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 (PCP), discovered in Germany during the 1920s, has become over the past four decades the number one drug of abuse in the United States. While briefly showing promise as being the "ultimate" anasthetic agent during the late 1950s, it very quickly fell into disfavor because of untoward side-effects during post-anesthetic emergence (1960s). Some few years later (1970s), PCP began its ascent in the illicit drug market. PCP is a drug with a broad range of pharmacological activity. It has been implicated as a major cause of psychiatric decompensation and has a number of clinical syndromes described in the literature. In addition, PCP has been shown to cause significant medical morbidity and mortality.
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PMID:Phencyclidine: pharmacologic and clinical review. 640 May 96

Phencyclidine (PCP) and d-amphetamine (AMP) had different effects upon homovanillic acid (HVA) levels in rat prefrontal cortex as compared to caudate. Lower doses of PCP increased HVA in prefrontal cortex only while lower doses of AMP decreased HVA in caudate alone. Higher doses of both drugs produced a decreased HVA in caudate and an increase in prefrontal cortex. At some doses PCP may selectively activate mesocortical dopaminergic neurons.
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PMID:Homovanillic acid in rat caudate and prefrontal cortex following phencyclidine and amphetamine. 643 82

Phencyclidine (PCP), haloperidol, and naloxone were administered alone and in combination to rats responding under a fixed-interval schedule for water presentation. Lower doses of PCP (0.25-2.0 mg/kg) and naloxone (0.001-0.1 mg/kg) produced increases while higher doses produced dose-dependent decreases in response rate. Haloperidol (0.0625-0.5 mg/kg) produced a monotonic dose-dependent decrease in responding. When a dose of naloxone (8.0 mg/kg) that did not alter responding was administered prior to the PCP, the PCP dose-response curve was shifted to 6.5-fold lower doses of PCP. When a dose of haloperidol (0.0625 mg/kg) that did not alter responding was administered prior to the PCP, the PCP dose-response curve was shifted to 1.5-fold higher dose of PCP. These observations are discussed in relation to current views of the mechanism of PCP action.
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PMID:Effects of phencyclidine, haloperidol, and naloxone on fixed-interval performance in rats. 643 87

The stimulation of motor activity by phencyclidine was found to differ significantly in BALB/c and C57Bl/6By inbred strains of mice. Phencyclidine-induced stimulation was compared for these strains, their reciprocal F1 hybrids, and their recombinant inbred offspring. There were significant differences in responsivity among the strains, suggesting a genetic influence on the PCP response; however, the strains did not segregate into two distinct groupings, suggesting that this genetic influence was not carried by a single gene. In addition, there was no relationship between the responsivity of these strains of mice to PCP and their previously-reported responses to amphetamine or scopolamine, which suggests that PCP-induced stimulation is not a simple cholinergic or amphetamine-like response.
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PMID:Genetic effects on PCP-induced stimulation in recombinant inbred strains of mice. 646 86

Male rats were given subcutaneous injections of saline or 0.25 to 5.0 mg/kg phencyclidine (PCP) either five or 35 minutes prior to being presented with 121 startling tactile (air-puff) stimuli at 15 second intervals. Phencyclidine increased startle with an inverted-U dose-response relationship, the maximal increase being produced by 1.0 mg/kg. Doses of 0.5 or 1.0 mg/kg PCP also produced a reduced rate of behavioral habituation, which, in the latter case, was shown to be independent of the time since drug administration. These results are interpreted as indicative of an impairment of behavioral habituation being the threshold effect of PCP on tactile startle.
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PMID:Increased startle responding in rats treated with phencyclidine. 647 61

Phencyclidine (PCP) is a drug of abuse which is commonly taken by inhalation or snorting. By this pathway, it comes in direct contact with the alveolar macrophages (AM) which phagocytize inhaled particles. The activated AM produce reactive oxidative products and release photons with resulting chemiluminescence (CL) that can be quantified in the presence of luminol. The effect of PCP on this functional ability has been studied. PCP-treated rat-AM in vitro causes a two-to threefold increase in CL emission, after challenging with zymosan particles. This CL augmentation by PCP appears not to be associated with increased phagocytosis. Several metabolic inhibitors have been studied, and only rotenone has been found to inhibit CL production to a greater degree with PCP than in its absence. It may be assumed that the enhanced CL produced in the presence of PCP is due to activation of the drug by some reactive oxygen state or states that are affected by rotenone.
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PMID:Phencyclidine-dependent chemiluminescence of rat alveolar macrophages. 657 14

Phencyclidine was introduced as an anaesthetic in 1960; and has now become a major drug of abuse in some countries. The rapid advance in the various fields of analytical chemistry during the past decades has made it possible to measure the levels of the compounds in tissues and body fluids. These methods may also be used to study the metabolism and pharmacokinetics of PCP. The resulting publication is an updated guide to these analyses particularly with the application of these techniques in human intoxication.
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PMID:Guide to the analysis of phencyclidine and its metabolites in biological material. 657 50

Phencyclidine (PCP), a semirigid molecule containing a cyclohexane ring with vicinally attached aromatic and piperidine rings, produces characteristic discriminative stimulus properties and pupillary miosis in rats. The effectiveness of a series of aromatic and nitrogen substituted analogs of PCP in producing PCP-like discriminative stimuli and changes in pupil diameter was determined in rats trained to discriminate between saline and 3.0 mg/kg of PCP. Dexoxadrol and its optical isomer levoxadrol were also evaluated for purposes of comparison. Analogs in which the electron-density of the aromatic ring was increased (3NH2-PCP) or only slightly reduced (3F-PCP) retained PCP-like activity. A loss of PCP-like activity occurred with analogs in which the electron-density of the aromatic ring was greatly reduced (3NO2-PCP) or extended to a larger system (1NCP and 2NCP). PCP-like activity also was abolished in analogs in which the distance between the aromatic ring and the remainder of the molecule was systematically increased by one, two or three methylene units. In contrast, substitutions on the nitrogen atom altered the potency, but not the efficacy, of such analogs. Dexoxadrol produced PCP-like activity whereas its optical enantiomer levoxadrol was devoid of such activity. These findings suggest a drug receptor surface with multiple domains or subsites which recognize regions of structural overlap among the phencyclidines, dioxolanes and psychotomimetic benzomorphan derivatives.
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PMID:Structure-activity relationship studies of phencyclidine derivatives in rats. 669 98

Phencyclidine (PCP), naloxone and haloperidol were administered alone and in combination to rats trained to drink sweetened-condensed milk during a 20 min daily session. PCP (1.0-16.0 mg/kg) produced a dose-dependent decrease in milk intake. All doses of naloxone (0.1-16.0 mg/kg) produced approximately a 30% decrease in milk intake. Haloperidol (0.125 mg/kg) had virtually no effect on milk intake. When a dose of naloxone which reduced milk intake by approximately 30% (8.0 mg/kg) was administered as a pretreatment to the PCP, the PCP curve was shifted to the left (lowered) to that degree. When haloperidol (0.125 mg/kg) was administered as a pretreatment to the PCP, the PCP dose-response curve was shifted 1.5 fold to the right. These interactions are similar to those observed in other behavioral paradigms and are discussed in reference to PCP's actions as an indirect dopaminergic agonist.
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PMID:Interactions of naloxone and haloperidol with phencyclidine: effects on milk intake. 670 72

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


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