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      Effects of Exogenous Androgen on Brain Androgen Receptors of the Fetal Rhesus Monkey

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          Abstract

          Testosterone secreted by the fetal testes masculinizes and defeminizes the nonhuman primate brain during a defined prenatal critical period. We previously demonstrated the presence of high-affinity, specific androgen receptors (AR) in the developing rhesus monkey brain, but did not present data concerning their capacity for activation. To achieve this end, we analyzed the AR content in brains from intact and gonadectomized rhesus monkey fetuses at approximately 125 days of gestation, 2 h after injection of either 500 µg dihydrotestosterone (DHT) or vehicle directly into the fetus. After treatment, plasma DHT concentrations increased five-fold in the fetal circulation. In gonad-intact fetuses, cytosolic AR decreased in preoptic area, medial basal hypothalamus, and septum following DHT treatment. No significant effect of DHT treatment on nuclear AR was seen. In contrast, the increased level of DHT in the maternal circulation decreased cytosolic AR and increased nuclear AR of the maternal myometrium. In gonadectomized fetuses, DHT treatment decreased cytosolic AR as it did in the intact group. In contrast, a significant increase in nuclear AR was seen in preoptic area, medial basal hypothalamus, and tegmentum of these fetuses. Thus AR in fetal rhesus brain can be activated by DHT when the gonads are removed, but not in the intact fetuses. These data suggest that AR in the developing nervous system of rhesus macaques can be activated by exogenous androgen and hence are probably functional.

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          Author and article information

          Journal
          NEN
          Neuroendocrinology
          10.1159/issn.0028-3835
          Neuroendocrinology
          S. Karger AG
          0028-3835
          1423-0194
          1994
          1994
          08 April 2008
          : 59
          : 3
          : 271-276
          Affiliations
          aDepartment of Physiology, School of Medicine, Oregon Health Sciences University, Portland, Oreg.; bDivision of Reproductive Sciences, Oregon Regional Primate Research Center, Beaverton, Oreg., USA
          Article
          126668 Neuroendocrinology 1994;59:271–276
          10.1159/000126668
          8159276
          © 1994 S. Karger AG, Basel

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          Page count
          Pages: 6
          Categories
          Hypothalamic-Gonadal Axis

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