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)

Open clinical trials have suggested that desipramine may be an effective agent for treatment of phencyclidine (PCP) or amphetamine dependence. Four pairs (eight subjects) with PCP and two pairs (four subjects) with amphetamine dependence were studied. One subject in each pair was given desipramine or placebo under double-blind conditions. Although desipramine clearly was no more effective than placebo in treatment of PCP dependence, subjects with amphetamine dependence who received desipramine remained in treatment longer and submitted more urine samples absent of amphetamine than did subjects who received placebo.
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PMID:Double-blind comparison of desipramine and placebo for treatment of phencyclidine or amphetamine dependence. 309 84

The effects of continuous i.v. phencyclidine (PCP) infusion and withdrawal on operant behavior were studied in rhesus monkeys. The monkeys were trained to lever press under a fixed-ratio 100 schedule of food presentation. They responded under this schedule during four daily 30-min periods conducted every 6 hr. After at least 5 days of continuous saline infusion through indwelling i.v. catheters, the subjects received 10 days of continuous infusion of 0.05 mg/kg/hr of PCP. During chronic PCP, rates of responding increased above saline control values. When saline was substituted for PCP, responding was suppressed markedly. This suppression of responding occurred within 8 hr of saline substitution and lasted several days. Mild signs of withdrawal were seen within 3 hr after saline substitution and dissipated by 48 hr. These signs included muscle tremors, oculomotor hyperactivity and increased aggressiveness. After responding during saline infusion had returned to control levels, continuous PCP infusion was resumed. Withdrawal effects on behavior decreased in intensity after repeated withdrawals and it was necessary to raise the infusion dose to produce consistent withdrawal disruption of behavior. Withdrawal-induced disruption in responding was reversed by acute pretreatment with PCP (0.01-0.3 mg/kg i.m.) in a dose-related fashion. Presession administration of naloxone (0.1-1.0 mg/kg i.m.) during chronic PCP infusion failed to precipitate withdrawal signs or disrupt operant responding, suggesting that PCP dependence is not of the opioid type. The results of this study indicate that operant behavior is disrupted during withdrawal from chronic PCP and can be used as evidence of behavioral dependence.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Behavioral dependence produced by continuous phencyclidine infusion in rhesus monkeys. 654 Mar 4

Rats were implanted with osmotic minipumps SC that infused either saline or 10 mg/kg/day phencyclidine (PCP) for 10 days, a regimen that produces dependence to PCP. At the end of this 10-day infusion period, the pumps were removed and the rats were sacrificed either immediately or at various time points (12 h, 1, 2, and 7 days) after pump removal. The saturation binding parameters of [3H]MK-801 were then determined in well-washed cortical/hippocampal membranes prepared from these rats. Neither the Bmax nor the Kd of [3H]MK-801 binding in membranes of PCP-treated rats differed from that determined using membranes from saline-treated rats at any time point studied. These results suggest that alterations in PCP receptors do not play a major role in the production of PCP dependence.
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PMID:[3H]MK-801 binding to well-washed rat brain membranes following cessation of chronic phencyclidine treatment. 766 65

Phencyclidine (PCP) is a drug of abuse that has rewarding and dysphoric effects in humans. The complex actions of PCP, and PCP withdrawal in particular, on brain reward function remain unclear. The purpose of the present study was to characterize the effects of withdrawal from acute and chronic PCP treatment on brain reward function in rats. A brain stimulation reward procedure was used to evaluate the effects of acute PCP injection (0, 5, or 10 mg/kg) or chronic PCP treatment (0, 10, 15, or 20 mg/kg/day for 14 days delivered via subcutaneous osmotic minipumps) on brain reward function. Withdrawal from acute administration of 5 and 10 mg/kg PCP produced a decrease in brain reward function as indicated by a sustained elevation in brain reward thresholds. When administered chronically, 10, 15, or 20 mg/kg/day PCP induced a progressive dose-dependent potentiation of brain stimulation reward, while cessation of the treatment resulted in significant elevations in reward thresholds reflecting diminished reward. Specifically, withdrawal from 15 or 20 mg/kg/day PCP induced a depression in brain reward function that lasted for the entire month of observation. These results indicate that prolonged continuous administration of high PCP doses facilitates brain stimulation reward, while withdrawal from acute high PCP doses or chronic PCP treatment results in a protracted depression of brain reward function that may be analogous to the dysphoric and anhedonic symptoms observed in PCP dependence, depression, and schizophrenia.
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PMID:Withdrawal from chronic phencyclidine treatment induces long-lasting depression in brain reward function. 1270 Jul