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)

Huntington's disease (HD) is an inherited neuropsychiatric degenerative process characterized by movement disorder, dementia, and, often, affective disorder (AfD) (seen in 38% of patients). Depression in HD is not just an understandable reaction to fatal illness: 10% of HD patients develop mania; AfD can occur 20 yr before neurological signs; and mood disorders are not randomly distributed, but occur in a subset of HD families. This evidence suggests that AfD in HD relates to brain pathophysiology. With its clear neuropathology, HD is proposed as one model for biological underpinnings of idiopathic AfD. There is striking atrophy and neuronal loss in HD neostriatum, particularly caudate. Caudate has rich connections to the limbic system. It is hypothesized that AfD in HD relates to dysfunction of the part of the neostriatum damaged earliest, dorsal medial caudate. Preliminary studies on neuropathological differences between HD patients with and without AfD are discussed. HD neurochemistry is reviewed, emphasizing the excitotoxin hypothesis, which involves dysfunction of the glutamate neurotransmitter system in HD (especially the NMDA receptor, which contains a channel with a phencyclidine (PCP) binding site). Based on the HD model, it is suggested that the glutamate system (particularly NMDA receptors) be examined in idiopathic AfD.
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PMID:Huntington's disease as a model for mood disorders. Clues from neuropathology and neurochemistry. 214 28

d-Amphetamine and phencyclidine (PCP) have both been reported to produce manic-like sequela in humans, effects that are reportedly antagonized by lithium. To test the hypothesis that the acute effects of these drugs in rats may serve as models of mania, the behaviors induced by d-amphetamine (3 mg/kg) or PCP (5 mg/kg) were quantified on behavioral rating scales subsequent to chronic dietary pretreatment with lithium carbonate or control diet. On day 14 of pretreatment, PCP-induced stereotyped behaviors and ataxia were potentiated in rats receiving lithium (plasma levels 1.0 +/- 0.23 mEq/l). PCP-induced locomotor activity was not affected by lithium pretreatment. Stereotypies and locomotion induced by d-amphetamine were also not significantly affected by lithium pretreatment. These results suggest that neither PCP nor amphetamine administered acutely to rats will be useful models to explore the manic-like symptoms produced by these drugs in humans.
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PMID:Effects of lithium on behaviour induced by phencyclidine and amphetamine in rats. 681 1

Phencyclidine (PCP), a widely abused drug currently, has multiple pharmacological actions, including psychotomimetic [1], anesthetic [2], sympathomimetic [2], anticholinergic [3-7], and dopaminergic [8-10]. Similarly, PCP intoxication in man can present with diverse symptoms: schizophrenia-like delusions and hallucinations; mania; violence, dyskinetic, catatonic, or stereotyped movements; hypertension; and coma [11, 12]. There is general agreement that the treatment of PCP intoxication includes support of vital functions and acidification of the urine [13]. However, there is no known specific antidote for PCP toxicity. Although diazepam [13], haloperidol [14, 15], and chlorpromazine [16] have been reported to improve the agitation and psychotic symptoms caused by PCP, the therapeutic efficacy of these agents has rarely been documented with objective clinical measures. Recently we found that intramuscular physostigmine and haloperidol [17, 18] improved several symptoms of acute PCP intoxication as measured by the Brief Psychiatric Rating Scale (BPRS) [19].
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PMID:Phencyclidine intoxication: assessment of possible antidotes. 713 17

Routine blood samples of 145 consecutive patients seen in the Los Angeles County Psychiatric Hospital Emergency Room during a 48-hour weekday period in June 1979 were examined for phencyclidine (PCP) using a sensitive and specific gas capillary gas chromatographic nitrogen detector (GC2-N) method. Of these 145 samples 63 (43.4%) were positive and PCP levels ranged 0.34 to 142.9 nanograms/ml (mean 14.6 ng/ml +/- 3.4 S.E.M.). An analysis of the records of these 63 patients revealed a wide variety of psychotic clinical pictures resembling mania, depression or schizophrenia with relatively few of the supposedly characteristic manifestations of PCP intoxication. Each of the 63 patients had at least one manifestation of toxic psychosis and/or acute delirium, in addition to the florid symptoms characteristic of functional states. PCP measurement, pharmacokinetics and the possible relationships of this intoxication to the psychiatric manifestations are discussed.
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PMID:The urban epidemic of phencyclidine (PCP) use: clinical and laboratory evidence from a public psychiatric hospital emergency service. 721 23

Frontal-subcortical circuits provide a comprehensive framework for understanding the anatomy, biochemistry, and pharmacology of behavior. The three principal behaviorally relevant circuits originate in the dorsolateral prefrontal cortex, orbitofrontal cortex, and anterior cingulate cortex, respectively. Circuit-specific marker behaviors associated with each circuit are executive dysfunction (dorsolateral prefrontal-subcortical circuit), disinhibition and OCD (orbitofrontal-subcortical circuit), and apathy (medial frontal-subcortical circuit). Environmental dependency is common to all prefrontal-subcortical syndromes and may reflect disruption of working memory. Depression, mania, and psychosis are mediated by structures involved in prefrontal-subcortical circuits and are circuit-related but not circuit-specific behaviors. The actions of PCP, LSD, serotonergic antidepressants, anxiolytics, sedative-hypnotics, antipsychotic agents, and ethanol may all be partially or primarily mediated through transmitter systems and receptor effects expressed through frontal-subcortical circuits.
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PMID:Anatomic and behavioral aspects of frontal-subcortical circuits. 859 19

Predictors of non-response were investigated in a 15-year follow-up (1981-1996) of 3,481 individuals in a probability sample from the household population of East Baltimore. Demographics (age, sex, race, education, marital status, and unemployment), household factors (living arrangements, household income, household size, and number of children), cultural variables (ancestral ethnicity and foreign language), social variables (social support and networks, committing felony, carrying a weapon, using an alias, and wandering), health factors (physical illness, health insurance, medical assistance, Medicare, receiving disability benefits, social security, and welfare), interviewer's observation, and psychopathologic variables (mental disorders, suicide behavior, comorbidity, and drug use) were collected at baseline in 1981 and in 1982, then linked to follow-up data between 1993 and 1996. A tracing process involving mail, phone, criss-cross directories, motor vehicle administration records, a commercial credit bureau, the state criminal justice system, hospital records, the US National Death Index, and field tracing were used to locate the original sample. A total of 3,066 respondents of the original sample (88.1%) were traced. Non-response was categorized into Sample Mortality (that part of the original sample that died during follow-up), Sample Loss (that part of the original sample that survived but could not be found) and Refusal (that part of the original sample that survived and was found but refused to participate). Stratified analysis and adjusted multiple logistic regression modeling found sample mortality and sample loss were strongly influenced by individual and household variables and by psychopathology. Sample mortality was influenced by specific mental disorders or conditions as mania, drug abuse/dependency, antisocial personality, cognitive impairment, alcohol abuse/dependency, phobia, drug use (except PCP), and comorbidity. Household factors protective against mortality include higher household income, not living as extended members in a married couple family, and living with children in the household. Persons who were unemployed, widowed or single, without high school education, male, and 65 years of age or older were more likely to die. Sample loss was influenced by cognitive impairment, antisocial personality, and cocaine use. Household factors linked to sample loss include living in female-headed families, or non-family households, and living alone. Young nonwhite, divorced/separated, without high school education, and unemployed were also harder to find. Refusal was associated with being white, with incomplete elementary education, living as a spouse in traditional married couple families, or as a child in female-headed families. Psychopathology did not influence refusal.
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PMID:Psychopathology and attrition in the Baltimore ECA 15-year follow-up 1981-1996. 1018 15

This exploratory study is an extension of previous studies which have applied personal construct theory (PCP) methodology toward a better understanding of the structure and dynamics of multidisciplinary mental (and physical) health care (Kirkcaldy and Pope, 1992; Kirkcaldy et al., 1993, 2000, 2005; Kirkcaldy and Siefen, 1999). In this study we wanted to use similar cluster statistical analyses, not unlike PCP analysis, to identify the diverse subjective models of psychological ailments such as anxiety, depression, psychosis, mania, obsessive compulsive disorder (OCD), post stress traumatic disorder (PTSD), etc., using not the idiosyncratic constructs generated by individual triadic element comparisons, but by selecting those constructs which have been clearly identified in various psychiatric and psychological rating scales (e.g. somatic preoccupation, social withdrawal, conceptual disorganization, hostility, disinhibition and controlling). Clinical experts (psychological psychotherapists, and medical psychotherapist and psychiatrist) each with over 25 years of clinical and research experience were required to complete the ratings of each disorder listed in terms of the pre-formulated behavioral, emotional and cognitive concepts. What emerged are several multivariate (grid) analyses based on mental health professionals' perception of diverse elements (disorders) and their interrelationship derived from the similarity of composite profiles of ill-related constructs. Overall, the analyses revealed clear associations between the subjective evaluations of psychological ailments suggesting some uniformity in mental health assessment of such disorders. The implications of these findings are discussed within the theoretical framework of improved mental health care.
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PMID:Subjective models of psychological disorders: mental health professional's perspectives. 2317 40