Protracted consumption of alcohol in high doses evokes significant metabolic changes in a body, resulting in the development of physical dependence via unclear neurochemical mehanisms. Evidence from recent studies increasingly points to the brain GABAergic system as being of fundamental importance in mediation of alcohol withdrawal signs, either at a receptor level or due to its metabolic role in the brain. It has been assumed that prolonged alcohol ingestion may be responsible for growing hyperexcitability of CNS owing to mulfunction of the inhibitory GABAergic system and deficiency of the neurotransmitter and rapid increasing of motor agitation after withdrawal. A minor GABA-shunt has been demonstrated early as an additional governor of basic brain metabolism and a deliverer of the Krebs’ cycle substrates in situations like ischemia, hypoxia, and drug intoxication. In this study we attempted to investigate whether the GABA catabolizing enzymes (GABA-transaminase (GABA-T) and succinic semialdehyde dehydrogenase (SSA-DH) could influence on Krebs’ cycle functioning through siccinate dehydrogenase (SDH) and NAD-isocitrate dehydrogenase (IDH) in cortex and cerebellum of rats chronically treated by ethanol solutions. Male heterogeneous stock rats were treated by chronic intragastrical infusion of 25% ethanol solution in the dose of 5g/kg of body weight, twice daily, within 14 and 29 days. Then ethanol-treated rats were decapitated 1 hour after the last alcohol injection. Control rats received intragastrically adequate volumes of water for the same period as the alcohol-treated animals. In cortex the reliable decrease in the activities of all the enzymes tested was observed 14 and 29 days after chronic alcohol ingestion (ChAI). In cerebellum the 14 days’ ChAI led to the reliable increase in the activities of SDH and SSA-DH, whereas prolongation of alcohol intoxication caused activation of both the GABA-catabolising and the TCA cycle enzymes. The shifts observed in the GABA shunt and the TCA enzymes activities are likely to be explained by indirect adaptation of the brain regions to protracted alcohol administration. These changes might partially be responsible for probable risk of severe withdrawal relapsing in alcohol addicts.

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