Adolescence appears to be a period during which both humans and animals display lower responses to many of alcohol’s aversive/moderate- to high-dose effects compared with their adult counterparts, which may promote excessive alcohol intake and the development of AD (Spear, Varlinskaya 2005;Ehlers et al. 2006;Spear 2000;Spear 2004;Witt 1994;Witt 2006). Clinically, it appears that adolescent individuals are also less affected by alcohol withdrawal than their adult counterparts (Martin, Winters 1998). Reports in the preclinical literature are much more abundant and specific on these developmental differences. For instance, there is evidence that during early and/or late alcohol withdrawal, adolescent, compared with adult, rats display (a) lower anxiety as measured using the elevated plus-maze (Doremus et al. 2003), (b) attenuated suppression of social interactions (Varlinskaya, Spear 2004); but see (Wills et al. 2008;Wills et al. 2009); (c) less distress as measured by ultrasonic vocalizations (Brasser, Spear 2002), and (d) decreased seizure threshold [ (Acheson et al. 1999) but see (Wills et al. 2008)]. Similarly, after an acute alcohol challenge, adolescent, compared with adult, rats display (a) shorter duration of the LORR and/or elevated
