Stress is typically defined as any stimulus that represents a perceived or actual threat to homeostatic functioning. The most common physiological response to stressful stimuli is the activation of the hypothalamic-pituitary-adrenal (HPA) axis which governs the neuroendocrine response to aversive stimuli. Activation of corticotropin releasing hormone (CRH) neurosecretory cells within the paraventricular nucleus of the hypothalamus (PVN) is the initiating step of the adrenocortical response to stress; the endpoint of which is the release of glucocorticoid hormones (corticosterone in rodents and cortisol in humans) into the general circulation. Glucocorticoids, in turn, promote glucose mobilization and redirect energy stores necessary for rapid, adaptive responses to stress (Pecoraro et al., 2006). At the central level, glucocorticoids can either mediate some of the responses to stress (e.g., activation of glutamate transmission in the hippocampus; (Karst et al., 2005)) or act to promote reinstatement in a system following a disturbance elicited by the stressful stimuli (e.g., suppression of CRH induction evoked by stressful stimuli; (Keller-Wood and Dallman, 1984)).
