Amplitude reduction of the P3 event-related potential (ERP) is well-documented in cases of alcoholism (Euser et al., 2012). Recently, this deficit in P3 amplitude (P3AR) has been extended to a broader spectrum of “externalizing” psychopathology which includes substance use disorders (SUDs) and disorders that often co-occur with SUDs such as antisociality and attention-deficit hyperactivity disorder (Iacono et al., 2002). A common externalizing dimension is thought to unite these disorders (Kendler et al., 2003; Krueger, 1999) and accounts for their relationship with P3AR (Patrick et al., 2006). This association between P3AR and externalizing is heritable (Gilmore et al., 2010b; Yoon et al., 2006) and genetically mediated (Hicks et al., 2007) and has been posited as an endophenotype for such disorders (Iacono and Malone, 2011) whereby a biological measure (e.g., P3 amplitude) is thought to be closer to genetic influence than otherwise complex symptomatology (e.g., alcohol dependence). Although substantial clinical and epidemiological evidence exists demonstrating P3AR’s robust association with SUDs and other externalizing disorders, possible mechanisms underlying this difference in brain response has received considerably less attention. The current study asks whether reduced P3-related phase-locking (arrhythmic brain responding) could account for the externalizing and effect.
