Sex-Related Differences in the Regulation of Cytoplasmie Estrogen Receptor Levels in Responsive Tissues of the Rat

Abstract

Cytoplasmic estrogen receptors were measured in the anterior pituitary and hypothalamus of intact adult Holtzman male and female rats at various time intervals following injection of 10 mug of 17beta-estradiol. Following equivalent depletion of receptors at 1 h in either sex, replenishment of cytosol receptor levels progressed at a greater rate and to a higher level in the male than in the female. Cycloheximide only partially inhibited replenishment, and its blocking effect was similar in males and females. The administration of 5 mug of 17beta-estradiol to adult males elicited less depletion than did 10 mug, and a completely cycloheximide-sensitive replenishment phase. Patterns of depletion and replenishment in immature rats following 0.1 mug of 17beta-estradiol were the same for males and females. In an analysis of the effects of neonatal androgenization, Charles River rats were used and it was initially demonstrated that no sex differences in receptor levels existed between normal males and females. After an injection of an androgenizing level of testosterone propionate on day 3 of age, a full normal complement of receptors was found in estrogen-responsive tissues at 90--100 days of age. The functional dynamics of receptor depletion and replenishment under the influence of exogenous estrogen, however, indicated that the anterior pituitary of the androgenized female responded differently from that of the untreated female, and similarly to that of the male. The hypothalamic receptor dynamics in the male were unaltered by early androgen administration, but estrogen-induced depletion of receptors in the female hypothalamus was considerably less extensive in the androgenized animal than in the untreated control. Whereas cytoplasmic estrogen receptor levels are essentially independent of sex in the rat, the present results indicate a sex-linked difference in the dynamics of receptor turnover in the anterior pituitary and hypothalamic response to 17beta-estradiol.