limited changes in the P300 following alcohol exposure (Benton and Tranel, 2000). Indeed, our results appear to be consistent with this notion. Taken together, and with regard to age-dependent effects on the P300, it appears that (a) relatively reduced cumulative alcohol exposure in adolescents versus adults, and/or (b) relative plasticity (as opposed to relative vulnerability) of the adolescent brain possibly moderated the relationship between AUDs and P300, thereby contributing to minimal changes in the P300 in the current adolescent sample. Nevertheless, further work is needed to characterize the consequences of alcohol exposure during the adolescent phase.
