183
hormone (ACTH) to the adrenal cortex, which emits cortisol (a glucocorticoid) (See Figure 3).20 Cortisol binds to the glucocorticoid receptors (GR) on the hippocampus, which inhibit the release of CRH to regulate the amount of cortisol in the body.22 Too much stress leads to chronic hyperactivity in these glands and ultimately hypercortisolism (a condition where one has too much cortisol in the body), which is linked to dysregulation of serotonin secretion.21 Having serotonin levels that are too low has been widely accepted as one of the main causes of depression. In 2001, Pariente et al. found that the function and expression of GR is reduced in patients with major depression, which would result in an increase in cortisol levels in the brain.22 According to Pariente et al., this is because reduced sensitivity to the inhibitory effects of the glucocorticoid receptors is a primary feature of HPA axis hyperactivity.22
Bear, Mark F. Neuroscience: Exploring the Brain. 3rd ed. N.p.: LWW, 2006. 21 Hernandez, María Eugenia, Danelia Mendieta, Mayra Pérez-Tapia, Rafael Bojalil, Iris Estrada-Garcia, and Sergio Estrada-Parra. "Effect of selective serotonin reuptake inhibitors and immunomodulator on cytokines levels: an alternative therapy for patients with major depressive disorder." Clinical and Developmental Immunology. 22 Pariente, CM. "Glucocorticoid receptors in major depression: relevance to pathophysiology and treatment." Biological Psychiatry 49, no. 5 (March 201): 391-404. 20