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 of ethanol-induced sedation (Lilijequist & Engel, 1982). In rats, ethanol enhances GABA receptor-mediated neurotransmission more powerfully through development (Li, Wilson, & Swartzwelder, 2003; Silveri & Spear, 2002), suggesting that as rats age, they are more sensitive to the inhibitory effects of ethanol such as sedation. While these findings cannot be directly translated to the human experience, changes in alcohol sensitivity as humans age may account for the intense, and quick sedation response seen in adults compared to adolescents (e.g., Little et al., 1996), and cause adults to stop drinking after a short period of time compared to teens. Thus, the neurological and physical growth that occurs over the course of adolescence is a key factor in understanding changes in alcohol sensitivity.
