Alcohol is a commonly used addictive substance with multiple behavioral and neurobiological effects. As a psychoactive compound, it can elicit a spectrum of behavioral effects, which include gregariousness, anxiolysis, aggression, loss of executive functions and cognitive deficits. A host of pharmacokinetic factors (i.e., absorption, distribution in the tissues, and rate of metabolism - primarily in the liver) contribute to the intensity and duration of ethanol’s effects, whereas an array of pharmacodynamic factors, determine the behavioral and subjective effects of ethanol on the brain. The spectrum of subjective responses to alcohol is attributed to the ability of ethanol to inhibit or to activate multiple neural pathways. Specifically, how a person responds to alcohol will ultimately depend on how the neural pathways are organized in that individual and the extent to which certain pathways are inhibited or activated. It is well known that there is substantial variability in the subjective response to alcohol and that differences in the subjective experiences of ethanol’s effects appear to play a significant role in the predisposition to alcohol abuse1 and dependence (e.g., Schuckit & Smith, 1996; Schuckit et al., 1996).
