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Suppression of testicular weight and activity induced in the hamster by light deprivation can be partially reversed by treatment with prolactin (PRL). The present study investigates the possibility that the stimulatory effect of PRL in this preparation may be mediated through increased LH binding. Hamsters exposed to 5 h light per day for two months to induce gonadal atrophy were injected daily for 2 1/2 weeks with saline, 250 mug PRLP, 20 MUG LH+150 mug FSH, or PRL+LH+FSH. Short light control animals exhibited significantly less LH binding than controls on 14 h of light per day. Treatment with LH+FSH had no effect on LH binding while PRL alone or in combination with LH+FSH increased binding to levels greater than the long light controls. Peripheral testosterone concentrations reflected the level of LH binding. Scatchard analysis indicates that the decreased binding in the short-day animals is due to reduced LH receptor numbers and that PRL treatment elevates receptor levels thereby increasing LH binding. These results suggest that the mechanism by which PRL stimulates testicular function in hamsters with regressed gonads is through increased binding of endogenously produced LH.

Transfer of adult male hamsters from a long to a short photoperiod causes testicular atrophy, which is accompanied by decreases in testicular LH receptors and in plasma PRL and testosterone levels. A decrease in plasma gonadotropin levels is also frequently observed. When the decline in peripheral PRL concentration is prevented by transplantation of homologous pituitary(ies) under the kidney capsule, testicular atrophy is delayed and incomplete. This appears to be due to the maintenance of testicular LH receptors by PRL secreted from the grafts and probably also to the stimulation of GSH release from the in situ pituitary. In hamsters maintained in a long photoperiod, ectopic pituitary homografts can increase testicular LH receptor levels, concentrations of testosterone and FSH in the plasma, and the weights of the testes and the seminal vesicles. In contrast to the findings obtained in rats and mice, chronic hyperprolactinemia in the male hamster does not inhibit gonadotropin release or interfere with copulatory behavior. These findings are consistent with our earlier suggestion that PRL plays an important part in the regulation of gonadal function in the male hamster but indicate that testicular atrophy in a short photoperiod cannot be explained solely by a reduction in PRL release.

In adult male hamsters, 2 months of exposure to a short photoperiod (5 h of light:19 h of darkness) caused testicular regression and a precipitous decline in plasma PRL, in agreement with earlier reports from other laboratories. Depressed release of PRL cannot be explained by a reduction in testicular steroidogenesis, because castration of males kept in a long photoperiod did not reduce PRL levels and administration of testosterone to males kept in a short photoperiod failed to reverse the decline in plasma PRL concentration. Treatment of such "regressed" animals with PRL, GH, or ectopic pituitary transplants stimulated growth of the testes and the accessory reproductive glands, increased the concentration of LH receptors in the testes, and elevated plasma testosterone levels. A single injection of 250 microgram PRL was sufficient to increase testicular LH binding, and chronic treatment with pituitary grafts completely reversed testicular regression. The effectiveness of exogenous PRL in stimulating testicular growth and LH receptors was significantly influenced by the timing of the injection. In some experiments, gonadotropin levels appeared elevated in animals injected with PRL, but these differences were not statistically significant. In hamsters with gonadal regression induced by exposure to a short photoperiod, daily administration of 20 microgram H and/or 150 microgram FSH had no apparent effect on testicular function. However, treatment with large doses of hCG and/or PMS gonadotropin resulted in significant stimulation of testicular growth and steroidogenesis. Chronic treatment of males maintained in a long photoperiod (14 h of light:10 h of darkness) with an inhibitor of PRL release, 2-Br-alpha-ergocryptine, resulted in a decreased weight of the testes and seminal vesicles. Administration of this inhibitor for a longer period (2 months) produced a significant increase in body weight but had little effect on testicular function. These results indicate that changes in the release of PRL (and possibly also GH) may plan an important role in mediating the effects of the photoperiod on testicular function in the golden hamster.

Hamster serum gonadotropins were measured by RIA at 4 h intervals during the estrous cycle. On the afternoon of proestrus both LH and FSH exhibited a surge, but unlike the situation in the rat and mouse FSH returned to "baseline" with LH by early evening of proestrus. Shortly following this return FSH concentrations increased and reached a second peak by noon on estrus which was equal in magnitude and longer in duration than that occurring on proestrus. FSH fell to its lowest levels on diestrus 2 (D2) and early proestrus. Serum gonadotropins were measured by RIA 6 h following unilateral ovariectomy on D2. A slight elevation of LH resulted while FSH increased to a level equal in magnitude to that found during the proestrous surge. In intact females administration of a total of 45 mug FSH in 5 injections on D2 resulted in ovulation of twice the normal number of eggs. The t1/2 of this rat FSH in the male hamster was found to be 122 minutes. The low levels of FSH during the cycle between D2 and proestrus, the large increase in serum FSH following unilateral ovariectomy, and the "doubled" ovulation in intact hamsters following the administration of FSH on D2, suggest that the serum FSH concentration on D2 is critical in determining the number of follicles which will be available for the subsequent ovulation.