The overall goal of this study is to determine to what extent common life stresses (i.e., dieting and psychological stress) impair fertility. It has been known for years that numerous forms of stress, including undernutrition, exercise, and psychological stress, can impair reproductive hormone secretion and can lead to decreased gonadal function, and impaired fertility, when the level of stress is severe. However, over the past several years, it has been shown for several different stresses (including both metabolic and psychological stresses) that mild, relatively acute forms of stress can also suppress reproductive hormone secretion; but we do not know if the effects of such stresses are great enough to actually impair fertility. These mild stresses are common in women's lives and if they play a role in impairing fertility, they could be a major factor contributing to infertility in our society. The projects in this research use a non- human primate model to determine if mild stress impact on fertility, and to study if the mechanisms underlying the suppression of reproductive hormone secretion my mild stress. A clinical component of this project begins to examine the role that mild stresses may play in the success rate of infertility treatment in women. Using this combined basic and clinical approach, the specific aims of this project are first, to define the impact of mild stress exposure on pregnancy rates in rhesus monkey; second, to identify the neural circuits which are responsible for mediating impairment of reproductive hormone secretion by mild stresses using a combined approach of pharmacological experiments and in vitro studies utilizing immunocytochemistry, in situ hybridization and confocal microscopy; and third, to determine if success rates in treating patients with tubal infertility by in vitro fertilization/embryo transfer (IVF-ET) are correlated with patient stress parameters. Together, the results of these studies will greatly increase our understanding of the role that common life stresses have on fertility in females, and will determine the underlying mechanisms whereby such stresses suppress reproductive function, providing information necessary for the future development of successful treatments for stress-induced infertility.
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