Estrogen-independent and estrogen-induced progesterone receptors, and their regulation by progestins in the hypothalamus and pituitary of the chick embryo: an immunohistochemical study.

The effects of an anti-estrogen and of progestins on the progesterone receptor (PR) in the hypothalamus and pituitary of 10-day-old chick embryos were studied by immunohistochemistry with an antibody to the receptor. In a first experiment, to determine if endogenous estrogens are responsible for the early appearance of PR in the chick embryo, a continuous treatment with the anti-estrogen. Tamoxifen, was applied from day 0 of incubation. In the hypothalamus and pars distalis of the pituitary a Tamoxifen treatment (10 micrograms every other day from day 0) did not modify the distribution of PR-positive cells or the intensity of PR immunoreactivity (PR-IR), compared to oil-injected embryos. In contrast, the same treatment totally blocked the increase of PR-IR in embryos administered estradiol (10 micrograms on day 7). Thus, the estradiol-induced PR-IR is inhibited by Tamoxifen, whereas the natural appearance of PR is not. We conclude that, in the chick embryo, the basal expression of PR is estradiol independent. In a second experiment, the regulation of PR by its own ligands (progesterone and the synthetic progestin, R5020) was studied. Progesterone (150 micrograms), administered to embryos 16 or 48 h before sacrifice on day 10, induced a slight increase in PR-IR in hypothalamus and anterior pituitary, whereas R5020 had no effect. In embryos treated with estradiol on day 7, R5020 decreased the PR-IR to a level comparable to that of control embryos. Thus R5020, a non metabolizable progestin, down-regulates the estradiol-induced PR-IR, but has no effect on the estradiol-independent, naturally expressed PR.(ABSTRACT TRUNCATED AT 250 WORDS)