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Titolo:
CHRONIC ETHANOL TREATMENT UP-REGULATES THE NMDA RECEPTOR FUNCTION ANDBINDING IN MAMMALIAN CORTICAL-NEURONS
Autore:
HU XJ; TICKU MK;
Indirizzi:
UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,7703 FLOYD CURL DR SAN ANTONIOTX 78284 UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL SAN ANTONIO TX 78284 UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT SAN ANTONIO TX 78284
Titolo Testata:
Molecular brain research
fascicolo: 2, volume: 30, anno: 1995,
pagine: 347 - 356
SICI:
0169-328X(1995)30:2<347:CETUTN>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
METHYL-D-ASPARTATE; SENSITIVE CALCIUM CHANNELS; RAT-BRAIN; WITHDRAWAL SEIZURES; GABAERGIC TRANSMISSION; IONOPHORE COMPLEX; CHRONIC EXPOSURE; UP-REGULATION; PC12 CELLS; ANTAGONIST;
Keywords:
ETHANOL; NMDA RECEPTOR; UP-REGULATION; CA2+; CORTICAL NEURON;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
61
Recensione:
Indirizzi per estratti:
Citazione:
X.J. Hu e M.K. Ticku, "CHRONIC ETHANOL TREATMENT UP-REGULATES THE NMDA RECEPTOR FUNCTION ANDBINDING IN MAMMALIAN CORTICAL-NEURONS", Molecular brain research, 30(2), 1995, pp. 347-356

Abstract

In the present study, we investigated the effects of chronic ethanol exposure on NMDA-mediated increase in intracellular calcium concentration ([Ca2+](i)) by means of fluorescent measurement of [Ca2+](i) with Fura-2AM in mammalian cortical cultured neurons, and the radioligand [H-3]MK-801 binding to cortical neuronal membranes. Chronic exposure ofthe cortical neurons to ethanol (50 mM, 5 days) did not produce any change in the cell protein, morphological appearance, and the resting [Ca2+](i); however, it significantly enhanced the NMDA-mediated increase in [Ca2+](i). The EC(50) value of NMDA was not significantly alteredfollowing chronic ethanol exposure, however, its E(max) value was increased by similar to 45%. Furthermore, chronic ethanol exposure increased the specific [H-3]MK-801 binding in cortical neuronal membrane preparation by similar to 30%. The enhancement of the NMDA-mediated increase in [Ca2+](i) and the increase in [H-3]MK-801 specific binding werereversed following 48 h ethanol withdrawal. Additionally, this enhanced NMDA response and the increased [H-3]MK-801 specific binding were susceptible to blockade by the concomitant chronic exposure of the cortical neurons to the NMDA receptor competitive (20 mu M CPP), and non-competitive (1 mu M MK-801) antagonists, but not by the non-NMDA receptor antagonist, CNQX (10 mu M), and the L-type calcium channel blocker,nitrendipine (10 mu M). Taken together, these results suggest that chronic ethanol exposure upregulated the NMDA receptor function and binding in cortical cultured neurons, and this increased NMDA receptor function is a NMDA receptor-mediated process. This altered NMDA receptor function may be responsible for the chronic ethanol-induced behavioralconsequences and withdrawal syndrome associated with chronic ethanol exposure.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 09:38:05