Initial responses to ethanol are highly informative predictors of AUD risk, with level of response (LR) being inversely correlated with susceptibility [15], [16], [17]. Similar inverse relationships between acute LR and ethanol consumption have been observed with a number of selectively bred or gene targeted rodent strains [18]. Therefore, an understanding of the molecular pathways initially perturbed by ethanol may identify important contributors to LR behaviors and elevated AUD susceptibility. As with humans, genetically diverse populations of mice exhibit a wide range of ethanol sensitivity. The B6 and D2 inbred strains are a particularly well documented example, with numerous studies reporting that ethanol induces significantly larger responses in D2 mice, when compared to B6, across a number of measures such as locomotor activation [19] and withdrawal severity [20].
