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)

Effects of acute and chronic administration of phencyclidine (PCP) on EEG activities and gross behavior were studied in monkeys with electrodes implanted in the brain. Administration of PCP (2.0 or 4.0 mg/kg i.v.) in monkeys produced a biphasic pattern of inhibition and excitation of behavior during 6-8 h observation period. The inhibitory phase appeared 1-3 min after PCP injection, and was uniquely characterized by high-voltage slow waves with delta waves (0.6-0.8 c/sec) in the parietal lobe and by those with theta waves (4-5 c/sec) in the occipital lobe and hippocampus during behavioral stupor. This inhibitory phase lasted 1-1.5 h, and subsequently, high-voltage fast wave with enhancement of theta waves and nystagmus appeared during behavioral arousal. Upon chronic PCP administration, the intensity and duration of the inhibitory phase progressively decreased, while the effects of the excitatory phase increased. The results suggest that PCP administration in monkeys produces a biphasic pattern of inhibitory and excitatory effects and upon chronic administration a tolerance develops to the inhibitory effect while an augmentation of the excitatory effect develops.
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PMID:Phencyclidine (PCP): effects of acute and chronic administration on EEG activities in the rhesus monkey. 257 2

Experiments were conducted to evaluate the degree of phencyclidine (PCP)-like activity associated with the dextro and levo enantiomers of the sigma agonist N-allylnormetazocine (NANM). In chronic spinal dogs, d- and l-NANM generally produced similar physiologic and gross animal behavior effects which included miosis, tachycardia, hyperthermia, increased secretory activity (lacrimation, rhinorrhea and salivation), nystagmus and stereotyped head movements. For these effects, d- and l-NANM were generally equal in potency and both were about 1/10th as potent as PCP. However, the NANM enantiomers could be differentiated on the basis of their effects on nociceptive reflexes. Comparisons of dose-response curves and efficacies demonstrated that d-NANM was more similar to PCP in its effectiveness in depressing the flexor and skin twitch reflexes than was l-NANM. In addition, naltrexone selectively antagonized or reduced only the effects of l-NANM on reflex activity. In intact dogs, d-NANM and PCP, but not l-NANM maintained self-administration behavior under FR15 or FI900 (FR10:S) schedules of reinforcement. This represented the most stereospecific action of the NANM enantiomers. Additionally, l-NANM failed to maintain self-administration behavior, even following pretreatment with naltrexone, thus suggesting that the opiate activity of l-NANM was not responsible for its lack of reinforcing efficacy. Taken together, the data demonstrate that both d- and l-NANM have PCP-like properties, but d-NANM is pharmacologically more equivalent than l-NANM to PCP and l-NANM has additional activity which is not PCP-like.
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PMID:Pharmacologic and reinforcing properties of phencyclidine and the enantiomers of N-allylnormetazocine in the dog. 378 Apr 14

Five infants and two young children were treated at a large children's hospital for phencyclidine intoxication. The clinical symptoms and signs were mostly neurologic, including diminished response to tactile and verbal stimuli (100%), ataxia (71%), nystagmus (57%), constricted pupils (57%), depressed sensorium, and stupor associated with a blank, expressionless stare (57%). Notably absent were the behavioral aberrations such as aggression, which are usually seen with PCP intoxication in older children and adults. The possibility of drug intoxication was denied by most of the parents or surrogate parents accompanying these small children and infants for treatment. It is suggested that a systematic investigation for possible PCP exposure, including a urine toxicology screen for PCP (preferably by immunoassay methods), be conducted whenever an infant or child is brought for emergency treatment of unresponsiveness, bizarre behavior, dyskinesis, dystonic posturing, atypical oculomotor and pupil findings, or evidence of hallucinations.
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PMID:PCP intoxication in seven young children. 379 69

Studies on the effects of PCP have been conducted in volunteers in the Army Laboratories and elsewhere and in illicit users. The present review has summarized the observations of many investigators which showed that the acute effects of PCP following several routes of administration were shown to be dose-related. High doses of PCP produce disturbing manifestations including psychosis, numbness, light-headedness, vertigo, ataxia, and nystagmus due to acute intoxication. Furthermore, some subjects became irritable, argumentative or negative under the conditions of social stress and demanding tasks. In addition to a variety of central action, PCP has also been shown to affect cardiovascular function, heat storage, and exercise performance. PCP can also induce, although rarely, prolonged toxic psychosis in chronic abusers and precipitate psychotic episodes in psychotic and prepsychotic personalities. Tolerance, but not physical dependence, develops to the effects of PCP. Psychologic dependence as indicated by craving for the drug has however been reported.
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PMID:Phencyclidine (PCP): some human studies. 651 53

Effects of acute and chronic administration of phencyclidine (PCP) on both neocortical and subcortical visual potentials (VEPs) and on spontaneous EEGs were studied in the rhesus monkeys with permanently implanted brain electrodes. VEPs were evoked by brief single photo-stimulator flashes (0.8 pps. 10 microsec duration). Injection of PCP (0.5 to 4.0 mg/kg doses, IV) in monkeys produced a significant inhibition on the peak-amplitude of major VEP components predominantly in the occipital lobe and hippocampus. The PCP-induced VEP inhibition persisted in the presence of occipital and hippocampal theta-activities. Nystagmus persisted throughout the 6 to 8 hours course of PCP-induced behavior. A biphasic pattern of inhibitory and excitatory effects on EEGs and behavior was also observed during the 6 to 8 hours observation period. Chronic administration of PCP (2.0 and 4.0 mg/kg dose IV daily) produced a significant decrease in its inhibitory effects on VEPs, suggesting tolerance development to the inhibitory effect on VEPs. The results suggest that the hippocampus has important implications in the modulation of PCP effects on CNS activities related to the visual function of the rhesus monkey.
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PMID:Effects of phencyclidine (PCP) on the visual evoked potentials in the rhesus monkey. 682 65

In 1,000 cases of phencyclidine (PCP) intoxication evaluated at the time of first examination in an emergency department, the incidence of "typical" findings was found to be lower than has been reported previously. Nystagmus and hypertension occurred in only 57% of our cases; some patients had only one of these findings and many had neither. The incidence of violence was 35%; bizarre behavior, 29%; and agitation, 34%. Changes in sensorium consisted of coma, lethargy/stupor, and acute brain syndrome; however, 46% of patients were alert and oriented. Motor signs included grand mal seizures, generalized rigidity, localized dystonias, catalepsy, and athetosis. Profuse diaphoresis, hypersalivation, bronchospasm, and urinary retention occurred in less than 5%. A small percentage had severe disturbances in vital signs, including three cases (0.3%) of cardiac arrest and 28 cases (2.8%) of apnea. Hypoglycemia and elevated serum CPK, uric acid, and SGOT/SPGT were common. Urine PCP levels did not correlate with the severity of the clinical findings.
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PMID:Acute phencyclidine intoxication: incidence of clinical findings in 1,000 cases. 722 71

Medical records of 107 consecutive patients with a diagnosis of phencyclidine (PCP) intoxication were reviewed and in 27 of these the diagnosis was confirmed by positive urine assay. In the 27 confirmed cases, the most common abnormalities present on physical examination were mental/behavioral (89%) and nystagmus (85%). Elevations in blood pressure, temperature, and heart rate that were statistically significant when compared with an age-matched control group also were noted. Review of available medical records disclosed that 13 of these patients had been evaluated previously at our institution for PCP intoxication. Toxicological screening tests including blood alcohol level, hypnotic screen, and urine test for alkaloids, were performed on 11 patients and found positive in four. The most common serious medical complication requiring hospitalization was rhabdomyolysis which occurred on three patients, two of whom developed acute renal failure. This complication may occur more frequently than previously recognized and should be excluded in patients with PCP intoxication.
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PMID:Phencyclidine intoxication: clinical experience in 27 cases confirmed by urine assay. 722 72

Six cases of PCP intoxication in young children age 5 years and younger seen at UCLA Medical Center recently and 10 other cases from the literature are described and their clinical findings summarized. PCP intoxication should be suspected in young children and infants presenting with rapid onset of lethargy or coma, strange behavior, staring spells, ataxia, and nystagmus. Other findings less frequent but still suspect are opisthotonos, hypertension, tachypnea or hyperpnea, miosis, hyperreflexia, hypertonia, and rigidity. Once suspected, the diagnosis is most easily made by finding PCP in the urine. Proper diagnosis of PCP intoxication is important to ensure that rapid, appropriate treatment is given, costly diagnostic workups are avoided, and family evaluations are instituted. One case strongly suggests that intoxication in infants may result from accidental inhalation when near individuals who are smoking PCP.
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PMID:PCP intoxication in young children and infants. 738 38

The non-competitive N-methyl-D-aspartate (NMDA) receptor antagonists phencyclidine (PCP) and dizocilpine maleate (MK801) cause nystagmus, tremor, and cerebellar ataxia at toxic doses. We have shown that PCP but not MK801 is toxic to rat cerebellar Purkinje cells. To study the mechanism and pathways of PCP and MK801 action, Fos protein expression was examined in the cerebellum and functionally related nuclei of the brainstem. PCP, 1-50 mg/kg i.p., induced Fos immunostaining in neurons of the inferior olive, cerebellar granule cell layer, and deep cerebellar and vestibular nuclei. At higher doses, PCP, 25-50 mg/kg, induced dense Fos immunoreactivity throughout the inferior olive except for rostral parts of medial accessory olive and caudal parts of principal olive. At lower doses of PCP, 1-10 mg/kg, Fos positive cells in inferior olive were concentrated in the subnucleus beta. In the cerebellum Fos positive granule cells were arranged in patches distributed throughout the cerebellar cortex following PCP, 1-50 mg/kg. Rare Fos positive Purkinje cells were observed adjacent to these patches. At the highest dose of PCP tested (50 mg/kg), Fos was expressed in the fastigial, interpositus, and dentate nuclei, and in vestibular nuclei, most prominently in the medial vestibular nucleus. At lower doses, Fos was expressed mainly in medial cerebellar output nuclei and in vestibular nuclei. MK801, 0.2-10 mg/kg i.p., induced Fos expression in the same regions as PCP. However, MK801-induced Fos expression in inferior olive was localized primarily to subnucleus beta. No apparent differences in the number or distribution of Fos positive neurons were observed at MK801 doses of 0.2-10 mg/kg. MK801 also induced Fos expression in fastigial and vestibular nuclei, but not in lateral (interpositus and dentate) cerebellar nuclei. MK801, 0.2-10 mg/kg, induced patchy Fos expression in cerebellar granule cells that was similar to PCP. These results support our earlier observations that PCP and MK801 have different actions in the cerebellum, although they both cause ataxia and indistinguishable behavioral symptoms. That high doses of PCP induce substantially more Fos expression in inferior olive than MK801 suggests that its toxicity to Purkinje cells is at least partially the result of excessive activity of climbing fibers, the excitatory neural input that arises from the inferior olive and synapses on Purkinje cell dentrities.
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PMID:FOS expression in the brainstem and cerebellum following phencyclidine and MK801. 882 Sep 68

Although there are many roadside testing devices available for the screening of abused drugs, none of them can be used for the detection of ketamine, a popular abused drug in Hong Kong. In connection to local drug driving legislation, effective roadside detection of ketamine in suspected drug-impaired drivers has to be established. According to the drug evaluation and classification program (DEC), ketamine is classified in the phencyclidine (PCP) category. However, no study has been performed regarding the signs and symptoms exhibited by users under the influence of ketamine. In a study to develop a protocol for effective roadside detection of drug-impaired drivers, 62 volunteers exiting from discos were assessed using field impairment tests (FIT) that included measurements of three vital signs (i.e. body temperature, pulse rate and blood pressure), three eye examinations [pupil size, lack of convergence (LOC) and horizontal gaze nystagmus (HGN)] and four divided attention tests (Romberg, one-leg stand, finger-to-nose and walk-and-turn tests). Subsequent laboratory analysis of oral fluid and urine samples from the participants revealed the presence of common abused drugs in both the urine and oral fluid samples of 55 subjects. The remaining 7 subjects with no drug in their oral fluid samples were used as drug-free subjects. In addition, 10 volunteers from the laboratory who were regarded as drug-free subjects were also assessed using the same FIT. Among the 62 volunteers, 39 of them were detected with ketamine in their oral fluid. Of these ketamine users, 21 of them (54%) with only ketamine found in their oral fluid samples while the rest (18 subjects) of them had other drugs (i.e. MA, MDMA, benzodiazepines and/or THC) in addition to ketamine. Of the 21 ketamine-only users, 15 of them (71%) were successfully identified by FIT. It was found that when salivary ketamine concentrations were greater than 300 ng/mL, signs of impairment became evident, with over 90% detection rate using the FIT. By comparing the FIT observations on the 21 ketamine-only users with the drug-free subjects, the typical signs and symptoms observable for subjects under the influence of ketamine included LOC, HGN, elevated pulse rate and in general, failing the divided attention tests, especially the walk-and-turn and one-leg stand.
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PMID:Roadside detection of impairment under the influence of ketamine--evaluation of ketamine impairment symptoms with reference to its concentration in oral fluid and urine. 1704 88


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