of ethanol, also differ in responses to the convulsant effects of GABAA receptor modulators, and to the locomotor-stimulant effects of benzodiazepines (Shen et al. 1998). Aside from selectively bred animals, inbred strains of mice also suggest a role for GABAA receptors. C57BL/6J mice are not only less sensitive to the sedative-hypnotic effects of ethanol than 129/SvJ mice but are also less sensitive to the GABA agonist propofol (Homanics et al. 1999b). Interestingly, the same study indicated that C57BL/6J mice are more sensitive to zolpidem and midazolam, but not Ro15-4513 and pentobarbital. Besides pharmacologic modifiers, molecular biological techniques have been used to assess the role of specific GABAA receptor subunits in innate tolerance. Using a coding polymorphism difference in C57BL/6J and DBA/2J mice, different lines of BXD recombinant inbred strains were used to determine whether variations in the gene for the GABAA receptor γ2 subunit correlated with ethanol-related behaviors. BXD lines with γ2 of DBA/2J origin were less ataxic on the screen test, but had greater ethanol-induced hypothermia (Hood and Buck 2000). A trend was also noted for sedative-hypnotic effects as well as a second motor ataxia test.
