GABAA receptor involvement in acute, rapid, and chronic ethanol tolerance has also been assessed in various animal models. For instance, selectively bred mice that differ in diazepam sensitivity also differ in rapid tolerance development. Mice that are more resistant to diazepam’s effects also develop more rapid tolerance than diazepam-sensitive mice (Gallaher and Gionet 1988). Inbred long-and short-sleep mice display differences in rapid tolerance. Long-sleep mice that display a greater response to ethanol’s sedative-hypnotic effects also develop greater rapid tolerance (Radcliffe et al. 2005). Indeed, these mice differ in GABAA receptor inhibitory post-synaptic responses (Proctor et al. 2004), suggesting the involvement of different GABAergic responses to ethanol. BXD mice have also been used to assess tolerance. Assessment of the parental strains, C57BL/6J and DBA/2J, indicates that although DBA/2J mice were more sensitive to ethanol’s motor ataxic effects, they also develop greater AFT (Gallaher et al. 1996). Subsequent tests show quantitative trait loci (QTL) for ethanol tolerance on chromosomes 9 and 11. While these studies did not identify a role for GABAA receptors in tolerance, it is possible that subunits from the
