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Mice, rats, and humans have two types of estrogen receptors, estrogen receptor-α (ERα) and estrogen receptor-β (ERβ). Estrogen receptor-α gene-disrupted (ERα-disrupted) mice bear two nonfunctional copies of the ERα gene. This mutation blocks the synthesis of full-length ERα, renders the animals infertile, and inhibits the induction of female sexual behaviors by estradiol and progesterone. It is likely that many of the processes contributing to the regulation of sexual receptivity by estradiol and progesterone are compromised in ERα-disrupted mice. However, given the importance of progesterone in the regulation of sexual receptivity and given the importance of progestin receptors (PRs) in mediating the responses of females to progesterone, we investigated the effects of ERα disruption on the induction of PRs by estradiol in the forebrain. We hypothesized that estradiol would induce PRs in wild-type mice but not in ERα-disrupted mice. Ovariectomized wild-type and ERα-disrupted mice were implanted with either estradiol-filled capsules or empty capsules for 5 d, after which their brains were processed for the immunocytochemical detection of PR. Estradiol increased the number of PR-immunoreactive cells in both wild-type and ERα-disrupted mice. The residual responsiveness of ERα-disrupted mice to estradiol could be accounted for by an ERβ-dependent mechanism or another as yet unidentified estrogen receptor; however, because ERα-immunoreactivity and PCR product representing the 3′ end of ERα mRNA were found in at least one PR-containing region of the ERα-disrupted mice, an ERα splice variant may also mediate the induction of PR-immunoreactivity in ERα-disrupted mice.

Induction of Progestin Receptors by Estradiol in the Forebrain of Estrogen Receptor-α Gene-Disrupted Mice