Facilitation and Inhibition of the Estrogen-Induced Luteinizing Hormone Surge in the Rat by Progesterone: Effects on Cytoplasmic and Nuclear Estrogen Receptors in the Hypothalamus-Preoptic Area, Pituitary, and Uterus*

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Abstract
The possibility that inhibition and facilitation of estrogen-induced LH surges by progesterone could be associated with effects of this steroid on the concentration, subcellular distribution, or molecular properties of estrogen receptors in the hypothalamus-preoptic area (HPOA) and pituitary was investigated. Immature rats (28 days old) that received Silastic capsules containing estradiol-17β in oil (150 μg/ml) at 0900 h had LH surges between 1700 and 2000 h on day 29. This treatment led to depletion of cytoplasmic estrogen receptors (to 25–35% of control levels) and their accumulation in the nucleus. Insertion of crystalline progesterone implants concomitantly with estradiol implants or 24 h later resulted in blockade or enhancement of the LH surge, respectively. Progesterone administered in either mode did not significantly alter the levels of estrogen receptors in the HPOA and pituitary; however, progesterone did suppress the quantity of both cytoplasmic and nuclear estrogen receptors in the uterus when administered in conjunction with estradiol for 24 h or for 8 h after 24-h estrogen priming. The binding affinity and sedimentation properties in sucrose gradients of cytoplasmic estrogen receptors were unchanged by progesterone treatment. The specificity of the effects of progesterone on LH secretion was examined. Testosterone, dexamethasone, and the synthetic progestin R5020 (17,21-dimethyl-19-nor-4,9-pregnadien-3,20- dione) also inhibited LH surges when injected 8 h after placement of estradiol implants in 28-day-old rats. Only progesterone and R5020 brought about premature and sustained LH release when given to estradiol-primed rats at 0900 h on day 29. None of these compounds interfered directly with the binding of [3H]estradiol to cytoplasmic or nuclear receptors. In conclusion, modulation by progesterone of the estrogeninduced LH surge does not seem to result from effects on neural and hypophysial estrogen receptors. In contrast, suppression of uterine estrogen receptors by progesterone may account in part for antagonism by this steroid of estrogen-stimulated uterine growth.