate with either duration of hospitalization or urine PCP levels, now were other measures of psychopathology found to distinguish these patients from patients with acute functional mental illness.
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PMID:Acute phencyclidine (PCP) intoxication: psychopathology and prognosis. 68 4

In fifteen patients hospitalized with phencyclidine (PCP) psychosis, several measures of psychopathology, including those of time distorsion, were examined in relationship to urine PCP levels and duration of hsopitalization. Impaired ability to estimate thirty seconds duration was found to correlate significantly with a higher urine PCP level and a longer hospitalization, the test for ability to estimate thirty seconds may be useful in clinical management of patients with PCP psychosis particularly when there is no urine PCP level available.
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PMID:Time distortion in acute phencyclidine (PCP) psychosis. A correlation between 30 seconds estimation and urine drugs levels. 71 Mar 64

Concentrations of phencyclidine in blood and liver are presented in five fatal cases occurring in Los Angeles County in 1976. Eleven other deaths in which phencyclidine contributed to death are described; acute psychotic reactions were observed in some of these cases. Two cases involved the drowning of individuals whose swimming capabilities may have been diminished from the effects of PCP. One case is presented in which a 20-year-old male took a massive overdose of phencyclidine for suicidal purposes.
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PMID:Phencyclidine-related deaths in Los Angeles County, 1976. 74 79

Adult mice were exposed to long-term phencyclidine (PCP) treatments as animal models for psychosis. The drug was administered via osmotic minipumps implanted subcutaneously in the backs of the mice. The treatments for 7 days with 2.5 and 1 mg/d/mouse and the treatment for 3 days with 1 mg/d/mouse differentially affected the release of dopamine and D-aspartate from striatal and frontal cortical slices. In frontal cortical slices the potassium-stimulated release of dopamine increased, whereas the release of D-aspartate varied with the PCP dose. In striatal slices the release of D-aspartate was either decreased or unchanged, whereas the release of dopamine was mostly unchanged. The 3-day treatment with PCP followed by the 3-day period of withdrawal increased the potassium-stimulated release of dopamine from frontal cortical slices and decreased that from striatal slices. In brain slices from untreated mice PCP increased the release of dopamine in vitro, whereas the release of D-aspartate was not affected. It seems that PCP has region-specific effects on both dopaminergic and glutamatergic transmission in the central nervous system, and it may thus serve as an interesting experimental model for further research on psychosis.
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PMID:Phencyclidine treatments differentially affect dopamine and D-aspartate release from frontal cortical and striatal slices from mice. 134 50

The psychotomimetic drug 1-(1-phenylcyclohexyl) piperidine (PCP, phencyclidine) was found to cause a deficit in the gating of the response of the hippocampal neuron to repeated auditory stimuli, which is similar to a particular physiological feature observed in human psychosis. Other drugs, with sigma agonist and/or N-methyl-D-aspartate (NMDA) antagonist effects, were administered and their ability to cause a loss of auditory gating was compared to that of PCP. The rank order of effectiveness was levoxodrol > PCP and (+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d)cyclohepten-5,10-imine maleate (MK-801) > N-allylnormetazocine (SKF 10047) > dexoxodrol > 3-(+/-)2-carboxypiperazine-4-yl) propyl-1-phosphonate (CPP). Further studies of two of the drugs, PCP and MK-801, showed that selective lesioning of the noradrenergic input with the neurotoxin DSP4, as well as less selective depletion of monoamines with reserpine, blocked the loss of gating. Phencyclidine, and other drugs with the same spectrum of action, most likely disrupt gating by increasing noradrenergic activity through a sigma mechanism.
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PMID:Phencyclidine and auditory sensory gating in the hippocampus of the rat. 143 86

The non-competitive NMDA receptor antagonists, PCP (phencyclidine), MK801, and ketamine produce psychosis in humans and abnormal vacuoles in posterior cingulate and retrosplenial rat cortical neurons. We show that PCP (> or = 5 mg/kg), MK801 (> or = 0.1 mg/kg), and ketamine (> 20 mg/kg) induce hsp70 mRNA and HSP70 heat shock protein in these vacuolated, injured neurons, and PCP also induces hsp70 in injured neocortical, piriform, and amygdala neurons. The PCP, MK801, and ketamine drug induced injury occurs in 30 day and older rats, but not in 0-20 day old rats, and is prevented by prior administration of the antipsychotic drugs haloperidol and rimcazole. Since haloperidol and rimcazole block dopamine and sigma receptors, and since M1 muscarinic cholinergic receptor antagonists also prevent the injury produced by PCP, MK801, and ketamine, future studies will be needed to determine whether dopamine, sigma, M1, or other receptors mediate the injury.
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PMID:Haloperidol prevents induction of the hsp70 heat shock gene in neurons injured by phencyclidine (PCP), MK801, and ketamine. 148 94

Drugs (e.g., PCP) which interfere with glutamatergic transmission at the N-methyl D-aspartate (NMDA) subclass of glutamate receptors precipitate both positive and negative symptoms of psychosis in humans. Based on a proposed "glutamatergic deficiency" in schizophrenia, pharmacologic facilitation of NMDA-mediated neural transmission by direct stimulation of the strychine-insensitive glycine binding site was attempted with "low-dose" milacemide, an acylated "prodrug" of glycine that readily crosses the blood brain barrier and is converted into glycine in the brain. In a prior study, "high-dose" milacemide proved to have no therapeutic utility in schizophrenia. The failure was thought, possibly, to be related to higher doses of milacemide having antagonist actions at the NMDA receptor complex. In the current study, "low-dose" milacemide (400 mg/day), as the sole pharmacotherapeutic agent, was also without significant clinical benefit. Despite our negative findings for milacemide, other strategies for facilitating NMDA-mediated neural transmission in schizophrenia might be worth pursuing.
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PMID:An NMDA intervention strategy in schizophrenia with "low-dose" milacemide. 153 74

Phencylidine (PCP) is a major drug of abuse in the United States. It produces a toxic confusional psychosis in man. We show here that nanomolar to micromolar concentrations of PCP and behaviorally active congeners selectively block voltage-regulated noninactivating (or very slowly inactivating) presynaptic K channels in the brain. The rank order of potency for blockage of these K channels parallels both the relative ability of these agents to produce characteristic behavioral deficits in rats and their ability to displace [3H]PCP from its high-affinity binding sites in brain. In view of the enhanced voltage-gated Ca influx that would be expected to accompany blockage of presynaptic K channels, this mechanism could explain the excessive neurotransmitter release that is characteristic of PCP intoxication.
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PMID:Phencyclidine in low doses selectively blocks a presynaptic voltage-regulated potassium channel in rat brain. 241 37

Hallucinogenic drugs are unique in that they produce the desired hallucinogenic effects at what are considered non-toxic doses. The hallucinogenic drugs can be categorised into 4 basic groups: indole alkaloid derivatives, piperidine derivatives, phenylethylamines and the cannabinols. The drugs reviewed include lysergic acid diethylamide (LSD), phencyclidine (PCP), cocaine, amphetamines, opiates, marijuana, psilocybin, mescaline, and 'designer drugs.' Particularly noteworthy is that each hallucinogen produces characteristic behavioural effects which are related to its serotonergic, dopaminergic or adrenergic activity. Cocaine produces simple hallucinations, PCP can produce complex hallucinations analogous to a paranoid psychosis, while LSD produces a combination of hallucinations, pseudohallucinations and illusions. Dose relationships with changes in the quality of the hallucinatory experience have been described with amphetamines and, to some extent, LSD. Flashbacks have been described with LSD and alcohol. Management of the intoxicated patient is dependent on the specific behavioural manifestation elicited by the drug. The principles involve differentiating the patient's symptoms from organic (medical or toxicological) and psychiatric aetiologies and identifying the symptom complex associated with the particular drug. Panic reactions may require treatment with a benzodiazepine or haloperidol. Patients with LSD psychosis may require an antipsychotic. Patients exhibiting prolonged drug-induced psychosis may require a variety of treatments including ECT, lithium and l-5-hydroxytryptophan.
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PMID:Clinical features and management of intoxication due to hallucinogenic drugs. 268 30


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