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) at high doses causes both excitation and depression in the rat. The visual evoked potential (VEP) was measured in rats following PCP administration in doses ranging from 1 mg/kg to 56 mg/kg. Consistent lengthening of VEP latencies suggests that PCP has an unusual inhibitory effect on visual function in the presence of the excitatory signs of bilaterally synchronous cortical spiking. The epileptogenic properties of PCP are quite evident in rats.
Brain Res Bull 1981 Sep
PMID:Phencyclidine-induced alterations of rat electrophysiology. 626 54

[3H]Phencyclidine ([3H]PCP) binds specifically to an apparently single class of binding sites on slide-mounted sections of rat olfactory bulb (Kd = 46 nM; Bmax = 10.5 fmol per slice). Bound [3H]PCP can be displaced by nonradioactive PCP and a series of its analogs with relative potencies that correlate closely (P less than 0.001) with values determined in a rat discrimination test that utilized PCP as a cue. Although morphine, naloxone, and opiate peptides do not displace bound [3H]PCP, psychotomimetic benzomorphans, classed as "sigma opiates," are quite potent displacers in vitro and have PCP-like behavioral properties in vivo. These results suggest that phencyclidine and the sigma opiates act at the same sites. [3H]PCP binding sites were visualized by using tritium-sensitive LKB film analyzed by computerized densitometry and color coding. The [3H]PCP binds most densely to cortical areas, diffusely in neocortex, and somewhat heterogeneously in the laminae of the hippocampal formation and dentate gyrus. Most of the brainstem and spinal cord show low specific [3H]PCP binding, with gray matter generally showing more binding than white.
Proc Natl Acad Sci U S A 1981 Sep
PMID:Phencyclidine (angel dust)/sigma "opiate" receptor: visualization by tritium-sensitive film. 627 22

Phencyclidine (PCP) is a major drug of abuse as well as a 'drug of choice' among substance abusers in the U. S. A. Unfortunately, PCP use may result in the development of psychotic behavior. PCP-induced psychosis is characterized by confusion, excitation, aggression, paranoia, hallucinations and delusions of grandeur and may evoke violent or suicidal behavior. Therefore, many patients suffering from PCP-induced psychosis have been diagnosed initially as schizophrenic. However, PCP-related research has not kept pace with the rise in abuse and PCP-induced psychosis. The neurochemical effects of PCP are not well defined at present, but both behavioral and biochemical studies suggest that it may interact with dopaminergic, cholinergic, noradrenergic, serotonergic, GABAergic and enkephalinergic systems. In addition, the specific reversible, saturable, high affinity 3H-PCP binding site is discovered recently in rat brain. On the other hand, there is now a large body of evidence to suggest that opiate receptors may be subdivided into mu, sigma, kappa and delta receptors. On the basis of behavioral and binding studies, it is proposed that the sigma receptor and the PCP binding site are one and the same. This receptor interacts with PCP and psychotomimetic opioids to produce their psychotomimetic effects. In connection with this receptor, a trial to isolate an endogenous ligand produces psychotomimetic effects, "angeldustin" is progressing. This review has served to illustrate the paucity of information currently available on the central effects of PCP. However, our current notions of the mechanisms of action of PCP are very complicate. Such a review inevitably raises more question than it answers but it is hoped that these may stimulate further investigation in this field.
Yakubutsu Seishin Kodo 1984 Sep
PMID:[Phencyclidine, a drug which induces psychosis: its neuropharmacological actions]. 639 56

Right ventricular involvement has been shown to be common in the acute phase of infero-posterior myocardial infarction. The aim of this prospective study was to assess the diagnostic and prognostic value of the different criteria obtained by clinical and paraclinical methods of investigation. Forty patients (35 men, 5 women: mean age 57,1 years) admitted consecutively with this type of transmural infarct without any other cause of acute or chronic volumic or barometric overload of the RV were investigated. In addition to clinical data, the following paraclinical investigations were carried out during the first three days of admission: ECG and vectorcardiogramme (VCG); transaminase levels (SGOT and SGPT), creatinine phosphokinase (CPK), alpha HBDH, serum creatinine, blood gases (pO2), M mode and 2 D echo, right heart catheterisation and cardiac output estimations, selective RV and pulmonary cineangiography centered on the LV in the monoplane 30 degrees LAO projection. Two groups of twenty patients were identified, comparable in age and sex, according to the angiographic extension of akinesia of the RV inferior wall: Group A: extensive akinesia (greater than or equal to 30 p. 100), Group B: very localised or no akinesia (less than 30 p. 100). Analysis of the results showed a number of features characterising patients in Group A: the high incidence of initial shock (45 p. 100 (A)/0 p. 100 (B] and signs of RV failure (85 p. 100/0 p. 100), higher SGOT, SEPT (p less than 0,05) and alpha HBDH (p less than 0,02) but not of CPK; much higher serum creatinine (p less than 0,01) and lower p02 (p less than 0,05); the ECG showed a high incidence (85 p. 100) and specificity (95 p. 100) of ST-T elevation in V3R and V4R, and also 2nd or 3rd degree AV block (60 p. 100/5 p. 100): there were no characteristic VCG changes. Catheterisation showed very significant increases (p less than 0,001) of mean RA, and RV end diastolic pressures, of the RA/mean pulmonary capillary pressure ratio and of Yu's index. There was a moderate increase in PCP (p less than 0,01), a drop in right ventricular systolic work index (RSSWI); adiastole was very common (90 p. 100) and very specific (95 p. 100); angiography showed an increase in RV end diastolic and end systolic volumes (p less than 0,05) and a fall in RV ejection fraction (p less than 0,05) but with a lot of individual variations; there were no significant differences between the two groups as regards the volumes, ejection fractions and p. 100 akinesia of the LV.(ABSTRACT TRUNCATED AT 400 WORDS)
Arch Mal Coeur Vaiss 1983 Sep
PMID:[Prospective study of the diagnostic and prognostic criteria of right ventricular involvement in the acute phase of inferoposterior infarction]. 641 16

All the components of phencyclidine(PCP)-induced stereotyped behaviors, including sniffing, backpedalling, turning and head weaving were significantly decreased in rats following kainic acid lesion of the striatum. In the 6-hydroxydopamine lesioned rats, the behavioral score of PCP-induced stereotyped sniffing was similar to that in the sham-operated rats, while other components were significantly decreased. In addition, only the PCP-induced backpedalling and head weaving were significantly attenuated in the 5,6-dihydroxytryptamine lesioned rats. These results suggest that not only dopaminergic but also serotonergic and other systems in the striatum may play important roles in PCP-induced stereotyped behaviors.
Eur J Pharmacol 1983 Sep 30
PMID:Phencyclidine-induced stereotyped behaviors in rats following specific neurotoxin lesions of the striatum. 641 71

Mice were used for a study of the interaction between morphine and phencyclidine (PCP) in relation to lethality, motor incoordination, locomotor activity and rearing, together with the half-life of PCP, following continuous administration of morphine by pellet (75 mg base) implantation for 72 h and after removal of the pellets for 6 and 24 h. PCP induced motor incoordination and suppressed locomotor activity and rearing; these effects were enhanced in morphine 'pellet-implanted' mice and were attenuated in morphine 'pellet-removed' groups. The enhancing effect of morphine on the PCP responses was attributable more to the presence of residual morphine than to the alterations in its disposition. The morphine-induced increase in locomotor activity and analgesia was attenuated in PCP (40 mg/kg per day i.p. for 5 days) tolerant mice. The rate of decay of PCP in serum and brain or morphine pellet-implanted animals was not different; however, in the 24 h 'pellet-removed' group, the rate of decay of PCP was increased. The results indicate that there is a two-way cross-tolerance development between PCP and morphine. The phenomenon appears to involve both dispositional and functional adaptation mechanisms.
Eur J Pharmacol 1984 Sep 17
PMID:Attenuation of pharmacological effects and increased metabolism of phencyclidine in morphine tolerant mice. 649 21

The effects of phencyclidine (PCP) (7.0, 11.7, 19.5, 32.6, and 54.4 mg/kg) on locomotor activity, stereotyped behavior (circling, backing up, and weaving frequency), and rotarod performance were evaluated. In addition, the frequency of other PCP-induced abnormal behaviors (head in corner, arched back, and cataleptic freeze) was determined. All doses of PCP produced a significant increase in locomotor activity and stereotyped behavior as well as an impairment of rotarod performance. Both the duration and the time to peak effects (with the exception of rotarod performance) of these PCP-induced behavioral changes appeared to be dose dependent. The delay in attaining peak effects for locomotor activity and stereotypy was attributed to PCP-induced gross motor ataxia, which became more severe and long lasting with increasing dose. Although the longest period of time that significant changes were seen in locomotor activity, stereotyped behavior, and rotarod performance was 12 hr, sporadic recurrences of stereotypy and a significant increase in cataleptic freeze were observed in the high-dose groups (19.5, 32.6, and 54.4 mg/kg) up to 21 days postadministration. These persistent behaviors (stereotypy and cataleptic freeze) are not unlike certain of the prolonged behaviors seen in man with PCP overdose (catatonic stupor along with repetitive orofacial and limb movements).
Toxicol Appl Pharmacol 1984 Sep 30
PMID:The effect of a single administration of phencyclidine on behavior in the rat over a 21-day period. 654 Sep 2

In four preparations/tests (isolated nerve, ventricular strip, rotarod, and mouse acute lethality), cis-N-phenyl-4-methyl-cyclohexyl piperidine (cis-MPCP) was consistently less active than PCP and trans-MPCP. As expected, cis-MPCP, at 10(-4)M, which did not depress the action potential evoked on frog sciatic nerves, reduced by half both the nerve block and prolongation of relative refractory period caused by PCP. However, cis-MPCP at 10(-6)M, which by itself had little effect, failed to reduce the positive inotropic effect of PCP on the field-stimulated rat ventricular strip. Cis-MPCP also failed to decrease the ataxic effect of 6 mg/kg PCP (ED80) in the mouse rotarod test. Finally, at a dose that was neither ataxic nor lethal to mice (20 mg/kg), cis-MPCP failed to reduce the 24-hour LD50 of PCP. These data suggest that the actions of PCP are mediated through a multiple receptor system.
Life Sci 1983 Sep 05
PMID:In vitro and in vivo evaluation of cis-methyl-phencyclidine (CIS-MPCP) as a potential antagonist of phencyclidine (PCP). 660 11

The use of phencyclidine (PCP) was investigated in the psychiatric population of an East Harlem, New York, hospital. Sixty-eight consecutive PCP-user admissions were interviewed through a 77-item questionnaire. The patient population served by the facility was 48 percent Hispanic and 32 percent black. The sample of PCP users was 86 percent black. This suggests that, in this area, either more blacks use PCP, or nonblack PCP users seek psychiatric help less frequently than black users. This study emphasizes the many problems affecting the sample population and shows evidence that a large portion of the sample is at risk to develop psychiatric symptoms.
J Natl Med Assoc 1983 Sep
PMID:Phencyclidine in an East Harlem psychiatric population. 663 93

Disposition of [3H] phencyclidine (5 mg kg-1 i.p.) in brain, liver and plasma of rats treated chronically with 0.9% saline or nicotine (1 mg kg-1 s.c. twice a day for 11 days) was studied using a method possessing high sensitivity and specificity for PCP. No significant differences were observed in the values of PCP in plasma and tissues and in brain or liver to plasma PCP concentration ratios in the 2 groups 0.5, 1, 2 hr after [3H] PCP injection. With the exception of the value of PCP metabolites in plasma at 0.5 hr, the PCP metabolites concentrations were also not significantly different in the 2 groups. Data suggested that chronic nicotine pretreatment of rats did not affect the disposition of PCP and the potentiation of PCP-induced locomotor stimulant effects by nicotine possibly involves the additive pharmacodynamic interaction of 2 compounds at the level of the central nervous system.
Arch Int Pharmacodyn Ther 1983 Sep
PMID:Effect of chronic nicotine pre-treatment on phencyclidine (PCP) disposition in the rat. 665 4


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