2010). Interestingly, measures of increased anxiety behavior in the Elevated Plus Maze in those rats exposed to prenatal nicotine were present in adulthood but not in adolescence, and although the result was more prominent in female rats, males also demonstrated the response (Eppolito
et al. 2010). The exposure to nicotine before and shortly after birth was associated with impairment to fear extinction (Eppolito et al. 2010), which replicated results from chronic nicotine exposure in adolescence but not adulthood (Smith et al. 2006). This may suggest that exposure to nicotine in high-activity neurodevelopmental periods may exert more deleterious Inhibitors,research,lifescience,medical effects than in adulthood. It is possible that chronic administration of nicotine, via altered nAChR activity, may influence gene expression and
plasticity in the medial PFC and amygdala (Brown and Kolb 2001; Li et al. 2004; Polesskaya et al. 2007). This interaction may underpin the lack of extinction learning displayed in rats that are exposed to chronic nicotine Inhibitors,research,lifescience,medical (Eppolito et al. 2010). Nicotine induces production of oxidative stress markers and reduces antioxidant defenses, contributing a major proportion of the net oxidative stress from cigarette use (Bhagwat et al. 1998; Yildiz et al. 1998; Guan et al. 2003; Qiao et al. 2005; Das et al. 2009), although nicotine is known exhibit Inhibitors,research,lifescience,medical both pro- and antioxidant effects (Li et al. 2000; Tizabi et al. 2003). Nicotine increases lipid peroxidation markers that can be prevented by coadministration of free radical scavenger vitamin E (Qiao et
al. 2005) and has demonstrated antimitotic properties (Qiao et al. 2003). Increased production of O&NS, and antimitotic properties, has been demonstrated during cell Inhibitors,research,lifescience,medical differentiation (in association with increased in nAChR density) (Qiao et al. 2003, 2005). It is possible that the balance between damaging and protective effects of nicotine may depend upon the degree of stimulated oxidative stress – a Inhibitors,research,lifescience,medical small amount of oxidative stress could have positive effects in stimulating normal cellular processes, but significantly increased oxidative stress could overwhelm protective mechanisms leading to direct cellular damage (Newman et al. GSK-3 2002a). Given the increased level of O&NS present in adolescence, it could be hypothesized that vulnerability to toxic effects of nicotine-induced oxidative stress would be heightened (Qiao et al. 2005). Nicotine has demonstrated adverse neurobiological effects during adolescence, with these effects seemingly dependent on only early small and infrequent exposure to nicotine (Abreu-Villaca et al. 2003b). In keeping with this hypothesis, administration of nicotine for 1 week to adolescent rats resulted in a significant increase in TBARS with effects that would have been observed at low levels of exposure (Qiao et al. 2005).