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 BALs upon recovery from alcohol-induced sedation (York, Chan 1993;Little et al. 1996;Pian et al. 2008;Silveri, Spear 1998); and (b) decreased motor impairment (Silveri, Spear 2001); (White et al. 2002a;White et al. 2002b). In addition, the existing literature suggests that adolescent rats develop tolerance to aversive/moderate- to high-dose effects of alcohol more quickly and/or to a greater extent than that observed in adult rats. These developmental differences for alcohol’s effects are seen when assessing (a) social interaction (Varlinskaya, Spear 2006), (b) LORR (Silveri, Spear 2004;Pian et al. 2008), (c) hypothermia (Swartzwelder et al. 1998), (d) motor impairment (Cook et al. 2008), and (e) electrophysiological effects (Pian et al. 2008). It is noteworthy that developmental differences in alcohol-associated pharmacokinetics cannot fully explain these findings [see (Spear, Varlinskaya 2006) for a cogent discussion and references], although clearly some of the variance is due to ontological differences in alcohol absorption and clearance (c.f. (Walker, Ehlers 2009).
