to withdrawal than wildtype control mice, possibly masking a difference between mouse lines (Blednov et al. 2003b). Studies have also assessed the role of β subunits in ethanol withdrawal seizure severity. β2-GABAA receptor knockout mice had increased HICs after chronic ethanol (Blednov et al. 2003b); however, knockouts had higher ethanol intake than controls. In other studies, β3 asparagine265 to methionine (N265M)-GABAA receptor knockin mice had enhanced withdrawal following chronic ethanol exposure (Sanchis-Segura et al. 2007). Withdrawal from acute high doses of ethanol has also been used to assess the role of specific GABAA receptor subtypes. The expression of γ2 subunits, which are involved in phasic inhibition, has also been thought to play a role. Work has shown that allelic variation in gabrg2, the gene encoding for the γ2 subunit, was correlated with withdrawal-related behavior (Hood and Buck 2000). However, γ2L-GABAA receptor knockouts had similar withdrawal-related HICs (Homanics et al. 1999a). In studies of subunits involved in tonic inhibition, δ-GABAA receptor knockout mice displayed decreased ethanol withdrawal HICs than controls; however, this effect was dependent on background strain of the mice (Mihalek et al. 2001). Interestingly, studies in α6-GABAA receptor knockout mice (which pairs with δ in the cerebellum) did not
