Abstract

Estrogen production by the female avian embryo induces development of a female phenotype of the reproductive organs whereas the low estrogen concentration in the male embryo results in a male phenotype. Treatment of female embryos with exogenous estrogens disrupts Müllerian duct development resulting in malformations and impaired oviductal function. Exposure of male embryos to estrogens results in ovotestis formation and persisting Müllerian ducts in the embryos and testicular malformations, reduced semen production and partially developed oviducts in the adult bird. Furthermore, studies in Japanese quail show that the male copulatory behavior is impaired by embryonic estrogen treatment. Results from our experiments with selective agonists for ERα and ERβ suggest that the effects of estrogens on the reproductive organs are mediated via activation of ERα. Abundant expression of ERα mRNA was shown in gonads and Müllerian ducts of early Japanese quail embryos. Both ERα and ERβ transcripts were detected by real-time PCR in early embryo brains of Japanese quail indicating that both receptors may be involved in sex differentiation of the brain. However, in 9-day-old quail embryo brains in situ hybridization showed expression of ERβ mRNA, but not of ERα mRNA, in the medial preoptic nucleus (POM) and the bed nucleus of the stria terminalis (BSTm), areas implicated in copulatory behavior of adult male quail. Furthermore, embryonic treatment with the selective ERα agonist propyl pyrazol triol (PPT) had no effect on the male copulatory behavior. These results suggest that ERβ may be important for the effects of estrogens on brain differentiation.

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