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N-methyl-D-aspartate receptors and ethanol: inhibition of calcium flux and cyclic GMP production

Hoffman, P.L.; Rabe, C.S.; Moses, F.; Tabakoff, B.

Journal of Neurochemistry 52(6): 1937-1940

1989


ISSN/ISBN: 0022-3042
PMID: 2542453
DOI: 10.1111/j.1471-4159.1989.tb07280.x
Accession: 040767884

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Measurements of calcium uptake and cyclic GMP production by cerebellar granule cells grown in primary culture demonstrated that ethanol preferentially inhibited N-methyl-D-aspartate (NMDA) receptor-gated cation channel function. Concentrations of ethanol as low as 10 mM inhibited NMDA-stimulated Ca2+ uptake by greater than 30%, and ethanol also inhibited NMDA-stimulated (Ca2+-dependent) cyclic GMP accumulation in a similar, dose-dependent manner. Responses to kainate were significantly less sensitive to ethanol. Studies using various concentrations of NMDA, as well as phencyclidine (PCP) and glycine, suggested that ethanol affected the "coagonist" binding site of the NMDA receptor-channel complex, rather than the PCP recognition site.

N-methyl-D-aspartate receptors and ethanol: inhibition of calcium flux and cyclic GMP production

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