, 2011). The study employing PCMS during adolescence also examined whether this experience protected against further stress exposures in adulthood. Interestingly,

they found rats given PCMS during adolescence were resistant to anxiety- and depressive-like behaviors induced by chronic unpredictable stress (CUS) later in adulthood (Suo et al., 2013). These data suggest that repeated exposure to Hydroxychloroquine cell line mild, predictable stressors during adolescence could immunize the animals against the negative behavioral effects often observed in adult animals induced by CUS (Willner, 1997). Along these lines, Buwalda and colleagues have investigated the short- and long-term effects of adolescent social stress on adult behaviors by exposing Wistar rats to older, more aggressive wild type Groningen (WTG) rats in either social defeat (Buwalda et al., 2013) or visible burrow system (VSB) paradigms (Buwalda et al., 2011). They find that when these Wistar rats

are again exposed to social defeat by WTG rats in adulthood, the Wistar rats that had experienced adolescent stress are attacked less and show greater resistance to anhedonia compared to Wistar rats that did not receive the aggressive, stressful interactions during adolescence (Buwalda et al., 2013 and Buwalda et al., 2011). These data add to the adolescent stress inoculation idea and broaden crotamiton it to ERK inhibitor include aspects of the “match-mismatch hypothesis”, which

basically states that the long-term costs of early life adversity are dependent on how well early life and later life environments match (less cost) or mismatch (greater cost) (Schmidt, 2011, Nederhof and Schmidt, 2012 and Daskalakis et al., 2013). Thus, adolescent stress exposure may instill greater resilience in an individual that will also have to experience similar stressors later in their adult environment. Gene and environment (G × E) interactions are another set of variables that need to be taken into consideration when discussing resilience and vulnerability to stressors (Nugent et al., 2011 and Caspi and Moffitt, 2006). That is, genetic differences can significantly influence the likelihood of developing a physiological or neurobehavioral dysfunction following exposure to stress. For instance, a notable G × E interaction study showed that the effect of early life stress on development of depression in adulthood was moderated in part by a polymorphism in the promoter region of the serotonin transporter gene (5-HTT). In this study it was found that individuals with one or two copies of the short allele of 5-HTT had greater levels of depression and suicidal ideation following early life stress than individuals homozygous for the long allele of 5-HTT (Caspi et al., 2003).