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Titolo:
The neuropsychopharmacology of phencyclidine: From NMDA receptor hypofunction to the dopamine hypothesis of schizophrenia
Autore:
Jentsch, JD; Roth, RH;
Indirizzi:
Yale Univ, Sch Med, Neurobiol Sect, New Haven, CT 06520 USA Yale Univ NewHaven CT USA 06520 Neurobiol Sect, New Haven, CT 06520 USA Yale Univ, Sch Med, Neuropsychpharmacol Res Unit, New Haven, CT 06520 USA Yale Univ New Haven CT USA 06520 rmacol Res Unit, New Haven, CT 06520 USA Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06520 USA Yale Univ New Haven CT USA 06520 , Dept Psychiat, New Haven, CT 06520 USA Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06520 USA Yale Univ NewHaven CT USA 06520 Dept Pharmacol, New Haven, CT 06520 USA
Titolo Testata:
NEUROPSYCHOPHARMACOLOGY
fascicolo: 3, volume: 20, anno: 1999,
pagine: 201 - 225
SICI:
0893-133X(199903)20:3<201:TNOPFN>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
SPATIAL WORKING-MEMORY; DORSOLATERAL PREFRONTAL CORTEX; CORTICAL ACETYLCHOLINE-RELEASE; EMISSION COMPUTED-TOMOGRAPHY; GLUTAMIC-ACID DECARBOXYLASE; VENTRAL TEGMENTAL AREA; CEREBRAL BLOOD-FLOW; RAT FRONTAL-CORTEX; CARD SORT TEST; NUCLEUS-ACCUMBENS;
Keywords:
ketamine; phencyclidine; psychotomimetic; memory; catecholamine; schizophrenia; prefrontal cortex; cognition; dopamine; glutamate;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
262
Recensione:
Indirizzi per estratti:
Indirizzo: Jentsch, JD Yale Univ, Sch Med, Neurobiol Sect, POB 208001, New Haven, CT 06520 USA Yale Univ POB 208001 New Haven CT USA 06520 aven, CT 06520 USA
Citazione:
J.D. Jentsch e R.H. Roth, "The neuropsychopharmacology of phencyclidine: From NMDA receptor hypofunction to the dopamine hypothesis of schizophrenia", NEUROPSYCH, 20(3), 1999, pp. 201-225

Abstract

Administration of noncompetitive NMDA/glutamate receptor antagonists, suchas phencyclidine (PCP) and ketamine, to humans induces a broad range of schizophrenic-like symptomatology,findings that have contributed to a hypoglutamatergic hypothesis of schizophrenia, Moreover, a history of eexperimental investigations of the effects of these drugs in animals suggests that NMDA receptor antagonists may model some behavioral symptoms of schizophrenia in nonhuman subjects. In this review, the usefulness of PCP administration as a potential animal model of schizophrenia is considered. To support the contention that NMDA receptor antagonist administration represents a viablemodel of schizophrenia, the behavioral and neurobiological effects of these drugs are discussed, especially with regard to differing profiles following single-dose and long-term exposure. The neurochemical effects of NMDA receptor antagonist administration are argued to support a neurobiological hypothesis of schizophrenia, which includes pathophysiology within several neurotransmitter systems, manifested in behavioral pathology. Future directions for the application of NMDA receptor antagonist models of schizophrenia to preclinical and pathophysiological research are offered. [Neuropsychopharmacology 20:201-225, 1999] (C) 1999 American College of Neuropsychopharmacology. Published by Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 09:36:35