Alcoholism is a complex neuropsychiatric condition with a multifactorial etiology that warrants the use of diverse neurobiological methods. This disorder not only involves effects of alcohol on brain structures but also subsequent alteration in brain electrophysiology potentiated by the addiction cycle. Alcoholism or alcohol use disorder (AUD) is a common familial disorder with increased risk among biological relatives of alcoholics (Goodwin et al., 1973; Cadoret et al., 1980; Bohman et al., 1987; Prescott, 2001). Family, twin, and adoption studies that highlight genetic contributions to AUDs suggest that both genders are equally vulnerable (Heath et al., 1997; Prescott et al., 1999). Yet AUDs may not be a specific disease but part of a spectrum of co-occurring disinhibitory disorders with overlapping genetic factors and shared underlying risk factors (Krueger et al., 2002; Kendler et al., 2003) and differential expression (Hicks et al., 2004). Thus, these behavioral phenomena – antisocial, impulsive traits, substance use disorders (SUDs), are variable expressions of a disinhibitory complex (Gorenstein and Newman, 1980) with AUD as one possible outcome in this spectrum. Understanding addictive behavior is complex and involves
