The alterations in GABAA receptor gene expression are regionally and temporally dependent. For example, chronic EtOH consumption produced a significant increase in the level of GABAA receptor α4 subunit peptide in the hippocampus following 40 days but not 14 days exposure (Matthews et al. 1998). The relative expression of hippocampal GABAA receptor α1, α2, α3, β(2/3), or γ2 subunits was not altered by either period of chronic EtOH exposure (Charlton et al. 1997; Matthews et al. 1998). Hippocampal α1 subunit immunoreactivity and mRNA content were also significantly reduced after 12 weeks of treatment, but not after 4 weeks of exposure. In contrast, α5 mRNA content was increased in this brain region. In marked contrast, chronic EtOH consumption for both 14 (Devaud et al. 1997) and 40 (Devaud et al. 1997; Matthews et al. 1998) days significantly increased the relative expression of cerebral cortical GABAA receptor α4 subunits and significantly decreased the relative expression of α1 subunits (Devaud et al. 1997; Matthews et al. 1998). These findings indicate that chronic EtOH consumption alters GABAA receptor gene expression in the hippocampus but
