Much stress research has focused on identifying factors that render an individual
vulnerable to the negative consequences of stressor exposure. The rationale is that by understanding mechanisms underlying vulnerability, susceptible individuals can be identified and vulnerability can be countered or attenuated. More recently, the concept of stress resilience has been embraced. Although inversely related to vulnerability, resilience is not simply its opposite as many examples presented in the following reviews in this issue illustrate. They discuss individual attributes that potentially confer resilience such as genetic make-up, developmental stage Galunisertib and sex, environmental factors including prenatal environment, social environment, and modifiers such as coping style, controllability, exercise and quality Idelalisib in vitro of sleep. The reviews raise a number of important questions that
can guide future research: Do different resilience factors converge on common mechanisms? Does resilience generalize across stressors? How long does resilience endure? Can the brain’s capacity for structural and functional plasticity be enhanced so as to compensate for and thereby alleviate the effects of adverse events earlier in the life course? Do our animal models of stress resilience translate sufficiently L-NAME HCl to allow us to make predictions in humans? Also emerging from these reviews is the concept that stressors are catalysts for brain evolution. Although this can have negative consequences that are expressed as dysfunctions and disease, positive adaptations can arise that protect against future traumas. The challenge lies in determining how we can take advantage of our knowledge of resilience to make the most of adversity. “
“The brain is the central organ of stress and
adaptation to stressors because it perceives what is potentially threatening and determines the behavioral and physiological responses (McEwen, 1998 and McEwen and Gianaros, 2011). Moreover, the brain is a target of stress and stressful experiences change its architecture, gene expression and function through internal neurobiological mechanisms in which circulating hormones play a role (Gray et al., 2013 and McEwen, 2007). In healthy young adult animals, neuroanatomical changes in response to repeated stress are largely reversible (Conrad et al., 1999 and Radley et al., 2005), or so it appears, based upon the restoration of dendritic length and branching and spine density. Yet there are underlying changes that can be seen at the level of gene expression and epigenetic regulation which indicate that the brain is continually changing (Gray et al., 2013, Hunter et al., 2013, McEwen, 2007 and Nasca et al., 2013).