Sexual receptivity facilitated by unesterified estradiol: Dependence on estrogen and progestin receptors and priming dose of estradiol benzoate.

Abstract

In some conditions, female sexual behavior in ovariectomized rats can be induced by continuous exposure of estradiol (E2) alone or by a single injection of a high dose of the long-lasting, esterified estradiol benzoate (EB). However, there are inconsistencies in the literature on the role of estrogens during priming or in the facilitation on female sexual behavior in EB-primed rats, as well as the cellular mechanisms involved. Either subcutaneous (sc) or intracerebral (icv) administration of some doses of free unesterified E2, induced lordosis in EB-primed rats. Either sc or icv injection of E2, immediately prior to testing, induced high levels of sexual receptivity when the female rats were primed with an EB sc injection of 2 μg EB. The roles of progesterone receptor (PR) and estrogen receptor on lordosis induced by sc or icv administration of E2 were explored. Tamoxifen or RU486 administrated sc or icv; each reduced lordosis induced by E2. Similarly, antisense oligonucleotides directed at PR-B or total PR (PR-A + PR-B) administrated icv immediately before EB injection inhibited lordosis induced by daily injections of EB. These results suggest that lordosis facilitated by free E2 is dependent on priming dose of EB. Furthermore both ERs and PRs are involved in this action of E2.