We have previously shown that an acute ethanol dose (1 g/kg), sufficient to impair the performance of a healthy rabbit, also reversibly depresses the activity of those limbic-cortex neurons that are specifically activated during recently learned behavioral acts. Our new morphological and neurophysiological data suggest a death of such neurons after 9-month chronic ethanol treatment. The effect of acute ethanol administration on neurons and performance speed in alcoholic rabbits was opposite to that found in healthy animals. Our results help to understand why neurocognition of alcoholics changes and why acute low-level alcohol ingestion influences them differently than healthy individuals. (C) 2000 Elsevier Science Inc.
- Cingulate cortex