The association between externalizing disorders and highly variable EEG phase (trial-to-trial “arrhythmia”) during the P3 time-window might provide insight into several differences in neurotransmission that have been implicated in the etiology of alcoholism and ADHD. Relative to non-preferring mice, the alcohol-preferring inbred mouse strain C57BL/6 also shows decrements in P3-related phase-locking in delta- and theta-frequencies (Criado and Ehlers, 2009). This mouse model of alcoholism exhibits decreased hippocampal acetylcholine concentrations (Imperato et al., 1996), decreased sensitivity to glutamate agonists (Kosobud and Crabbe, 1990), and has been suggested to have deficits in γ-aminobutyric-acid (GABA) receptor function (Metten and Crabbe, 2005). Such associations between EEG and human alcoholism have also been supported by linkage to genes with cholinergic, glutamatergic, and GABAergic functions (for review, see Rangaswamy and Porjesz, 2008). Reduced theta-band phase-locking in the time-window between stimulus and button-response has also been observed 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
