Dopamine D1 receptor expression is greater than D2 receptor expression in the prefrontal cortex (e.g. 20-fold increase of D1 relative to D2 in primates) (Lidow, Goldman-Rakic, Gallager & Rakic, 1991). Animal models of working memory have shown that pharmacologically enhancing D1 receptor function in prefrontal cortex can compensate for dopamine dysfunction and facilitate long-lasting recovery of cognitive and behavioral functions (Williams & Castner, 2006). There is indirect but strong evidence that the major alleles of rs4532 and rs265978 increase D1 expression via linkage disequilibrium with rs686, a known functional 3′ untranslated region (3′ UTR) DRD1 polymorphism that affects D1 receptor expression levels (Huang et al., 2008). As such, we speculate that in the current study, allelic variation moderated the developmental dynamics of DRD1 gene expression and function in a way that positively modified cognitive growth in a subgroup of ADHD probands to help them overcome some of their early difficulties with inattention, hyperactivity and impulsivity. Alternatively, our results could be reflecting the impact of DRD1 on changes in attentional control on working memory performance rather than vice versa. However, we
