Rat anterior pituitary estrogen receptor mRNA levels after estrogen and progesterone treatment

Previous work from our laboratory has demonstrated that progesterone can induce a rapid decrease in estrogen receptor (ER) binding in the anterior pituitary of the rat. This effect of progesterone on ER correlates well with the loss of estrogen action. The objectives of this study were to determine whether the rapid decrease in ER binding in the rat pituitary after a single injection of estradiol and the decrease in ER binding induced by progesterone in the estrogen-primed rat could be due to a suppression of mRNA levels for the estrogen receptor. Ovariectomy for 14 days decreased ER mRNA levels and injection of 2 μg of estradiol in ethanol:saline for 3 days increased ER mRNA levels. A single injection of 1 μg of estradiol brought about no change in ER mRNA levels in the pituitary of ovariectomized rats within 1 h of administration. Five micrograms of estradiol increased the ER mRNA levels, whereas 10 μg of estradiol brought about a decrease in ER mRNA levels. Thus, the reported decrease in pituitary ER binding after 1 and 5 μg of estradiol was not accompanied by a similar change in ER mRNA levels, suggesting that the decrease in ER binding may be due to accelerated processing of ER or to decreased translation of ER mRNA. When 2 μg of estradiol was injected into estrogen-primed ovariectomized rats, the recovery of ER binding at 18 h was preceded by an increase in ER mRNA levels at 12 h, suggesting new ER synthesis during the recovery process. Progesterone (0.8 mg/kg body wt), in the absence of estradiol-priming, increased ER mRNA levels in the pituitary at 1, 6, and 12 h and decreased them at 18 h. In estrogen-primed animals, the changes in ER mRNA levels brought about by progesterone combined with estradiol were similar to those observed with estradiol alone, with the exception that ER mRNA levels were elevated in the progesterone-treated group at 1 h, a time when ER binding was further suppressed. Thus the progesterone-induced decrease in ER binding was not due to a suppression of ER mRNA levels. In estrogen-primed rats 0.8 and 4.0 mg/kg body wt doses of progesterone increased ER mRNA levels, whereas the 2.0 mg/kg body wt dose did not. These results indicate that estradiol alone has a time- and dose-dependent effect on ER mRNA levels in the anterior pituitary. Progesterone by itself and in the presence of estrogen priming has a dose-related effect on anterior pituitary ER mRNA levels. Furthermore, the effect of progesterone on decreasing ER binding appears to be due either to a post-transcriptional effect and/or to accelerated receptor processing.