The objective of this research program is to study the hormonal mechanism(s) acting during prenatal life to determine sexual behavior differentiation. Normal and prenatally stressed rats and guinea pigs will be utilized. We previously had found that exposure to environmental stressors during prenatal life feminizes and demasculinizes sexual behavior in male rats. The complex of changes characteristic of such animals has been termed the prenatal stress syndrome. The etiology of the syndrome appears to be a deficiency in testicular testosterone release on day 18 of gestation. Our research has shown that in normal male fetusus, maximal testosterone titers occur on day 18 of pregnancy. The proposed research will compare fetal plasma LH, pituitary LH and brain LHRH levels as well as the aromatization capacity of specific brain areas during prenatal development with the pattern of plasma testosterone release previously shown to characterize normal and stressed fetuses. The degree to which high testosterone titers on day 18 of gestation are critical to the development of normal male behavior potentials will be probed further by androgenizing females and stressing males during a variety of stages in perinatal life. A more detailed appraisal of the extent to which sexual behavior potentials are altered in prenatally stressed males will be made through adult androgen treatment, exposure to stress in adulthood, or injections of low doses of estradiol. The possible interaction of prenatal stress with prepuberal socializing experiences will be assessed and we plan to test the generality of this syndrome in species other than the rat. Finally, the effects of prenatal stress on the development of reproductive potentials in females will be reevaluated.
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