which the subject has self-reported feelings of “highness” (Wang et al., 2000) and mood alteration (de Wit et al., 1990). This decrease is observed in cortical areas, including PFC, with little change seen in basal ganglia and corpus callosum (Volkow et al., 1990). While these studies were performed with moderate doses of EtOH, low doses have also been shown to reduce glucose metabolism, although behavioral deficits were not reported at this low dose (Volkow et al., 2006). Transcranial magnetic stimulation (TMS) has been combined with brain imaging to probe changes in PFC activity, and healthy social drinkers show decreased TMS-induced prefrontal activity after 0.8 g/kg EtOH (Kahkonen et al., 2003). These results are congruent with studies that have shown decreases in prefrontal glucose metabolism in the PFC after acute EtOH administration (de Wit et al., 1990; Volkow et al., 1990). The deleterious effects of acute EtOH on PFC-dependent behaviors may also result from the breakdown of functional specificity in different brain regions. Indeed, recent work has demonstrated a decrease in functional heterogeneity in right prefrontal cortex following ethanol administration (Volkow et al., 2008). A decrease in asymmetry has also been observed while inebriated patients participated in a verbal fluency task
