The objective of this investigation is to examine the effects of maternal alcohol treatment on perinatal differentiation of the sexually dimorphic nucleus of the preoptic area (SDN-POA). Maternal alcohol consumption during pregnancy has been shown to be detrimental to development of the fetal central nervous system. Alcohol consumption also results in depression of the gonadal steroids in male rats. Since masculine differentiation of the SDN-POA is dependent upon the presence of fetal androgens during a critical period of brain development, maternal alcohol consumption may result in the alteration of androgen dependent neuronal development producing permanent structural alteration of the SDN-POA neurons in the male offspring. The ability for maternal alcoholization to induce this defect will be examined by allowing pregnant female rats to consume an alcohol diet during gestation and then assess the structural and biochemical changes induced in the SDN-POA in male offspring. Possible mechanisms by which this developmental effect occurs will be investigated by examining brain and serum androgen levels in neonates from alcohol-treated mothers, neuronal testosterone binding in the SDN-POA region and the ability of the SDN-POA to aromatize testosterone. The reduction of androgen secretion by the perinatal tests, the loss of neuronal androgen binding or the reduction of the ability of the neonatal brain to convert testoterone to estrogen may be an indication of the mechanism by which demasculinization of the neonatal brain occurs. The alteration of fetal neuronal sexual differentiation by maternal alcohol consumption could result in abnormalities in the adult of the neuroendocrine control of reproductive events, reduced fertility, behavioral changes or yet undefined consequences.
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