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 mRNA and increased α6 subunit mRNA (Mhatre and Ticku 1992; Morrow et al. 1992). Chronic EtOH administration also decreased the polypeptide levels of the δ subunit of GABAA receptors in the rat cerebellum and hippocampus, whereas there were no changes in the δ subunit polypeptide levels in the rat cerebral cortex (Marutha Ravindran et al. 2007). Furthermore, chronic EtOH administration caused a down-regulation of native δ subunit-containing GABAA receptor assemblies in the rat cerebellum as determined by [(3)H]muscimol binding to the immunoprecipitated receptor assemblies (Marutha Ravindran et al. 2007).
