and not its physical features [53]. Across numerous ERP studies in alcoholism, the robust and consistent finding is that alcoholics and their high-risk offspring show reduced P3 amplitude across a variety of tasks and modalities (see [42,54] for reviews). Furthermore, the P3 component is highly heritable [55-59] and has proven to be useful as an endophenotypic marker of alcoholism. However, a reduction of P3 amplitude has not been found to be specific to alcoholism, but is also found in other related externalizing or disinhibitory disorders, such as substance use disorders (SUDs), conduct disorder (CD), antisocial personality disorder (ASPD), oppositional defiance disorder, (ODD), and attention deficit hyperactivity disorder (ADHD) [60,61]. In SUDs, reduced P3 amplitudes have been observed in individuals with dependence/abuse for tobacco [62], cocaine [63], cannabis [64,65], and ‘ecstacy’ or methylene-dioxy-methamphetamine (MDMA) [66]. Thus, reduced P3, while not specific to alcoholism, is a marker of alcoholism and related externalizing or disinhibitory disorders. However, the P3 component is not a unitary electrophysiological phenomenon elicited during cognitive processing; but emanates from multiple sources in the brain with contributions from frontal cortex (including anterior cingulate), parietal cortex, and hippocampus [7,67-71]; furthermore, it is primarily the outcome of event-related delta (concentrated more posteriorly)
