The hypothalamic-pituitary-adrenal (HPA) axis governs the neuroendocrine adrenocortical response to aversive stimuli. Corticotropin releasing hormone (CRH) neurosecretory cells within the paraventricular nucleus of the hypothalamus (PVN) integrate input from other regions of the nervous system and activation of these cells is the initiating step of the adrenocortical response to stress. The endpoint of HPA axis activation is the release of glucocorticoid hormones, such as corticosterone, from the adrenal cortex into the general circulation. Among other effects, glucocorticoids promote glucose mobilization and redirect energy stores necessary for rapid, adaptive responses to stress (Pecoraro et al., 2006). While the HPA axis is ubiquitously activated in response to aversive stimuli, the up-stream neural circuits mediating this activation depend on the nature of the stressor. “Physiological” stressors, which evoke disturbances in internal homeostasis, activate the HPA axis via a bottom-up circuit in which brainstem nuclei recruit the HPA axis directly, while “psychological” stressors elicit a neuroendocrine response through top-down processes (Pecoraro et al., 2006; Sawchenko et al., 2000; Herman et al., 2003). In this circuit, psychological stressors activate corticothalamic sensory systems, which convey information
