Effect of prenatal exposure to aromatase inhibitor, testosterone, or antiandrogen on the development of feminine sexual behavior in ferrets of both sexes
Experiments were conducted to assess the role of prenatal exposure of the brain to estrogen in controlling the development of proceptive and receptive feminine sexual behavior in ferrets of both sexes. Female ferrets, deprived prenatally of estrogen via maternal ovariectomy on gestational day 30 (42-day gestation) plus SC implantation of an aromatase inhibitor, 1,4,6-androstatriene-3,17-dione (ATD), into their mothers, were significantly less receptive than control females when tested in adulthood after ovariectomy and administration of low (5 and 10 μg/kg) dosages of estradiol benzoate (EB). However, they were no less receptive than control females in response to a high (15 μg/kg) dosage of EB. Estrogen-deprived females showed EB-induced reductions in approach latencies to a stud male (proceptive responses) which were equivalent to those of control females. These results suggest that estrogenic stimulation of the female brain during fetal development enhances later receptive responsiveness to estradiol. However, prenatal estrogen appears not to be an absolute requirement for the development of receptive or proceptive coital capacity in females. In a previous study castrated male ferrets failed to show EB-induced reductions in the latency to approach a sexually active male, indicating that they were proceptively defeminized. In the present study females exposed prenatally to exogenous testosterone also failed to display significant EB-induced reductions in approach latencies to a sexually active male. Males deprived prenatally of estrogen ran faster to a stud male after adult administration of increasing dosages of EB. By contrast, control males as well as males exposed prenatally to androgen receptor antagonist, flutamide, displayed no EB-induced reduction in approach latencies. This suggests that in male ferrets prenatal neural aromatization of androgen to estrogen normally contributes to the process of proceptive defeminization.
