Abstract # 140:

Scheduled for Sunday, September 18, 2011 01:05 PM-02:05 PM: Session 19 (Salon F (Sixth Floor)) Oral Presentation


J. L. Cameron
University of Pittsburgh, Department of Psychiatry, Pittsburgh, PA 15213, USA
     Everyday life stresses (i.e., mild psychosocial stress, moderate metabolic stress caused by dieting and exercise) can precipitate reproductive dysfunction, particularly in females. However, some individuals are more vulnerable and will rapidly lose menstrual cycles (i.e., are stress-sensitive), while others are more resilient and maintain normal cyclicity even when exposed to substantial stress (i.e., are stress-resilient). Women prone to stress-induced infertility generally are not exposed to severe psychological stresses, but they rate the stresses in their lives as more stressful. To identify neural underpinnings of stress sensitivity we have used female cynomolgus macaques as an experimental model as they have menstrual cycles throughout the year like women, and live in complex social environments. We have found sensitivity to stress-induced reproductive dysfunction is a stable characteristic of an individual. Even in the absence of stress, stress-sensitive monkeys have lower secretion of the ovarian steroids, estrogen and progesterone, higher heart rates, lower serotonin secretion in the CNS, fewer serotonin neurons and alterations in expression of pivotal serotonin-related genes, along with higher gene expression of GAD67 and CRH in the hypothalamus. Several of these differences are likely to lead to decreased activity of the reproductive axis, and we have shown that treatment with a serotonin reuptake inhibitor to increase synaptic serotonin levels will increase reproductive hormone secretion in stress-sensitive individuals. Current studies are showing that individuals who are sensitive to stress-induced reproductive dysfunction are also sensitive to other stress sensitive health problems, such as increased anxiety. Supported by NIH grants (NS09561, HD18185, HD062618).