Effects of selective and combined activation of estrogen receptor a and ß on reproductive organ development and sexual behaviour in Japanese quail (Coturnix japonica)

Abstract

Excess estrogen exposure of avian embryos perturbs reproductive organ development in both sexes and demasculinizes the reproductive behaviors of adult males. We have previously shown that these characteristic effects on the reproductive organs also can be induced by exposure of Japanese quail (Coturnix japonica) embryos to selective agonists of estrogen receptor alpha (ERa). In contrast, the male copulatory behavior is only weakly affected by developmental exposure to an ERa agonist. To further elucidate the respective roles of ERa and ERß in estrogen-induced disruption of sexual differentiation, we exposed Japanese quail embryos in ovo to the selective ERa agonist 16a-lactone-estradiol (16aLE2), the selective ERß agonist WAY-200070, or both substances in combination. The ERa agonist feminized the testes in male embryos and reduced cloacal gland size in adult males. Furthermore, anomalous retention and malformations of the Müllerian ducts/oviducts were seen in embryos and juveniles of both sexes. The ERß agonist did not induce any of these effects and did not influence the action of the ERa agonist. Male copulatory behavior was not affected by embryonic exposure to either the ERa- or the ERß-selective agonist but was slightly suppressed by treatment with the two compounds combined. Our results suggest that the reproductive organs become sexually differentiated consequent to activation of ERa by endogenous estrogens; excessive activation of ERa, but not ERß, during embryonic development may disrupt this process. Our results also suggest that the demasculinizing effect of estrogens on male copulatory behavior is only partly mediated by ERa and ERß, and may rather involve other estrogen-responsive pathways.