Abstract

Administration of a single dose of ethanol decreases cyclic GMP levels in all brain areas and cyclic AMP levels in the cerebral cortex, cerebellum, and pons-medulla oblongata. The cyclic AMP decrease is probably not mediated by an effect of ethanol on adenylate cyclase or phosphodiesterase activities. Low doses of ethanol increase the postdecapitation-induced rise of cyclic AMP in pons-medulla oblongata while high ethanol doses decrease the postdecapitation-induced rise in all brain areas. This decrease might be due to the inhibited conversion of ATP into adenosine in ethanol-treated animals. Chronic administration of ethanol prevents the cyclic AMP-lowering effect of an acute ethanol dose, while the decrease of cyclic GMP is still present. During ethanol withdrawal cyclic AMP levels are increased in the cerebral cortex and pons-medulla oblongata. An inverse relationship between cyclic GMP and GABA levels in the cerebellum of rats undergoing withdrawal was observed and it might be related to some symptoms of ethanol withdrawal. Levels of cyclic nucleotides and GABA were correlated also in some other brain areas indicating that cyclic nucleotides in these areas might be involved in ethanol withdrawal.

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