In cultured chick neurons, 5–10 mM ethanol elicited maximal GABA response potentiation [38]. Potentiation of IGABA by ethanol (20 mM) has also been seen in cultured mouse cortical neurons [27]. There have been few successful studies in attempts to replicate these findings in more intact systems, however. The effect of acute alcohol exposure on GABA responses has also been examined in the piriform cortex of adult rats subjected to chronic ethanol treatment. Acute ethanol (10 mM) modulated GABA in both chronic drinking and control groups, but a higher percentage of ethanol-induced potentiation was seen in the chronic ethanol group [39]. This was despite the observation that responsiveness to GABA was decreased in the chronic drinking group, indicating that chronic ethanol attenuates sensitivity to GABA, while increasing sensitivity to ethanol-induced GABA potentiation. In the lateral orbital frontal cortex in mice, 11 mM acute ethanol decreased spike frequency and input resistance supporting the idea of an inhibitory action of acute alcohol on excitability via a chloride channel [40]. Other studies have also investigated ethanol modulation of glutamatergic responses. It has been shown
