The regulation of various GABAA receptor subunits by ethanol differs across brain regions (Grobin et al. 2000). For example, chronic ethanol consumption for 14 days increases GABAA receptor α4 subunit peptide expression in the cerebral cortex and the hypothalamus (Devaud et al. 1997), decreases α4 subunit peptide levels in the amygdala and nucleus accumbens (Papadeas et al. 2001), and does not alter α4 subunit peptide levels in the hippocampus or ventral tegmental area (Matthews et al. 1998; Papadeas et al. 2001). However, repeated ethanol withdrawals or longer ethanol exposure increases α4 subunit peptide expression in the hippocampus (Cagetti et al. 2003; Matthews et al. 1998) and these effects are associated with alterations in the pharmacological responses of GABAA receptors to benzodiazepine agonists and inverse agonists (Cagetti et al. 2003). Furthermore, in cerebellum, α6 subunit mRNA and peptide levels are increased while α1 subunit peptide and mRNA are decreased following chronic ethanol administration (Mhatre et al. 1993; Morrow et al. 1992). Therefore, it is clear that adaptation in GABAA receptor subunits expression caused by chronic ethanol administration is not universal across
