Effects of immunoneutralization of luteinizing hormone (LH)-releasing hormone on testicular prolactin and LH receptors in the golden hamster and on LH receptors in the Djungarian hamster.

In male Syrian hamsters, seasonal transitions between reproductive activity and quiescence are accompanied by major alterations in testicular binding of LH/hCG and PRL. These alterations are believed to be due to the photoperiod-induced changes in PRL secretion, but other adenohypophyseal hormones appear to be involved as well. To elucidate the role of LH and FSH in the control of testicular LH/hCG and PRL receptors, we have examined the consequences of selective suppression of gonadotropin release by immunoneutralization of endogenous LHRH. In adult Syrian hamsters, four weekly injections of LHRH antiserum produced significant reductions in plasma levels of LH, FSH, and testosterone and in the weights of the testes and the seminal vesicles; no change in plasma PRL; and a significant reduction in the total content (femtomoles per testis) of testicular LH/hCG and PRL receptors. The concentration of LH/hCG receptors (femtomoles per mg protein) was significantly increased. In adult males of another seasonally breeding species, the Djungarian hamster (Phodopus sungorus), four weekly injections of LHRH antiserum produced suppression of plasma LH and FSH, no change in plasma PRL, a reduction in the weights of the testes and the seminal vesicles, an increase in the concentration of testicular LH/hCG receptors, and a decrease in their total content. Alterations in testicular LH and PRL binding induced by treatment with LHRH antiserum in the present study were qualitatively similar to changes induced by exposure to short photoperiod or by treatment with bromocriptine. We conclude that gonadotropins normally participate in the regulation of testicular LH/hCG and PRL receptors in the Syrian hamster and LH/hCG receptors in the Djungarian hamster. Seasonal changes in the content of LH/hCG and PRL receptors in the testes appear to be due to photoperiod-induced alterations in the secretion of both PRL and gonadotropins.