Stress Response Paper

Now, before I get into the paper, I first would like to give some background on stress, the HPA axis, cortisol, and oxytocin. I will first start off with defining what exactly stress is. Stress is formally defined as a state of real or perceived threat to homeostasis. In order to maintain homeostasis in the presence of stimuli that act as stressors, various different systems in the human body are activated, including the endocrine, nervous, and immune systems. These collectively are known as the stress response. Activation of the stress response initiates a number of behavioral and physiological changes that improve an individual's chance of survival when faced with these challenges. Behavioral effects of the stress response include increased

awareness, improved cognition, and general euphoria. There are also several physiological adaptations that result from the stress response, including increased respiratory rate and metabolism (which results from sympathetic nervous system activation) and suppression of digestion and growth, or the parasympathetic nervous system. Due to the broad spectrum of physiologic and effects of the stress response, there are several neuronal and endocrine systems that function in order to regulate this adaptive process.
Now, the HPA axis is one of the primary effectors of the stress response.

The HPA axis, which is formally known as hypothalamic-pituitary-adrenal (HPA) axis, is composed of the following central nervous system structures: the paraventricular nucleus (PVN) of the hypothalamus, the anterior lobe of the pituitary gland, and the adrenal gland. The HPA axis is a very integral part of the stress response, and it works in a fairly straightforward manner. The HPA axis response is characterized by the release of corticotropin-releasing factor (CRF) from the hyporthalamus when presented with a stress-inducing external stimulus. CRF is also known as CRH or corticotropin-releasing hormone. When CRF binds to CRF receptors on the anterior pituitary gland, adrenocorticotropic hormone (ACTH) is released. ACTH then travels through the bloodstream and binds to receptors on the adrenal cortex and stimulates the release of the hormone, cortisol. In response to stressors, cortisol can typically be released for up to several hours, so blood concentration of cortisol could be high a while after the stressor was initially presented. At a certain blood concentration of cortisol, the cortisol eventually exerts negative feedback to the hypothalamic release of CRF and the pituitary release of ACTH. After this is eventually achieved, homeostasis

returns.