Any intrinsic or extrinsic stimulus that evokes a biological response is known as stress. Based on the type, timing and severity of the applied stimulus, stress can exert various actions on the body ranging from alterations in homeostasis to life-threatening effects and death.4 In addition to its paramount role in normal daily function, cortisol is a key player in the stress response. In the presence of a physical or psychological threat, cortisol levels surge to provide the energy and substrate necessary to cope with stress-provoking stimuli or escape from danger. However, although a stress-induced increase in cortisol secretion is adaptive in the short-term, excessive or prolonged cortisol secretion may have crippling effects, both physically and psychologically.3
The hypothalamic-pituitary-adrenal axis (HPA axis) is an interactive neuroendocrine unit comprising of the hypothalamus, the pituitary gland, and the adrenal glands. The hypothalamus is located in the brain and the pituitary at the base of it, whereas the adrenals are on top of the kidneys.
The HPA axis plays key roles in basal homeostasis and in the body's response to stress. The major pathway of the axis results in the production and secretion of cortisol. The hypothalamus responds to basal neural input which follows a circadian rhythm and input as a result of stress by increasing the secretion of corticotrophin-releasing hormone (CRH) from the hypothalamus.
Hypothalamic-pituitary-adrenal (HPA) axis appears to play a key role in the pathogenesis of major depressive disorders (MDD). Treatment of certain selective serotonin reuptake inhibitors (SSRIs) has been shown to reduce the activity of corticotropin-releasing hormone (CRH) neurons and may contribute to their therapeutic action. It has been proposed that the downregulation of CRH activity is final and common step of antidepressant treatment.1
Related to:
Cortisol, Corticotropin-releasing hormone, CRH, MDD, Anxiety