and antisocial behavior (Euser et al., 2012; Porjesz et al., 2005). Twin studies of primarily White samples have shown that the association between P3 amplitude and externalizing behaviors are due, in part, to genetic correlation (i.e. shared genetic influences; 4.8% of variance is shared) between these phenotypes (Gilmore, Malone, Bernat, & Iacono, 2010; Hicks et al., 2007; Yoon, Iacono, Malone, & McGue, 2006). Based on twin and family data, low P3 amplitude has been identified as a candidate endophenotype for externalizing behaviors (Iacono & Malone, 2011; Porjesz et al., 2005), suggesting that the neurophysiological characteristics of which P3 amplitude is a marker may mediate genetic liability. However, this evidence is based on the estimation of latent genetic factors. To our knowledge, no studies have employed measured genetic liability to provide direct tests of the hypothesis that P3 amplitude mediates the association between genetic predispositions and externalizing behaviors.
