Prolactin (PRL), Follicle-Stimulating Hormone, and Luteinizing Hormone Are Regulators of Testicular PRL Receptors in Golden Hamsters*

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Abstract
The ability of PRL, FSH, and LH to regulate testicular PRL receptors in golden hamsters was evaluated using a variety of experimental protocols. Exposure to a photoperiod of 5 h of light and 19 h of darkness (5L:19D) for 11 weeks precipitated a 94% reduction in content (femtomoles per testes) of testicular PRL receptors and, concomitantly, a decrease (P < 0.05) in plasma PRL, but not LH or FSH. One pituitary gland under the kidney capsule in 5L:19D-housed hamsters increased (P < 0.05) both the concentration (femtomoles per mg protein) and content of PRL receptors, as well as those of plasma PRL and FSH. Similar treatment in 14L:10D-housed hamsters produced comparable changes in plasma PRL and FSH without affecting PRL receptors. Injections of l-dopa for 7 days into hamsters housed in 5L:19D for 11 weeks significantly elevated serum FSH concentrations, had no measurable effect on serum PRL and LH, and induced a greater than 2-fold increase in PRL receptor levels. In a separate study, hamsters housed in 5L:19D for 12 weeks were injected for 3 days with 250 ng ovine (o) PRL, 25 μg oLH, or 5 μg oFSH, and results were compared with vehicle-injected, 5L:19D- and 14L:10D-housed controls. Injections of oPRL and oLH increased (P < 0.05) PRL receptor concentration and content, with PRL being more efficacious. No anti-oPRL antibodies were produced by oPRL injections. In this study, injections of oFSH were without effect on PRL receptors. To ascertain the effects of each hormone in the absence of other trophic influences, experiments were conducted in hypophysectomized hamsters injected daily for 3 days (2–4 days posthypophysectomy) with one of the following: 5 or 25 μg oLH; 10, 50, or 250 μg oPRL; or 1 or 5 μg oFSH. Hypophysectomy reduced the concentration and content of PRL receptors by 85%, and treatment with 50 or 250 μg oPRL increased (P < 0.05) these low levels almost 3-fold. Again, no anti-oPRL antibodies were induced. Injection of 5 ng oLH or 25 μg oFSH also induced increases (P < 0.05) in PRL receptors. Hypophysectomy reduced basal and hCG-stimulated in vitro testicular testosterone production (nanograms per testes/4 h) to levels less than 20% of control values. None of the hormonal treatments affected (P < 0.05) basal testosterone production in vitro. However, injections of 5 or 25 μg oLH or 5 μg oFSH elevated (P < 0.05) hCG-stimulated testosterone production. oPRL produced a modest but significant increase in the ratio of hCG-stimulated to basal testosterone production. These data indicate a multihormonal regulatory mechanism of testicular PRL receptors in golden hamsters which involves PRL, FSH, and LH. The effects of FSH are presumably indirect and probably involve a Sertoli cell-derived intercellular messenger. Although PRL had the greatest effect on testicular PRL receptors and produced a modest but significant increase in responsiveness to hCG stimulation, it was incapable of reversing other cellular defects, and allowing for more nearly normal testosterone production. (Endocrinology118: 773–782, 1986)