the inhibition of Pyk2 (protein tyrosine kinase 2), which results in the disinhibition of Rac1 (Ras-related C3 botulinum toxin substrate 1) that in turn can facilitate the proper assembly of dendritic spines (see Figure 8 in Suo et al., 2012). Mutations and deletions in Gatad2b have been associated with intellectual disabilities (e.g., Tim-Aroon et al., 2017). Perhaps more pertinent for the current study, the ENIGMA consortium has found that SNPs associated with both Gatad2b and Dlg2 are associated with differences in putamen size (Chen et al., 2017). The coexpression and physical interaction partners for Dlg2 are shown in Figure 1. Key partners include a number of genes encoding glutamate receptor subunits (e.g., Grin2b and Grid1) and genes encoding glutamate associated membrane proteins (e.g., Dlg1, Dlg4, and Dlgap1). Bell et al. (2016) have reviewed the literature associated with ethanol risk, ethanol effects and glutamate reward circuitry; importantly, these authors noted when comparing the P and NP rats, there were a number of differences in glutamate signaling genes that predate ethanol exposure. Clinical studies have shown that in family history positive (FHP) individuals there is an altered response to both alcohol and the NMDA antagonist ketamine, suggesting a genetic link between alcoholism
