We have previously proposed that the ERN might be a useful endophenotype for internalizing disorders (Hajcak, Franklin, Foa, & Simons, 2007). In particular, the ERN might reflect information-processing abnormalities that mediate the pathway between genetic predisposition and disease states (Gottesmann & Gould 2003). Gottesmann and Gould (2003) highlighted several characteristics of endophenotypes. First, an endophenotype should be associated with a disease. Several studies have shown that increased error-related brain activity characterizes patients with anxious (Gehring, Himle, & Nisenson, 2000; Hajcak et al., 2003a; Hajcak, McDonald et al., 2004; Hajcak & Simons, 2002; Ruchsow, Spitzer et al., 2005) and depressive symptoms (Chiu & Deldin, 2007). Additionally, an endophenotype should be state-independent. This has been verified in anxiety disorders, with studies showing no change in ERN amplitude during symptom provocation (Moser et al., 2005) or after successful treatment (Hajcak et al., 2007; Ladouceur et al., 2007). To our knowledge, though, there have been no research studies to date that have looked at state changes in symptoms of depressed patients. Endophenotypes must also be heritable. Preliminary studies reported by Anohkin, Golosheykin, and Myers
