One of the key risk factors for addiction in general, as well as for nicotine dependence in particular, is early onset of substance use, as assessed by retrospectively reported age at first use or age at onset of regular use (Robins and Przybeck 1985; Breslau et al. 1993; Breslau and Peterson 1996; Grant and Dawson 1997; Grant et al. 2006; Grucza et al. 2008; Agrawal et al. 2009). Recently, advances in developmental neurobiology have pointed to adolescence as a potential critical period of vulnerability for the development of substance use disorders (Chambers et al. 2003; Crews et al. 2007). The development of adolescent animal models for nicotine dependence has enabled researchers to show that both neurobiological changes and long-term behavioral sequelae differ for adolescent as compared to adult nicotine exposure (Trauth et al. 2000; Trauth et al. 2001; Slotkin 2002; Adriani and Laviola 2004; Slotkin et al. 2008; Kota et al. 2009; Slotkin and Seidler 2009). Hence, the molecular mechanisms and neuroadaptive processes involved in adolescent exposure and adult exposure may differ considerably. The ramifications of these animal models for
