Testicular LH binding in the hamster: modification by photoperiod and prolactin.
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.
D000818:Animals; D006224:Cricetinae; D003624:Darkness; D005640:Follicle Stimulating Hormone / Q000494:pharmacology; D008027:Light; D007986:Luteinizing Hormone / Q000378:metabolism* / Q000494:pharmacology; D008297:Male; D011388:Prolactin / Q000494:pharmacology*; D013737:Testis / Q000187:drug effects / Q000378:metabolism*; D013739:Testosterone / Q000378:metabolism
D013739:Testosterone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone