facilitating addiction in A1 carriers and high P3 amplitude acting as a protective factor. According to this hypothesis, P3 is a moderator, rather than mediator, of genetic risk (Anokhin et al., 1999a). This hypothesis is consistent with the notion that P3 (which is ubiquitous across a variety of cognitive tasks) reflects the recruitment of cognitive control network, with higher P3 indicating higher cognitive control capacity and thus better impulse control. The proposed interpretation of P3 as an indicator of general, non-specific cognitive control capacity is supported by fMRI studies using oddball tasks(reviewed in Kiehl et al., 2005; Linden, 2005; Polich, 2007; Soltani and Knight, 2000) showing significant activation in frontal and parietal regions that are broadly consistent with regions implicated in a common, “superordinate” fronto-parietal system cognitive control network (Dosenbach et al., 2007; Naghavi and Nyberg, 2005; Niendam et al., 2012) as well as dorsal frontopriatal attention network supporting goal-directed (top-down) selection for stimuli and responses (Corbetta and Shulman, 2002).
