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

Most street hallucinogens contain either LSD or phenycyclidine HCl (PCP). Because the acute phase of LSD and PCP mimic several other drugs and conditions, it is important to exclude these other possibilities. When faced with LSD or PCP, "talking down" usually suffices for the mild case; management becomes more complex should hyperpyrexia, coma, seizures or a hypertensive crisis ensue. Diazepam, not a phenothiazine, is preferred for sedation.
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PMID:Management of hallucinogen abuse. 106 15

In this review phencyclidine and related arylcyclohexylamines and hallucinogens, using LSD as the prototype, are considered as two distinct classes of abused drugs. Within these classes drugs that are found on the street are discussed, and a current epidemiological summary is provided. The abuse liability and dependence potential of these drugs are evaluated by considering four major determinants of their abuse. First, is the ability of a drug to function as a positive reinforcer and increase the probability of operant behavior leading to its delivery. Animal data describing the reinforcing effects of PCP are reviewed with respect to the influence of variables controlling drug-reinforced behavior; however, there are no animal models of hallucinogen-reinforced behavior. Several methods of quantifying reinforcing efficacy are discussed. A second determinant is the subjective effects of the respective drugs. These effects are described and compared across drugs based on clinical reports in humans and drug discrimination studies in animals. A third determinant is the behavioral and physiological toxicity that results from acute and chronic use of these drugs. Clinical reports and results of sensitive tests that have been developed for laboratory animals are reviewed. A fourth determinant is the dependence potential that exists with these drugs, measured by tolerance development and the extent to which behavioral and physiological disturbances occur when drug use is terminated.
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PMID:PCP and hallucinogens. 219 84

Patterns of adolescent drug use in Greece (N = 174) and the United States (N = 2,610) are compared. The rates of self-reported lifetime alcohol and cigarette use are rather similar. For other drugs (marijuana, amphetamines, depressants, cocaine, LSD, PCP, and heroin) there is much more drug use in the United States. A causal model employing variables from social control and social learning theories is applied to drug use in both samples. We conclude that American theories of adolescent deviance assume certain cultural conditions, and therefore may need revision before they can be fruitfully applied to the behavior of young people in other cultures.
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PMID:Cultural patterns and causal processes in adolescent drug use: the case of Greeks versus Americans. 326 93

The dorsal root potential (DRP) evoked by stimulation of the inferior central nucleus (ICN) of the cat is affected by administration of a variety of hallucinogenic agents. It has been previously shown that a single low dose of LSD is unique in that it potentiates this DRP, while injections of 5-methoxy-N,N- dimethyltryptamine (5-MeODMT), ketamine or phencyclidine (PCP) inhibit its production. Tolerance develops to the facilitatory effect of low doses of LSD on the DRP, but not to the inhibitory action of 5-MeODMT. Repeated injections of ketamine every 30 minutes also fail to produce tachyphylaxis to the inhibitory effect of this dissociative anesthetic. The raphe-evoked DRP is a long latency potential that is inhibited by a wide variety of putative serotonin antagonists and has therefore been traditionally thought to be mediated by serotonin. However, in light of the inability of either tryptophan or fluoxetine to potentiate this DRP, and the resistance of this DRP to blockade by parachlorophenylalanine, reserpine or intrathecally administered 5,7-dihydroxytryptamine, it appears that this potential may in fact be mediated, at least in part, by a non-serotonergic transmitter.
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PMID:Action of hallucinogens on raphe-evoked dorsal root potentials (DRPs) in the cat. 395 25

Although barbiturates are often effective as therapeutic agents in several types of brain ischemia, there is no consensus as to their mechanisms of action. Exactly why other intravenous anesthetics such as ketamine are not effective therapies in brain ischemia is not known. Structural analogs of ketamine such as phencyclidine (PCP) not only exert potent hallucinogenic properties and are widely abused drugs, but often result in hypertensive encephalopathies and death. In view of the paucity of information on the cerebral circulatory actions of barbiturates, ketamine and PCP (and analogs), in-vivo (microcirculatory) and in-vitro studies were undertaken. Barbiturates, in anesthetic concentrations (e.g., 10(-5) to 10(-4) M), were found to exert direct vasodilator actions on cerebral arterial smooth muscle; these relaxant actions appear to be related to inhibition of calcium ion (Ca2+) influx in cerebral vessels. The latter may be important in the salutory actions of barbiturates in brain ischemia, head trauma and cerebrovasospasm. Unlike barbiturates, ketamine was found to exert spasmogenic actions on cerebral arteries, which may aid in explaining the inability of this anesthetic to be of therapeutic value in brain ischemia. PCP and its analogs, as well as other hallucinogenic molecules (e.g., LSD, mescaline) produced spasms in cerebral arterioles, venules and arteries in concentrations which mimic their hallucinogenic potencies. Distinct PCP-like receptors which subserve contraction appear to exist on large as well as microscopic cerebral blood vessels. Spasms induced by PCP, its analogs and ketamine can be readily reversed or prevented completely by calcium channel blockers. The latter agents could be quite useful, clinically, in prevention of cerebral infarction, hypertension and fatality associated with PCP (and analogs) intoxication.
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PMID:Effects of barbiturates, phencyclidine, ketamine and analogs on cerebral circulation and cerebrovascular muscle. 640 Apr 29

Groups of rats, acclimated to drinking both water and 10% v/v ethanol were implanted with a variety of slow-release devices containing d-amphetamine (d-amp), nicotine, caffeine, phencyclidine (PCP), secobarbital, LSD, mescaline or haloperidol. Ethanol intake was elevated only during treatment with d-amp or nicotine; none of the other drugs affected ethanol consumption even though the amounts of all drugs released were pharmacologically sufficient to affect behavior. Nicotine treated rats were not simply seeking calories provided by the EtOH solution, since nicotine treatment did not enhance intake of a distinctively flavored solution isocaloric to 10% ethanol. These results support a self-medication model of ethanol intake.
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PMID:Ethanol intake increases during continuous administration of amphetamine and nicotine, but not several other drugs. 686 54

Four hundred forty-three impoverished medical patients, many of whom were homeless, were studied to determine whether homelessness is an independent predictor of current substance use. Twenty-four percent of the sample of patients were frequent alcohol users (i.e., daily or almost daily), and 18% had recently used illegal drugs (cocaine, heroin, PCP, LSD). Marijuana use was not included in the drug use variable. Bivariate analyses revealed that frequent alcohol was associated with being homeless, male, less educated, a veteran, unemployed, and having more children. Frequent alcohol users also were more likely to be sexually active, have had suicidal thoughts, a previous psychiatric hospitalization or felony conviction, an accident or injury, and poor physical health. Self-reported use of illegal drugs was associated with being younger, U.S. born, never married, having a poor mood, and a mental health problem or substance use by a parent. Use of illegal drugs was associated with being homeless, male, less educated, sexually active, and having a previous felony conviction or psychiatric hospitalization. Once demographic and family characteristics were controlled for, housing status was not related to either frequent alcohol or illegal drug use. Substance use among impoverished patients was a reflection of their historical social backgrounds rather than of their current housing status. Helping these patients to obtain stable housing may not impact the substance use of homeless persons.
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PMID:Substance use among impoverished medical patients: the effect of housing status and other factors. 836 78

A social control drug progression model was delineated and tested using a sample of 2,626 high school students from the southwestern United States. Along with the social control constructs of parental attachment, educational attachment, religious attachment, and conventional values, we incorporated alcohol, cigarette, and marijuana use into the model as intervening variables. The model explains 39% of the variation in the self-reported amphetamine use and 24% of the variation in "hard drug" use (cocaine, heroin, LSD, and PCP). The findings suggest that the integration of social control theory and drug progression improves the predictive power of the model of adolescent drug use.
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PMID:Drug progression model: a social control test. 853 Feb 12

Frontal-subcortical circuits provide a comprehensive framework for understanding the anatomy, biochemistry, and pharmacology of behavior. The three principal behaviorally relevant circuits originate in the dorsolateral prefrontal cortex, orbitofrontal cortex, and anterior cingulate cortex, respectively. Circuit-specific marker behaviors associated with each circuit are executive dysfunction (dorsolateral prefrontal-subcortical circuit), disinhibition and OCD (orbitofrontal-subcortical circuit), and apathy (medial frontal-subcortical circuit). Environmental dependency is common to all prefrontal-subcortical syndromes and may reflect disruption of working memory. Depression, mania, and psychosis are mediated by structures involved in prefrontal-subcortical circuits and are circuit-related but not circuit-specific behaviors. The actions of PCP, LSD, serotonergic antidepressants, anxiolytics, sedative-hypnotics, antipsychotic agents, and ethanol may all be partially or primarily mediated through transmitter systems and receptor effects expressed through frontal-subcortical circuits.
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PMID:Anatomic and behavioral aspects of frontal-subcortical circuits. 859 19


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