title: N-methyl-D-aspartate receptors and ethanol: inhibition of calcium flux and cyclic GMP production.
abstract: 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.
authors.affiliation: Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland.
authors.forename: P L
authors.initials: PL
authors.lastname: Hoffman
authors.forename: C S
authors.initials: CS
authors.lastname: Rabe
authors.forename: F
authors.initials: F
authors.lastname: Moses
authors.forename: B
authors.initials: B
authors.lastname: Tabakoff
mesh_terms: D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000502:physiology; D002118:Calcium / Q000037:antagonists & inhibitors*; D002478:Cells, Cultured; D002531:Cerebellum / Q000166:cytology / Q000378:metabolism; D006152:Cyclic GMP / Q000096:biosynthesis*; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000494:pharmacology*; D005998:Glycine / Q000494:pharmacology; D006098:Granulocytes / Q000378:metabolism; D016202:N-Methylaspartate; D009994:Osmolar Concentration; D010622:Phencyclidine / Q000494:pharmacology; D010852:Picrotoxin / Q000494:pharmacology
chemical_list: D001224:Aspartic Acid; D002118:Calcium; D006152:Cyclic GMP; D000431:Ethanol; D005998:Glycine; D016202:N-Methylaspartate; D010622:Phencyclidine; D010852:Picrotoxin