Recovery of neuropsychological functions during reduction in use of phencyclidine

Cosgrove, J. Michael; Newell, Terry G.

doi:10.1002/1097-4679(199101)47:1<159::aid-jclp2270470125>3.0.co;2-o

Cited by 131 publications

(64 citation statements)

References 17 publications

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“…The results of this and a previous (Balla et al, 2001b) study suggest that ongoing NMDA receptor dysfunction would be sufficient to account for dopaminergic hyperactivity within PFC and striatum. Chronic PCP abuse is associated with cognitive dysfunction that develops during the course of abuse but resolves significantly following discontinuation (Cosgrove and Newell, 1991). Thus, the pattern of cognitive dysfunction in humans exposed to PCP follows the pattern of dopaminergic hyperactivity observed in the present study.…”

Section: Implications For Schizophrenia and Drug Abusesupporting

confidence: 75%

Subchronic Continuous Phencyclidine Administration Potentiates Amphetamine-Induced Frontal Cortex Dopamine Release

Balla

Sershen

Serra

et al. 2003

Neuropsychopharmacol

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Functional dopaminergic hyperactivity is a key feature of schizophrenia. Etiology of this dopaminergic hyperactivity, however, is unknown. We have recently demonstrated that subchronic phencyclidine (PCP) treatment in rodents induces striatal dopaminergic hyperactivity similar to that observed in schizophrenia. The present study investigates the ability of PCP to potentiate amphetamine-induced dopamine release in prefrontal cortex (PFC) and nucleus accumbens (NAc) shell. Prefrontal dopaminergic hyperactivity is postulated to underlie cognitive dysfunction in schizophrenia. In contrast, the degree of NAc involvement is unknown and recent studies have suggested that PCP-induced hyperactivity in rodents may correlate with PFC, rather than NAc, dopamine levels. Rats were treated with 5-20 mg/kg/day PCP for 3-14 days by osmotic minipump. PFC and NAc dopamine release to amphetamine challenge (1 mg/kg) was monitored by in vivo microdialysis and HPLC-EC. Doses of 10 mg/kg/day and above produced serum PCP concentrations (50-150 ng/ml) most associated with PCP psychosis in humans. PCP-treated rats showed significant, dose-dependent enhancement in amphetamine-induced dopamine release in PFC but not NAc, along with significantly enhanced locomotor activity. Enhanced response was observed following 3-day, as well as 14-day, treatment and resolved within 4 days of PCP treatment withdrawal. These findings support the concept that endogenous NMDA receptor dysfunction could account for the pattern of dopaminergic dysfunction observed in schizophrenia, and suggest that even short duration abuse of PCP-like agents may greatly potentiate behavioral effects of psychostimulants in drug abuse situations. Finally, these studies provide a model system in which to evaluate effects of potential psychotherapeutic agents.

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Section: Implications For Schizophrenia and Drug Abusesupporting

confidence: 75%

Subchronic Continuous Phencyclidine Administration Potentiates Amphetamine-Induced Frontal Cortex Dopamine Release

Balla

Sershen

Serra

et al. 2003

Neuropsychopharmacol

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“…Ketamine may increase only secondary negative symptoms in the NVs (secondary to experiencing altered perceptual experience for example). Reports of acute PCP intoxication in humans account primarily productive states (Pearlson 1981) whereas descriptions of chronic PCP abuse include characteristics of dulled thinking and lethargy (Cosgrove and Newell 1991). Others have reported ketamine-induced changes in negative symptoms, both in patient and NVs (Malhotra et al 1997a).…”

Section: Discussionmentioning

confidence: 99%

Effects of Ketamine in Normal and Schizophrenic Volunteers

Lahti

Weiler

Michaelidis

et al. 2001

Neuropsychopharmacology

590

355

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“…Drug addicts who predominantly abuse amphetamine, cocaine, heroin, alcohol or phencyclidine exhibit performance deficits on tasks that require response inhibition, decision making and/or cognitive flexibility (Cosgrove and Newell 1991;McKetin and Mattick 1998;O'Malley et al 1992;Rogers et al 1999;Ornstein et al 2000;Grant et al 2000). The deficits exhibited by drug abusers include impairments of set shifting, planning (Ornstein et al 2000) and decision-making (Rogers et al 1999;Grant et al 2000).…”

Section: Relation To Neuropsychological Studies In Drug Addictionmentioning

confidence: 99%

Impairments of Reversal Learning and Response Perseveration after Repeated, Intermittent Cocaine Administrations to Monkeys

Jentsch

Olausson

Garza

et al. 2002

Neuropsychopharmacology

254

217

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The current experiments examined the effects of acute or repeated, intermittent administrations of cocaine on the acquisition and reversal of object discriminations by Vervet monkeys in order to test the hypothesis that cocaine treatment affects performance of tasks that depend upon the functions of the orbitofrontal cortex and amygdala. An acute dose of cocaine (1 mg/kg; 20 min prior to testing) impaired reversal of a previously learned object discrimination but had no effect on acquisition of a novel one. Specific impairments of reversal learning were also observed in monkeys 9 and 30 days after repeated administrations of cocaine (2 or The compulsive drug seeking and taking behavior that is characteristic of drug addiction has recently been attributed to complex, inter-related dysfunctions in neural systems mediating incentive motivation and behavioral regulation (e.g., the striatum, amygdala and ventral frontal cortex; Jentsch and Taylor 1999;Robbins and Everitt 1999; Volkow and Folwer 2000;Berke and Hyman 2000). Several lines of evidence support this hypothesis. First, drug addicts exhibit altered cerebral blood flow and metabolism within the striatum, amygdala and frontal cortex both at baseline and after drug-induced craving (c.f. Volkow and Fowler 2000;London et al. 2000). Second, chronic drug administration affects the neurochemistry and anatomy of these brain regions in animal models (Nestler and Aghajanian 1997;Robinson and Kolb 1997;Wolf 1998;Berke and Hyman 2000; Vandershuren and Kalivas 2000;Robinson et al. 2001 (Post et al. 1976), altered incentive motivation (Shippenberg and Heidbreder 1995;Taylor and Horger 1999;Robbins and Everitt 1999) and impaired cognitive and executive function (Jentsch et al. 1997(Jentsch et al. , 2000Rogers et al. 1999;Robbins and Everitt 1999;Grant et al. 2000;Ornstein et al. 2000) after chronic stimulant drug administration.Because of its important role in decision-making (Bechara et al. 2000) and inhibitory control over pre-potent behavior (Roberts and Wallis 2000), an involvement of ventromedial regions of the frontal cortex in drug abuse has been proposed. In essence, impairments of frontal lobe function are thought to effectively 'un-gate' subcortically-mediated, conditioned tendencies (such as established instrumental responses to obtain and consume drugs), resulting in the compulsive drug seeking and taking that characterize addiction (Jentsch and Taylor 1999). Nevertheless, few studies have directly investigated the long-term consequences of prolonged exposure to addictive drugs on frontal cortex cognitive function, particularly in non-human primates.The aim of the current studies was to directly evaluate the function of the prefrontocortico-amygdalo-striatal system after repeated, intermittent cocaine administrations to monkeys. Using an animal model in which drug treatment (schedule and dosing) and withdrawal can be experimentally controlled, we employed a wellcharacterized behavioral task, the acquisition and reversal of a 3-choice object discrimination. T...

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Recovery of neuropsychological functions during reduction in use of phencyclidine

Cited by 131 publications

References 17 publications

Subchronic Continuous Phencyclidine Administration Potentiates Amphetamine-Induced Frontal Cortex Dopamine Release

Subchronic Continuous Phencyclidine Administration Potentiates Amphetamine-Induced Frontal Cortex Dopamine Release

Effects of Ketamine in Normal and Schizophrenic Volunteers

Impairments of Reversal Learning and Response Perseveration after Repeated, Intermittent Cocaine Administrations to Monkeys

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