The lack of an effect of a gabra2 deletion on drinking behaviour seems at first sight to be in disagreement with the human literature suggesting that polymorphisms of the α2-subunit are involved in ethanol dependence [1], [2]. Both risk and protective haplotypes have been identified, but it is currently unknown if and how these haplotypes translate into expression differences and if they would be in any way analogous to the constitutive mouse knockout. One factor that should be considered is how variations in the α2-subunit may interact with other intrinsic or environmental influences. Recent evidence suggests that the α2-subunit plays a role in ethanol dependence only in those who have been subjected to childhood trauma [11]. Since our mice received no developmental stress, it is perhaps unlikely that they would reveal a role of α2-subunit containing receptors in motivation to drink ethanol.
