Adolescence is best defined by characteristic behaviors including high social interaction and play behavior, high levels of risk-taking, high activity and exploration, impulsivity, and novelty and sensation seeking (Ernst et al., 2009; Spear, 2000). Adolescent behaviors are shared across many species, from humans (12 to 20–25 years of age) to mice (post-natal days 28 to 42) and others (Spear, 2000). Recent studies indicate that adolescent brain structural development coincides with consolidation of adult abilities (Blakemore and Choudhury, 2006), including intelligence (Shaw et al., 2006) and behavioral control of executive functions (Ernst et al., 2009). Adolescent brain maturation involves peaks in cholinergic, dopaminergic, and serotoninergic inputs to frontal cortex, as well as cortical width peaking during adolescence and then declining to stable adult levels (Giedd, 2004; Giedd et al., 2008; Gould et al., 1991; Kalsbeek et al., 1988; Kostovic, 1990; Rosenberg and Lewis, 1994; Spear, 2000). Developing systems are sensitive to ethanol neurotoxicity. Rat models of adolescent binge drinking find significant frontal neurodegeneration (Crews et al., 2000a) and loss of neurogenesis (Crews et al., 2006), suggesting that the adolescent brain is uniquely sensitive to ethanol neurotoxicity (Crews et al., 2007).
