Brain Tissue Transplants and Reproductive Function
In many species, there are marked sex differences in the neural control of a variety of endocrine and behavioral processes. These sex differences in CNS function in the adult are due, in large part, to the hormonally induced sexual differentiation of the brain during development; in fact, the mammalian brain is inherently female or at least bipotential. Specifically, sexual differentiation of the neural mechanisms controlling reproductive function in mammals, with respect to both sexual behavior and gonadotropin secretion, results from exposure of the brain of the male to his testicular hormones during a restricted period of brain development.1, 2 In the rat, this “critical period” for sex steroid action apparently begins several days before birth and extends into the early postnatal period.3, 4 In contrast, it is the absence in the female of testicular secretions during the critical period that permits the development by adulthood of a neural substrate that subserves feminine behavior and the cyclical pattern of luteinizing hormone (LH) secretion necessary for ovulation. If, however, the inherently female brain is exposed to exogenous testicular hormones (i. e., testosterone) during the critical period, sexual differentiation (masculinization) of the brain will occur, resulting in the development of masculine sexual behavioral potential and a noncyclic or tonic pattern of LH secretion during adulthood.1, 2 It must be emphasized that considerable evidence suggests that, in the rat, testosterone does not act directly to masculinize the brain, but rather that it is aromatized within steroid-sensitive regions to estrogen intraneuronally, which then acts to masculinize brain function.4
KeywordsLuteinizing Hormone Sexual Differentiation Preoptic Area Gonadal Steroid Testosterone Propionate
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