Genetically modified mouse models such as transgenics and global knockouts have increased our understanding of GABAA receptor involvement in behavioral ethanol actions (see Boehm et al. 2006, 2004b; Crabbe et al. 2006 for more detailed reviews). For instance, the locomotor-stimulant effects of ethanol appear to be modulated by α1-GABAA receptors. The α1-GABAA receptor knockout mice have increased ethanol-induced activity (Blednov et al. 2003b; June et al. 2007; Kralic et al. 2003). Ethanol’s sedative-hypnotic effects may also involve interactions with α1-GABAA receptors since male α1-GABAA receptor knockout mice have reduced loss of righting reflex duration (Blednov et al. 2003a). However, this effect was not observed in other studies (Kralic et al. 2003), possibly due to variation in genetic background of the strains used to create separate knockout mouse lines. Further, α2-GABAA receptors are implicated in the sedative-hypnotic effects of ethanol, as shown by reduced ethanol-induced loss of righting reflex in α2- GABAA receptor knockout animals (Boehm et al. 2004b). Studies using benzodiazepine-insensitive histidine101 to arginine (H101R) knockin mice have also indicated a role for α2-GABAA receptors in ethanol’s sedative-hypnotic effects. The
