A HORMONAL STUDY ON THE EFFECT OF ANESTHESIA ON MOOD AND DEPRESSION

Abstract

Interest in mood disorders among women has increased, and epidemiological studies suggest that the incidence of major depressive disorder is higher among women than men, even across different nation and cultures. Women who present episodes of depression associated with reproductive events (i.e., premenstrual, postpartum, menopausal transition) may be particularly prone to experiencing depression because of a heightened sensitivity to intense hormonal fluctuations. The hypothesis that sex hormone fluctuations that occur in female reproductive events could influence neurochemical pathways linked to depression is supported with existing animal and human studies and with clinical data (Lee et al., 2015). Female depression and female effective behaviors are influenced by estradiol levels (Borrowand Cameron, 2014).There are multiple activities of estrogens on brain neurotransmitters involving various genomic and nongenomic mechanisms.Estradiolmodulates dopaminergic activity at various steps of dopamine transmission (i.e dopamine release and metabolism, pre and postsynaptic dopamine receptors and transporter (Cyr et al., 2002). Estrogen receptors and serotonin receptors coexist in cells in a wide variety of tissues. Many of 17-β estradiol (E2) effectsare mediated by changes in the actions of serotonin (5-HT). Serotonin is usually considered to be a neurotransmitter, but surprisingly, only 1% of serotonin in the human body is found in the central nervous system. the remaining 99% is found in other tissues, primarily plasma, the gastrointestinal tract and immune tissues where serotonin acts as hormone regulating various physiological functions including vasodilation, clotting, recruitment of immune cells and gastrointestinal motility and iniation of uterine contraction. Both naturally – occurring and pharmacologically – induced changes in E2 alter the concentration of serotonin through two mechanisms. First E2 increases production of tryptophan hydroxylase (TPH, the rate limitating step in synthesis of serotonin in the body) increasing the concentration of serotonin in the body. Second E2 inhibits the expression of the gene for the serotonin reuptake transporter (SERT) and acts as antagonists at the SERT thus promoting the actions of serotonin by increasing the time that it remains available in synapsesand interstitial spaces (Rybaczyket al., 2005).