Estrogen induction of progestin receptors in the hypothalamus of male and female rats which differ in their ability to exhibit cyclic gonadotropin secretion and female sexual behavior.

Abstract

This study examined whether estrogen induction of cytoplasmic progestin receptors in the hypothalamus of male and female rats is sufficient to facilitate feminine sexual behaviors and/or cyclic gonadotropin secretion. Newborn male rats were injected with oil (M) or were castrated at birth and injected with oil (D1-M) or 10 μg of testosterone propionate (TP) (l0-TP-M); neonatal females were treated with oil (F), 10 μg of TP (10-TP-F), or 500 μg of TP (500-TP-F). In adulthood, females were tested for estrous cyclicity by taking vaginal smears. Following adrenalectomygonadectomy, all animals received estrogen plus progesterone and were tested for the display of receptive and proceptive components of female sexual behavior. After hormone withdrawal, animals were injected with oil or 5 μg of estradiol benzoate (EB) 24 and 48 h before sacrifice, the same dose and times of EB injection used in behavioral testing, and the concentrations of cytoplasmic progestin receptors in the hypothalamus-preoptic area (HPOA) were determined using 3H-R5020. Only control females (F) exhibited vaginal cyclicity and corpora lutea as adults. F, 10-TP-F, D1-M, and 10-TP-M groups all showed high levels of receptive hehavior (lordosis); however, only F showed high levels of proceptive behavior (ear wiggling, hopping, and darting). Neither M nor 500-TP-F groups displayed significant levels of any female sexual behaviors. Despite these large differences in the capacity of neonatally manipulated rats to respond to estrogen and progesterone with gonadotropin release and female reproductive behaviors, EB treatment produced identical, twofold increases in cytoplasmic progestin receptor levels in the HPOA of all animals. These results demonstrate that estrogen-induced elevation of neural progestin receptor concentrations alone is not sufficient to mediate the preovulatory surge of gonadotropins, to facilitate female sexual behavior, or to underlie male-female differences in the sensitivity of these responses to estrogen and progesterone.