Effects of prolactin on testicular regression and recrudescence in the golden hamster.

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.