An increase in phase locking at beta frequencies, in frontal cortex, was found to correlate selectively and significantly with the human participant’s overall ratings of their level of ethanol intoxication. Beta activity in the EEG has also been long associated with risk for the development of alcoholism (Campanella et al., 2009; Ehlers and Schuckit, 1990; Porjesz et al., 2005; Rangaswamy et al., 2004). Findings from the Collaborative Study on the Genetics of Alcoholism (COGA) have demonstrated that genetic linkage and linkage disequilibrium between the beta frequencies of the EEG and a GABAA receptor gene on chromosome 4 (Porjesz et al., 2002). The GABAA receptor gene has also been found to be associated with the diagnosis of alcohol dependence in that dataset (Edenberg et al., 2004). Interestingly, many of the behavioral effects of ethanol overlap with the effects of GABAA receptor agonists, whereas decreases in ethanol responses can be produced by inverse agonists and antagonists (see Grobin et al., 1998; Kumar et al., 2009, for reviews). Although some of the effects of low doses of ethanol (30-100 nM) appear to be
