, 2010). Animal models of social stress have shed some light on the etiology of stress-related urological disorders. For example, rats exposed to social defeat stress exhibit urinary retention (Wood et al., 2009 and Desjardins et al., 1973). Recent studies confirmed that this stress-related urinary dysfunction is mediated by increases in CRF within Barrington’s nucleus, a brain region involved in micturition (Wood et al., 2013b); both a CRF1 antagonist and shRNA targeted knockdown of CRF in Barrington’s nucleus inhibited the development of urinary dysfunction evident in socially defeat rats. These studies did identify that

bladder hypertrophy was negatively correlated with the latency to assume a submissive posture, demonstrating an association between passive coping see more and bladder dysfunction (Wood et al., 2009). However, preclinical studies identifying mechanisms of individual differences in susceptibility Autophagy signaling inhibitor to stress-related urological dysfunction are lacking. Overall, it seems clear that there are multiple neural determinants of resilience or vulnerability to stress. Peptides such as CRF and NPY and the VTA/dopamine system have been the

best-characterized mediators of resilience or vulnerability. The bulk of evidence suggests that resilience is not simply the opposite of vulnerability because there are some mechanisms that are dichotomous in resilient vs. vulnerable animals. How these diverse mechanisms interact with one another to produce a resilient or vulnerable phenotype is challenging. Resilience is also a dynamic process (Bracha et al., 2004 and Rutter, 2006). The phenotypes associated with resilience

may be stressor specific so that an individual resilient in one stress context to certain outcomes may not be resilient in a different context and/or to other outcomes. Maintaining the same resilient phenotype when the stressful environment shifts may not necessarily be adaptive so resilience phenotypes may have to be adjusted to suit Liothyronine Sodium changing environments. Efforts of SW were supported by a Beginning Grant in Aid from the American Heart Association13BGIA14370026 and the National Institute of Health (NIGMS) grant 5P20GM103641. Efforts of SB were supported by a grant from the “Enabling Stress Resistance” program at the Defense Advanced Research Projects Agency (DARPA) and the U. S. Army Research Office under grant number W911NF1010093. “
“It is not stress that kills us, it is our reaction to it”. Stress is an event that threatens the homeostasis of the organism and as a result causes physiological and behavioural responses that attempt to reinstate equilibrium (McEwen and Wingfield, 2003, de Kloet et al., 2005 and Day, 2005). Allostasis can be defined as the collection of processes that are required to achieve internal and external stability in the face of a changing environment thus maintaining homeostasis (McEwen and Wingfield, 2003, de Kloet et al., 2005 and Day, 2005).