in PFC volume) may reflect premorbid characteristics that serve to increase risk for early alcohol use (e.g., De Bellis et al., 2005). Thus, early use of alcohol may not necessarily be causal in producing these neural alterations or the elevated risk for dependence, although findings from several recent longitudinal studies provide preliminary evidence for lasting consequences of early use of alcohol and other drugs (e.g., Odgers et al., 2008). Definitive evidence is still needed to convincingly demonstrate that adolescent alcohol use is causal in producing lasting neural alterations and later abuse or dependence (see Clark et al., 2008). Controlled experiments with laboratory animals may prove helpful in determining whether brain development in adolescence is particularly vulnerable to alcohol toxicity. Some studies with laboratory animals have reported that exposure to alcohol during adolescence can exert long-term influences on the brain (e.g., Crews et al., 2000; Slotkin et al., 2002; Hargreaves et al., 2008; Sabeti & Gruol, 2008) and elevate intake of alcohol in adulthood in some cases (e.g., Rodd-Henricks et al., 2002), with some evidence of age-specific differences in the timing of exposure during the broad adolescent period as well (Sabeti & Gruol, 2008). These basic science studies are at their
