Alcohol sensitivity refers to both objective (e.g., body sway) and subjective (e.g., self-reports of level of intoxication) measures of alcohol effects. It is hypothesized that low response to alcohol may be indicative of a genetic vulnerability to problem drinking (e.g., Schuckit & Gold, 1988). Due to ethical considerations regarding administering alcohol to youth for research, most of what we know about developmental differences in absorption and elimination of alcohol has been extrapolated from animal studies. Animal models suggest that across species adolescents are less sensitive to the negative consequences of alcohol use, such as loss of motor coordination (White et al., 2002), sedation (Little, Kuhn, Wilson, & Swartzwelder, 1996), and withdrawal symptoms/hangover effects (Acheson, Richardson, & Swartzwelder, 1999), than their more mature counterparts. Although no definitive conclusions have been reached regarding adolescents’ reduced sensitivity to the unpleasant effects of alcohol, the developmental status of the GABA and dopamine systems have been implicated as a mechanism responsible for these observed differences (Moy, Duncan, Knapp, & Breese, 1998). GABAA receptor activation, which promotes neuronal inhibition, is thought to be a primary mechanism
