NEUROENDOCRINE MEDIATION OF SOCIALLY INDUCED ANOVULATION

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Studies have continued this year assessing the consequences of psychosocial stress, resulting from social subordination, on metabolic, reproductive, and behavioral outcomes I adult female rhesus monkeys. In addition, the contribution of polymorphisms in the gene that encodes the serotonin reuptake transporter (5HTTLPR) was evaluated as other studies show individuals carrying one or both alleles of the short promoter length variant (s-variant) are more vulnerable to the adverse consequences of psychosocial stress than females homozygous for the long promoter length (l/l). Two experiments were conducted in the current year. The initial study assessed the effects of supplementation of leptin to test the hypothesis that leptin acts centrally to minimize the response to psychosocial stressors and to determine whether leptin normalizes thyroid hormone levels known to be depressed by social subordination. The second experiment tested the hypothesis that allopregnanolone, a neuroactive metabolite of progesterone, would be anxiolytic and reduce activation of the hypothalamic pituitary adrenal axis to novel situations. The analyses of the data from both of these experiments are still under way. In the coming year, we will assess the effects of a corticotropin releasing hormone (CRH) antagonist on a number of metabolic and reproductive endpoints to test the hypothesis that the reproductive deficits observed in subordinate females are the result of an up-regulation of CRH, and will provide insights into possible treatment strategies for women suffering from stress-induced infertility.