Stress, a word usually associated with experiences that are challenging both emotionally and physiologically, is an internal or external signal alluding to potential threats. Understanding stress is of utmost importance as it is important biologically, enabling adaptive processes to one’s ever-changing environment (Gunnar & Quevedo, 2007). Animal stress responses are composed of the activation of neurobiological systems that help preserve viability through allostasis, an active process by which the body responds to daily events and maintains a state of equilibrium (McEwen, 2007).
There are two systems in which the stress responses of mammals are affected: the sympathetic-adrenomedullary system (SAM) and the hypothalamic-pituitary-adrenocortical system (HPA axis). The SAM is part of the system which releases adrenaline/epinephrine from the center of the adrenal gland. These increases in the circulation of epinephrine enable rapid mobilization of metabolic resources and organization of the fight or flight response. In contrast, the production of glucocorticoids by the HPA axis takes time and is able to pass through the blood brain barrier (Gunnar & Quevedo, 2007; McEwen, 2007). But what is the method behind the HPA axis?
The anatomical structures known to mediate the stress response are found within both the central nervous system and peripheral tissues. If one were to take a deeper look into the HPA axis, it would be clear that the effectors of this stress response are localized within the paraventricular nucleus of the hypothalamus (PVN), the anterior lobe of the pituitary gland, and adrenal glands. Neurons localized in the PVN synthesize corticotropin releasing factor (CRF) and vasopressin. CRF, a key neuropeptide, has been implicated in initiating many of the responses to stress such as endocrine, autonomic, and behavioral responses (Shekhar, Truitt, Rainnie, & Sajdyk, 2005).
As a response to stressor stimuli, CRF is released and transported to the anterior pituitary gland, where it binds its receptor and induces the release of adrenocorticotropic hormone (ACTH) into the systemic circulation. The circulating ACTH reaches its principal target, the adrenal cortex, where it stimulates glucocorticoid synthesis and secretion. Not only are glucocorticoids effectors of the HPA axis, helping to control body homeostasis and response to stress, they also play a regulatory role in the termination of the stress response via negative glucocorticoid feedback. It is believed that glucocorticoids exert inhibition effects through genomic alterations (Tsigos, 2002). Simply put, the PVN receives input from several areas of the brain, including brainstem nuclei, limbic centers, and circumventricular organs. The PVN integrates these signals and activates the HPA axis cascade, resulting in the release of cortisol from the adrenal cortex. Although the stress response is a complex cascade of biochemical events, studies on specific elements can provide tremendous...