In the human genome, the majority of GABAA subunit genes are clustered on four chromosomes: 4p12 (β1, α4, α2, γ1), 5q34 (β2, α6, α1, γ2), 15q11 (β3, α5, γ3) and Xq28 (θ, α3, ε) (Steiger and Russek, 2004). Homologous clusters of genes are found on mouse chromosomes 5, 11, 7 and × and are thought to have derived from a single ancestral αβγ cluster by gene duplication (Russek, 1999). Positioning of GABAA genes in tandem is believed to facilitate coordinated and tissue-specific co-regulation of gene expression by allowing clustered genes to share regulatory elements (Steiger and Russek, 2004, Barnard et al., 1998). Co-regulation of genes encoding the GABAA receptor subunits is evidenced by variation in RNA levels in post-mortem human brain samples over a range of developmental ages. At earlier stages of development, chr4p12 GABAA genes are expressed at higher levels than chromosome 5q34 genes. However, during development, chr4p12 genes are down regulated while chromosome 5q34 genes are up regulated (Fillman et al., 2010). Similarly, in rhesus monkeys, there is a developmental up regulation of the α1 subunit and a
