It has been previously demonstrated that fetal alcohol response can feminize the expression of adult male sexually dimorphic behaviors in the rat. These long-term behavioral alterations are hypothesized to result from an alcohol-induced disruption of androgenic status in the male fetus during the critical prenatal period for sexual differentiation of the brain. Data outlined in the progress report support this hypothesis by demonstrating the absence of a prenatal surge of testosterone in fetal alcohol exposed (FAE) male fetuses on days 18-19 of gestation. In addition, light microscopic examination of the testes of males at birth revealed morphologic damage due to fetal alcohol exposure. As adults, FAE males were found to exhibit feminized or demasculinized patterns of behavior in scent marking, water consumption, saccharin preference, and sexual behavior. Studies outlined in the present proposal are designed to examine in detail alcohol-induced alterations in the mechanisms involved in the perinatal organization of masculine differentiation of the brains. In addition, behavioral studies are proposed to explore whether replacement of the prenatal or postnatal surge of testosterone in FAE males will normalize adult behavior patterns. These studies will provide new and valuable information which will enhance our understanding of how prenatal alcohol exposure feminize males and will aid in the eventual development of clinical strategies to treat FAE children.
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