Biology of Reproduction, Vol 24, 306-310, Copyright © 1981 by Society for the Study of Reproduction

Hormone-Dependent Subpopulation of Rat Testicular Luteinizing Hormone (LH) Receptors

¹ Department of Pediatrics, Children’s Hospital, College of Medicine, The Ohio State University, Columbus, Ohio 43205
² Department of Pychology, College of Medicine, The Ohio State University, Columbus, Ohio 43205

The effects of prolactin (PRL), growth hormone (GH), and luteinizing hormone (LU) treatment on testicular LH receptor content were studied in the hypophysectomized adult male rat. One and 2 weeks after hypophysectomy, testicular LH receptor binding capacity, as determined by [¹²⁵I]-hCG binding to whole testicular homogenates, was 14% and 16% of normal values, respectively. Seven days of s.c. LH treatment (5 µg/day), begun 1 week after hypophysectomy, caused a significant additional reduction of [¹²⁵I]-hCG binding capacity to 10% of control values. Growth hormone administration (100 µg/day) for 7 days, begun 1 week after hypophysectomy, caused an increase in binding to 31% of control values, but simultaneous administration of LH (5 µg/day) prevented this GH-induced increase in binding capacity. Seven days of PRL treatment (100 µg/day) also caused a significant increase in [¹²⁵I]-hCG binding above the 2 week hypophysectomized control values (24%), but adding PRL to GH treatments did not result in an increase in [¹²⁵I]-hCG binding above that seen with GH or PRL alone. However, simultaneous administration of LH with PRL caused the induction of additional new receptors and returned total binding to 44% of normal intact control values. Combination of all three treatments (GH, PRL, and LH) showed an additive effect of the residual and PRL + LH treatment regimens and increased [¹²⁵I]-hCG binding to 52% of that of normal controls. These experiments suggest 1) GM and PRL are capable of inducing new LH receptors in the regressed testis of the hypophysectomized rat, 2) PRL allows LH or LH allows PRL to induce a new LH receptor population resistant to LH down-regulation, 3) GH causes the induction of a new population of LH receptors sensitive to LH down-regulation. These observations raise the possibility that subpopulations of Leydig cell LH receptors with different hormonal sensitivities reside within the testes.

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ACKNOWLEDGMENTS The author would like to thank Mrs. Sara Amin and Mr. John Wukie for their skilled technical help with the studies and Ms. Janet Worthington and Mrs. Judy D’Angelo for their expert secretarial assistance in preparation of this manuscript. We also thank NIAMDD Pituitary Distribution Program for the hormone preparation used in this study. This study was supported by CHRF Grant 74-220.