Evidence Against a Role of Acetaldehyde in Electroencephalographic Signs of Ethanol-Induced Intoxication

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Abstract
Acetaldehyde, the proximate metabolite of ethanol, when injected intravenously in rats produced electroencephalogram (EEG) changes similar to those observed after ethanol administration; that is, low doses activated the cortical EEG and higher doses caused activation followed by synchronization. However, when acetaldehyde was administered as a continuous infusion to simulate production of ethanol-derived acetaldehyde, only synchronization occurred, and then only at the higher doses. At low infusion dosage when the EEG was unaffected, concentrations of acetaldehyde in the blood were equal to or greater than those which occur during intoxication. Thus, acetaldehyde by itself cannot account for ethanol-induced EEG synchronization.