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. 1994 Feb;18(1):81-5.
doi: 10.1111/j.1530-0277.1994.tb00884.x.

Involvement of protein kinase C in ethanol-induced inhibition of NMDA receptor function in cerebellar granule cells

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Involvement of protein kinase C in ethanol-induced inhibition of NMDA receptor function in cerebellar granule cells

L D Snell et al. Alcohol Clin Exp Res. 1994 Feb.

Abstract

Ethanol inhibits N-methyl-D-aspartate (NMDA)-stimulated increases in intracellular Ca2+ in cerebellar granule cells apparently by reducing the potency of glycine to act as a co-agonist at the NMDA receptor. The inhibitory effect of ethanol on the NMDA response in these cells can be reversed not only by a high concentration of glycine, but also by the protein kinase inhibitors, staurosporine and calphostin C. We previously showed that activation of protein kinase C in cerebellar granule cells also resulted in inhibition of the NMDA response, and in decreased potency of glycine at the NMDA receptor. Furthermore, the inhibitory effects of ethanol and protein kinase C activation are not additive. These results suggest a role for protein kinase C in ethanol inhibition of NMDA responses in cerebellar granule cells. In contrast, although ethanol can inhibit the response to kainate in these cells in a "competitive" manner, this response is not affected by activation of protein kinase C.

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