Analysis of the Effect of Progesteronein Vivoon Estrogen Receptor Distribution in the Rat Anterior Pituitary and Hypothalamus*

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Abstract
An acute injection of estradiol is known to cause a rapid redistribution of estrogen receptors in responsive cells, measurable as depletion of the cytosol receptor content with accompanying accumulation in the nucleus. The effects of progesterone on this process were examined in the anterior pituitary and hypothalamus using an animal model in which sensitivity to steroidal feedback control of gonadotropin secretion was defined. Ovariectomized immature rats were administered low dose estrogen replacement for 4 days. On the morning of the 5th day, groups of animals were injected according to one of the following protocols: vehicle alone; 5 or 10 .mu.g estradiol; and 0.8 or 3.2 mg progesterone, followed 1 h later by vehicle or 5 or 10 .mu.g estradiol. All animals were killed 1 h after estradiol (or vehicle) injection, and levels of cytosol and nuclear estrogen receptors were measured. The only change occasioned by progesterone treatment was a decrease in anterior pituitary nuclear estrogen receptor levels. At the 5-.mu.g dose of estradiol, 0.8 and 3.2 mg progesterone were equally effective in diminishing nuclear estrogen receptor binding. When 10 .mu.g estradiol were used to cause receptor redistribution, only the higher 3.2 mg dose of progesterone significantly depressed nuclear receptor binding. If ovariectomized animals were maintained in the absence of estrogen replacement, progesterone at either the 0.8- or 3.2 mg dosage was completely ineffective in altering the patterns of estradiol-induced cytosol or nuclear estrogen receptor levels. A tissue-specific inhibitory action of progesterone on estrogen-induced enhancement of nuclear estrogen receptor binding was demonstrated. This inhibition can be partially overcome by increasing the level of estrogen used to effect receptor redistribution. The requirement for maintenance of a background level of estrogen suggests that the inhibitory action of progesterone is mediated through progesterone receptor interactions.

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