in ADHD (McLoughlin et al., 2014). Several candidate gene studies suggest abnormal neurotransmission in ADHD (particularly genes related to catecholamine function; Faraone et al., 2005), but what these mean for P3-related delta and theta expression remains unclear. Because differences in evoked energy are thought to reflect changes in the number of neurons directly activated by sensory stimulation and differences in phase-locking are thought to be influenced by “top down” neuromodulatory mechanisms (Sauseng et al., 2007), perhaps decrements in phase-locking for externalizing individuals is at least partly due to dysfunctional “tuning” of ongoing EEG rhythms by GABAergic interneurons, particularly in the theta-band (Cobb et al., 1995).
