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Ethanol is primarily responsible for the behavioural effects of acute alcoholic beverage consumption, which involves central nervous system dysfunction. The mechanisms of ethanol action in the nervous system are poorly understood, particularly those related to the neurotoxicity of high acute ethanol consumption. We now describe a simple experiment showing that a concentration of ethanol, which is reached in the plasma after high acute ethanol intake, disrupts rat brain nerve terminals, as measured by the release of lactate dehydrogenase. This cytolytic action of ethanol was further enhanced upon depolarisation of the nerve terminals suggesting that the mechanism of action of ethanol might not be related to modification of lipid bilayer properties.
Keywords: Nerve terminals; Neurotoxicity; Ethanol; Neurochemistry; Synaptosomes*Corresponding author. Tel./fax: 351-21 7936787
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