Increases in ovarian GnRH receptors by following GnRH treatment.

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Abstract
Using a gonadotropin-releasing hormone (GnRH) analog, [D-Ser (tBu6)] des-Gly10-GnRH-N-ethylamide (GnRHa) as a ligand the binding capacity of the rat ovary to GnRH during sexual maturation and the mechanism regulating GnRH binding capacity were examined. Specific high affinity binding sites for GnRH were observed in the ovary and the Kd values for the granulosa cells and the residual tissue were similar to those of whole ovary. During sexual maturation, the GnRH binding capacity of the ovary rose from 7 days of age to a peak at 28 days and declined during the prepubertal period. The treatment with PMSG [pregnant mare''s serum gonadotropin] decreased GnRH binding capacity in the residual tissue as well as in the whole ovary but did not change the binding capacity in the granulosa cells in diethylstilbestrol (DES) primed hypophysectomized rats. Repeated injections of GnRH caused a significant increase in the number of GnRH receptors of the ovary in PMSG treated DES primed hypophysectomized rats but not in the saline treated rat. The granulosa cells exhibited increases in GnRH binding capacity following repeated administrations of GnRH more than the residual tissue did. In GnRH treated DES primed hypophysectomized rats, increasing doses of PMSG increased the binding capacity of the granulosa cells but decreased the binding capacity in the residual tissue. GnRH in combination with PMSG seems to have stimulatory effects on GnRH binding capacity and to increase the sensitivity to GnRH in the granulosa cells.