This work was supported by National Science Foundation Award #1257162 to AB, and NIH/NIMH BRAINS Innovation award #MH087495 to DK. “
“It is well established that prolonged or chronic exposure to stress can lead to a variety of adverse physiological and psychological consequences, including obesity, drug abuse, and mood disorders (McEwen, 2005, McEwen, 2007 and de Kloet BGJ398 in vivo et al., 1998). Furthermore, a growing body of evidence indicates that periods marked by significant brain maturation and plasticity, such as perinatal and adolescent development, may be especially vulnerable to these disruptive effects of stress (Romeo et al., 2009 and Eiland

and Romeo, 2013). Less appreciated, however, is the fact that not all individuals exposed to extended or repeated stressors necessarily go on to develop neurobehavioral dysfunctions. The factors that mediate this resilience to stress-induced vulnerabilities are unclear, but likely involve an interaction between genetic and environmental variables (Rutter, 2013 and Southwick and Charney, 2012). The purpose of this review is to discuss possible mechanisms that may contribute to stress resilience, particularly during the adolescent stage of development. Given

the scarcity of data that directly addresses stress resilience during adolescence, this review will also suggest potential future lines of research to help fill this gap in our understanding. An emergent body of research has begun to show the Bosutinib clinical trial short- and long-term effects of exposure to stress during adolescence on a

diverse set of negative physiological and neurobehavioral outcomes (Eiland and Romeo, 2013, McCormick and Green, 2013, McCormick, 2010, Hollis et al., 2013, McCormick and Mathews, 2010 and McCormick et al., 2010). It has been proposed that over adolescents may show a heightened sensitivity to stressors based on at least three converging factors (Romeo, 2013). First, animal studies have indicated that peripubertal individuals display greater hormonal stress responses compared to adults following a variety of physical and psychological stressors (Romeo, 2010a, Romeo, 2010b and McCormick and Mathews, 2007). Second, neuroanatomical studies have reported that the brain areas known to be highly sensitive to stressors in adulthood, namely the amygdala, hippocampus, and prefrontal cortex, all continue to mature during adolescence (Giedd and Rapoport, 2010). Third, the adolescent brain may be more responsive to the stress-related hormones than the more mature brain, as a previous study in rats showed that exposure to similar levels of corticosterone increased gene expression for glutamate receptor subunits to a greater degree in the adolescent compared to adult hippocampus (Lee et al., 2003).