Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Therapeutic implications of the hyperglutamatergic effects of NMDA antagonists
Autore:
Krystal, JH; Belger, A; DSouza, DC; Anand, A; Charney, DS; Aghajanian, GK; Moghaddam, B;
Indirizzi:
VA Connecticut Healthcare Syst, Psychiat Serv 116A, W Haven, CT 06516 USA VA Connecticut Healthcare Syst W Haven CT USA 06516 W Haven, CT 06516 USA Connecticut Mental Hlth Ctr, Abraham Ribicoff Res Facil, New Haven, CT 06519 USA Connecticut Mental Hlth Ctr New Haven CT USA 06519 ew Haven, CT 06519 USA Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA Yale Univ New Haven CT USA iv, Sch Med, Dept Psychiat, New Haven, CT USA
Titolo Testata:
NEUROPSYCHOPHARMACOLOGY
fascicolo: 6, volume: 21, anno: 1999, supplemento:, S
pagine: S143 - S157
SICI:
0893-133X(199912)21:6<S143:TIOTHE>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
METHYL-D-ASPARTATE; PRIMATE PREFRONTAL CORTEX; CENTRAL-NERVOUS-SYSTEM; SCHIZOPHRENIC-PATIENTS; CEREBRAL-CORTEX; NEGATIVE SYMPTOMS; INDUCED PSYCHOSIS; ANTIPSYCHOTIC ACTION; RECEPTOR ANTAGONISM; GLUCOSE-UTILIZATION;
Keywords:
glutamate; NMDA; ketamine; schizophrenia; frontal cortex; attention; cognitive function; pharmacotherapy; lamotrigine; serotonin; 5-HT2A; LY354740; M100907; MDL 100,907;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
148
Recensione:
Indirizzi per estratti:
Indirizzo: Krystal, JH VA Connecticut Healthcare Syst, Psychiat Serv 116A, 950 Campbell Ave, W Haven, CT 06516 USA VA Connecticut Healthcare Syst 950 Campbell Ave W Haven CT USA 06516
Citazione:
J.H. Krystal et al., "Therapeutic implications of the hyperglutamatergic effects of NMDA antagonists", NEUROPSYCH, 21(6), 1999, pp. S143-S157

Abstract

Antagonists of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor produce transient effects in healthy human subjects that resemble symptoms observed in some schizophrenic patients. NMDA antagonists also impair aspects of human corticolimbic information processing in a fashion that resembles deficits associated with schizophrenia, as measured by electrophysiologic and functional neuroimaging paradigms. Although all current antipsychotics block dopamine-2 (D-2) receptors, recent studies question the centrality of D-2-receptor stimulation to the NMDA-antagonist psychosis. For example, pretreatment with haloperidol fails to attenuate the psychotic effects ofketamine in healthy human subjects. Also, pretreatment with amphetamine fails to increase these effects of ketamine. Both preclinical and clinical studies suggest that subanesthetic doses of NMDA antagonists activate glutamate neurons in the cerebral cortex and hippocampus. Recent preclinical and clinical studies also suggest that duties that attenuate glutamate release, including group II/III metabotropic glutamate-receptor agonists, drugs thatblock voltage-dependent ion channels, and serotonin-2A (5-HT2A)-receptor antagonists may attenuate NMDA antagonist effects. To the extent that NMDA antagonist effects provide insight into the pathophysiology of schizophrenia, these novel pharmacologic strategies and others may provide a rationale for the exploration of new treatments that do not involve D-2-receptor blockade. If schizophrenia, like NMDA-antagonist effects, involves hyperglutamatergic states, then these novel pharmacotherapeutic strategies also may haveneuroprotective or neurotrophic consequences that influence the course of schizophrenia. [Neuropsychopharmacology 22:S143-S157, 1999] (C) 1999 American College of Neuropsychopharmacology. Published by Elseiver Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/01/20 alle ore 07:12:47