Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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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

[3H]Phencyclidine (PCP) bound specifically and with high affinity (Kd = 0.15 microM at pH 7.4) to a single saturable class of binding sites in rat brain membrane preparations. Specific binding constituted approximately 70% of total binding at 0 degrees C and 33% of total binding at 37 degrees C (at 10 nM [3H]PCP). Bound [3H]PCP could be displaced by nonradioactive PCP, a series of its derivatives, and the psychotomimetic opiate N-allylnorcyclazocine (SKF 10,047) with relative potencies that closely paralleled those determined in animal behavioral tests. Muscarinic cholinergic ligands inhibited [3H]PCP binding, but only at 0.1 mM and in rank order at variance with that for binding to muscarinic sites or for pharmacological potencies. Other drugs, including opiates other than SKF 10,047, were unable to displace specifically bound [3H]PCP at 0.1 mM. [3H]PCP binding was most enriched in crude synaptosomal subcellular fractions, and was about three times higher in hippocampus (region of highest density) than in cervical spinal cord (region of lowest density). Trypsin and Pronase reduced specific [3H]PCP binding. Thus, PCP may exert its effects on the central nervous system via binding to specific brain receptor sites.
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PMID:Specific [3H]phencyclidine binding in rat central nervous system. 29 53

Phencyclidine (PCP) is a potent sympathomimetic and hallucinogenic dissociative anesthetic agent. As an abused street drug, it is most often smoked, thus allowing the user to titrate the dose. The clinical signs of PCP intoxication can be viewed in three dose-related stages, but waxing and waning of signs through the three stages is not uncommon. Treatment protocols for each stage address drug therapy and both clinical and psychological supportive measures.
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PMID:Emergency management of acute phencyclidine intoxication. 43 46

Phencyclidine (PCP) impaired spatial alternation performance in rats. This effects was mimicked by antimuscarinic anticholinergics (scopolamine, atropine) and PCP derivatives (ketamine, cyclohexamine) but not by a variety of other agents. Muscarinic cholinergic agonists antagonized PCP. Impairment of spatial alteration performance by PCP appears to be mediated, at least in part, by and anticholinergic action; this is the first instance of a behavioral effect of PCP that can be largely attributed to a specific mechanism.
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PMID:Anticholinergic behavioral effect of phencyclidine. 51 Mar 89

Phencyclidine (PCP) is an illicit drug with a high potential for negative effects. It is easy to synthesize and difficult to control because the precursors are easy to obtain. DAWN data shows that PCP episodes in emergency rooms and hospitals have increased from the twenty-third most frequently observed drug in 1973 to sixteenth in 1975. One explanation for the increase in PCP use is the change in the mode of administration from pill to smoking. An exploratory study of a local outbreak of PCP describes the effects of PCP and the dilemma facing the user. Regular PCP use is difficult to hide, but since stigma is attached to PCP use, the PCP user is reluctant to admit to regular use.
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PMID:Phencyclidine (PCP): a local and national perspective. 61 89

Phencyclidine (PCP) is a dissociative veterinary anesthetic and tranquilizer that at present is being abused as a psychedelic and hallucinogenic agent with increasing frequency. The cases of two young patients suffering from phencyclidine toxicity are reported. In each, central nervous system depression was accompanied by an acute dystonic motor reaction resulting in acute rhabdomyolysis and myoglobinuria. Skeletal muscle injury was felt to be the result of excessive involuntary isometrimc motor activity rather than a direct effect of phencyclidine on skeletal muscle. Patients suffering from phencyclidine intoxication should be screened for acute rhabdomyolysis. Phencyclidine intoxication should be included in the differential of nontraumatic rhabdomyolysis and should be considered among the potential causes of acute myoglobinuric renal failure.
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PMID:Phencyclidine-associated acute rhabdomyolysis. 62 51

delta9-Tetrahydrocannabinol (THC; 2.5, 5.0, 10.0 mg/kg, PO) impaired avoidance and rotarod performance, and caused bradycardia and hypothermia. Phencyclidine (PCP; 1.25, 2.5, 5.0 mg/kg, IP) impaired avoidance and rotarod performance and caused a marked increase in photocell activity. When combined, the depressant properties of each drug were enhanced and the stimulation of photocell activity cg/kg THC and its interactions with PCP followed subacute treatment for six days, whereas many of the effects of PCP were enhanced after subacute treatment with a dose of 2.5 mg/kg. Open-field behavior was affected by each drug alone and in combination in a similar way as photocell activity, but the depression caused by their interaction was greater; both drugs caused an increase in urination. Response rates on an FR-10 schedule of food reinforcement were decreased by 2.5 mg/kg PCP, but not by 5.0 mg/kg THC; the combination caused greater response suppression than either drug alone. The functional interactions between THC and PCP were not related to changes in the concentrations of 14C or 3H in plasma or brain derived from 14C-delta9-THC and 3H-PCP, respectively.
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PMID:Interactions between delta9-tetrahydrocannabinol and phencyclidine hydrochloride in rats. 85 Jun 86

1. Phencyclidine (PCP) block of Ca2+ channel current in enzymatically dissociated neurones from the CA1 region of the adult guinea-pig hippocampus was studied using whole-cell voltage clamp techniques. Ca2+ channel current was recorded with 3 mM-Ba2+ as the charge carrier. Na+ currents were blocked with tetrodotoxin and K+ currents were eliminated by using tetraethylammonium and N-methyl-D-glucamine as the predominant extracellular and intracellular cations, respectively. 2. Peak Ca2+ channel current evoked by depolarization from -80 to -10 mV was reduced in a use-dependent fashion by PCP. The apparent forward and reverse rate constants for block at the depolarized voltage were 10(6) s-1 M-1 and 11-14 s-1, respectively. These values were at least 60 times faster than the corresponding rates at the resting voltage. The steady-state block produced by PCP increased in a concentration-dependent fashion with an IC50 of 7 microM. Other dissociative anaesthetic drugs were substantially weaker inhibitors of the current (tiletamine > dizocilpine (MK-801) > ketamine). 3. The Ca2+ channel current recorded under identical conditions in rat dorsal root ganglion neurones was less sensitive to blockade by PCP (IC50, 90 microM). 4. PCP block of the hippocampal Ca2+ channel current occurred in a voltage-dependent fashion with the fractional block decreasing at positive membrane potentials. Analysis indicated that the PCP blocking site senses 56% of the transmembrane electric field. 5. Analysis of tail currents recorded at -80 mV demonstrated that PCP does not affect the voltage-dependent or time-dependent activation or deactivation of the Ca2+ channel current. 6. The rate and extent of inactivation of the Ca2+ channel current was maximal at -10 mV and diminished at more positive potentials. Experiments with Ba(2+)-free external solution demonstrated that inactivation of the Ca2+ channels is largely voltage-dependent and is not affected by Ba2+ influx. 7. PCP markedly increased the apparent extent of inactivation of the Ca2+ channel current during prolonged voltage steps. This increase in apparent inactivation was more pronounced at depolarized potentials. Inactivation at -10 mV proceeded in two exponential phases; PCP had little effect on the fast decay phase and caused a moderate speeding of the slow decay phase. Although block of the activated state evolved on the same time scale as inactivation, the apparent rate of inactivation was not increased in a concentration-dependent fashion by PCP indicating that the block does not occur by a conventional open channel mechanism.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Phencyclidine block of calcium current in isolated guinea-pig hippocampal neurones. 133 8

The effects of N-methyl-D-aspartic acid (NMDA) and phencyclidine (PCP) on extracellular levels of dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) in the striatum of the rat were studied using in vivo microdialysis. Intrastriatal infusion of NMDA produced a significant dose-dependent increase in extracellular DA and a decrease in concentrations of DOPAC. Whereas both 2-amino-5-phosphonovalerate (APV) and PCP antagonized the NMDA-induced increase in extracellular levels of DA, the effect on NMDA-induced changes in extracellular concentrations of DOPAC were different for the two compounds. The APV significantly attenuated the decrease in extracellular DOPAC produced by smaller concentrations of NMDA, whereas PCP did not prevent decrease in DOPAC produced by any concentrations of NMDA. Phencyclidine alone produced a dose-dependent increase in extracellular DA but had no effect on the extracellular concentration of DOPAC. This study demonstrated that PCP, at concentrations which did not produce an increase in extracellular DA, antagonized the effect of the NMDA on DA. The data also indicated that both APV and PCP antagonized the NMDA-evoked release of DA over a range of concentrations of NMDA, even though they did so by different mechanisms.
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PMID:The effect of phencyclidine and DL-2-amino-5-phosphonovaleric acid on N-methyl-D-aspartic acid induced changes in extracellular concentration of dopamine and DOPAC in the rat neostriatum. 134 11

Phencyclidine (PCP), a drug inducing schizophrenia-like symptoms in humans, is reported to be a non-competitive antagonist at the N-methyl-D-aspartate (NMDA) subtype of excitatory amino acid receptors. In rats, PCP produces three dose-dependent stages of EEG patterns: 1) increase of cortical desynchronization duration; 2) increase of the amplitude of the high-frequency (20-30 Hz) low-voltage (30-50 microV) cortical background activity; 3) appearance of cortical slow (2-3 Hz) wave-sharp wave complexes. These EEG changes are accompanied by stimulatory-depressive effects such as stereotypy (circling, head weaving) and ataxia. In the present study, the EEG and behavioural effects induced by systemic administration of the NMDA antagonists dizocilpine (MK 801), dextromethorphan (DM), [(+)-alpha-(4-chlorophenyl)-4- [(phenyl)methyl-1-piperidine ethanol] (SL 82.0715), (+)3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), cis-4-phosphonomethyl-2-piperidine-carboxylic acid (CGS 19755) have been compared to those of PCP in rats. The rank of potency for inducing PCP-like EEG stages 1-3 was as follows: MK 801 > PCP > CGS 19755 > CPP. These drugs also induced PCP-like behavioural effects. On the contrary, DM and SL 82.0715, administered up to the dose of 100 mg/kg IP, failed to induce PCP-like behavioural effects and elicited only the stage 1 of PCP-like EEG. These results strongly suggest the involvement of NMDA neurotransmission in the behavioral and EEG effects of PCP.
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PMID:Different capability of N-methyl-D-aspartate antagonists to elicit EEG and behavioural phencyclidine-like effects in rats. 136 27


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