With the development of more sophisticated fine-mapping techniques, studies on GABAA receptor subunit expression have been associated to specific genotypes. Thus, Dodd and colleagues reported that the GABRB2 gene, which encodes for the β2 subunit, did not influence the β2 subunit expression; rather, expression of β3 subunit was increased in controls with GABRB2-1,2 genotype, but not in alcoholics with the same genotype (Dodd et al. 2004). Furthermore, aldehyde dehydrogenase ADH1C, D2 dopamine receptor DRD2B, excitatory amino acid transporter 2 EAAT2, and apolipoprotein E APOE genotypes modulate GABAA receptor β subunit expression in superior frontal cortex toward a less-effective form of the receptor (Dodd et al. 2004, 2006). Alleles associated with alcoholism also appear to reduce the β3:β2 ratios in alcoholic’s superior frontal cortex. GABAA receptors with the β2 subunit are less efficacious at mediating chloride flux in response to any GABA concentration, so this subunit switching would have the effect of attenuating GABAA receptor-mediated inhibition and may make this brain region more susceptible to the neuropathological consequences of chronic alcoholism (Buckley et al. 2006). More recently, Haughey et al. (2008)
