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Titolo:
ETHANOL, STROKE, BRAIN-DAMAGE, AND EXCITOTOXICITY
Autore:
CREWS FT; STECK JC; CHANDLER LJ; YU CJ; DAY A;
Indirizzi:
UNIV N CAROLINA,SCH MED,CTR ALCOHOL STUDIES,CB 7178,1021 THURSTON BOWLES BLDG CHAPEL HILL NC 27599 UNIV FLORIDA,DEPT NEUROL SURG GAINESVILLE FL 32610 LOUISIANA STATE UNIV SHREVEPORT LA 71105
Titolo Testata:
Pharmacology, biochemistry and behavior
fascicolo: 4, volume: 59, anno: 1998,
pagine: 981 - 991
SICI:
0091-3057(1998)59:4<981:ESBAE>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
D-ASPARTATE RECEPTORS; ISCHEMIC NEURONAL INJURY; TRANSIENT FOREBRAIN ISCHEMIA; NITRIC-OXIDE SYNTHASE; GLUTAMATE NEUROTOXICITY; CORTICAL-NEURONS; SUBUNIT COMPOSITION; CEREBRAL-ISCHEMIA; NMDA ANTAGONISTS; RAT HIPPOCAMPUS;
Keywords:
ETHANOL; STROKE; EXCITOTOXICITY; NMDA; NITRIC OXIDE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
59
Recensione:
Indirizzi per estratti:
Citazione:
F.T. Crews et al., "ETHANOL, STROKE, BRAIN-DAMAGE, AND EXCITOTOXICITY", Pharmacology, biochemistry and behavior, 59(4), 1998, pp. 981-991

Abstract

The N-methyl-d-aspartate (NMDA)-glutamate receptor could contribute to stroke, trauma, and alcohol-induced brain damage through activation of nitric oxide formation and excitotoxicity. In rat primary cortical cultures NMDA was more potent at activating nitric oxide formation than triggering excitotoxicity. Ethanol dose dependently inhibited both responses. In contrast, treatment of neuronal cultures with ethanol (100 mM) for 4 days significantly increased NMDA stimulated nitric oxide formation and excitotoxicity. These findings suggest that ethanol acutely inhibits but chronically causes supersensitivity to NMDA-induced excitotoxicity in neuronal cultures. To investigate ethanol's interaction with stroke induced damage models of global cerebral ischemia were studied. Transient global ischemia resulted in a loss of hippocampal CA1 pyramidal neurons over a 3- to 5-day period. Determinations of the NMDA receptor ligand binding stoichiometry or postischemic receptor binding changes did not show differences between neurons that undergo delayed neuronal death following ischemia and those that show no toxicity, for example, CA1 and dentate gyrus, respectively. Acute ethanol (3 g/kg) was found to protect against ischemia-induced CA1 hippocampal damage by lowering body temperature, but not under temperature controledconditions. These studies indicate that the factors contributing to stroke-induced brain damage are complex, although they are consistent with chronic ethanol increasing stroke-induced brain damage by increasing NMDA excitotoxicity. (C) 1998 Elsevier Science Inc.

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Documento generato il 02/12/20 alle ore 18:31:33