Chronic EtOH administration differentially altered the expression of distinct GABAA receptor subunit mRNAs and peptide levels in various brain regions. In the cerebral cortex, both mRNA and peptide levels for GABAA receptor α1, α2, and α3 subunits were decreased (Devaud et al. 1995, 1997). In contrast, both α4, β1, β2, β3, γ1 and γ2 subunit mRNA and peptide levels were increased (Devaud et al. 1995, 1997). These alterations in the subunit expression affect the GABAA receptor assemblage and consequently, also affect receptor function and binding. It has been reported that recombinant GABAA receptors with α4β2γ2 subunits are less sensitive to GABA and benzodiazepines compared to α1β2γ2 receptors (Whittemore et al. 1996). Therefore, these alterations may account for the decreased sensitivity to GABA in cerebral cortical synaptoneurosomes (Morrow et al. 1988) and benzodiazepines in cortical membrane vesicles (microsacs) (Buck and Harris 1990). Following chronic EtOH exposure, acute EtOH did not facilitate the GABA or muscimol-stimulated Cl- uptake in cortex (Morrow et al. 1988) and in cerebellum (Allan and Harris 1987). In the cerebellum, chronic EtOH exposure decreased GABAA receptor α1 subunit
