Ischemia-induced glutamate release in rat frontoparietal cortex after chronic alcohol and withdrawal

High doses of ethanol increase stroke risk: in this context, a role for excitatory amino acids has been proposed. The present results show that, in frontoparietal cerebral cortex, chronic ethanol treatment (10% v/v in drinking water for 28 days) was able to slightly reduce glutamate release (evaluated through transdialysis coupled with high-pressure liquid chromatography) following focal ischemia as regards non-treated ischemic rats. This reduction was, however, not associated with decreased cerebral damage. In 24-h withdrawing rats, histological and morphometric analyzes showed an exacerbated cerebral damage coupled with higher glutamate and aspartate release compared to controls. These results suggest that adaptive changes following chronic ethanol consumption lead to an increased excitotoxicity that is particularly evident during the withdrawal condition.