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N ‐Methyl‐D‐Aspartate Receptors and Ethanol: Inhibition of Calcium Flux and Cyclic GMP Production
Author(s) -
Hoffman Paula L.,
Rabe Carolyn S.,
Moses Frances,
Tabakoff Boris
Publication year - 1989
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1989.tb07280.x
Subject(s) - nmda receptor , phencyclidine , kainate receptor , ethanol , chemistry , calcium , biophysics , biochemistry , receptor , glycine , glutamate receptor , biology , ampa receptor , amino acid , organic chemistry
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 m M inhibited NMDA‐stimulated Ca 2+ uptake by >30%, and ethanol also inhibited NMDA‐stimulated (Ca 2+ ‐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.