A preliminary account of some of this work was presented previously (Rabe and Tabakoff, 1988).
N-Methyl-D-Aspartate Receptors and Ethanol: Inhibition of Calcium Flux and Cyclic GMP Production
Article first published online: 5 OCT 2006
Journal of Neurochemistry
Volume 52, Issue 6, pages 1937–1940, June 1989
How to Cite
Hoffman, P. L., Rabe, C. S., Moses, F. and Tabakoff, B. (1989), N-Methyl-D-Aspartate Receptors and Ethanol: Inhibition of Calcium Flux and Cyclic GMP Production. Journal of Neurochemistry, 52: 1937–1940. doi: 10.1111/j.1471-4159.1989.tb07280.x
- Issue published online: 5 OCT 2006
- Article first published online: 5 OCT 2006
- Received February 13, 1989; accepted February 21, 1989
- N-Methyl-D-aspartate receptor-gated ion channel;
- Cyclic GMP accumulation;
- Cerebellar granule cells;
- Kainate receptor
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 >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.