Effects of chronic consumption of alcohol and other drugs of abuse include tolerance and dependence and these neuroadaptations arise, at least in part, from changes in gene expression [1], [2]. Several studies show changes in gene expression in autopsy brain tissue from human alcoholics [3]–[5], potentially providing therapeutic targets for new treatments for alcoholism. However, drug development requires testing in animal models and there is only limited information on brain gene expression changes in rodent models of chronic alcohol consumption [1]. For the Preferring (P) line of rats, three studies of ethanol consumption found changes in gene expression that often varied between brain regions [6]–[8]. Mice are widely used to study alcohol consumption but analyses of brain gene expression profiles following chronic alcohol drinking are remarkably limited for mouse models [1], [9], [10] and there are no direct comparisons of genomic changes in different animal models. One theme that has emerged from studies of gene expression in human alcoholism is the role of neuroimmune genes [3], [11], [12] and differential expression of this category of genes is also seen in
