Effects of an lhrh agonist and gonadotropins on testicular prolactin receptors

Abstract Effects of administration of the LHRH agonist D-Leu 6 -LHRH ethylamide (LHRH-A), gonadotropin (PMS), and their interaction on testicular prolactin (PRL) receptor levels were investigated in rats. LHRH-A (2 μg/100 g body wt.) or saline was injected SC daily, and PMS (5 IU) injected every other day. In intact rats, the testicular PRL receptor levels were about 400 fmoles/testis after either 1 or 7 daily injections of saline. Administration of LHRH-A decreased PRL receptors to 12% of that of saline-injected control rats at day 1, and to 20% at day 2, and PRL receptor levels were partially restored to 55% at day 7. In hypophysectomized rats given daily injections of saline for 7 days PRL receptor levels were only 20% of those in saline-injected intact rats. Injections of LHRH-A in hypophysectomized animals did not further decrease PRL receptor numbers at this time. Administration of PMS to hypophysectomized rats for 7 days partially reversed the reduction of PRL receptors that occurred after hypophysectomy, to 46% of those in intact controls. Injections of LHRH-A into hypophysectomized, PMS-treated animals did not significantly alter PRL receptors on day 1 (117% of that of saline-injected, hypophysectomized, PMS-treated rats at day 1) or day 2 (96% of same-day controls), but decreased PRL receptors on day 7 to 102 fmoles/testis (55% of same-day controls). This latter concentration is nearly the same as that in saline-injected, 7-day hypophysectomized rats not treated with PMS. These findings suggest that: (1) the effects of LHRH-A on testicular PRL receptors differ depending on the presence or absence of gonadotropin, (2) gonadotropin, primarily FSH, maintains some population of testicular PRL receptors, and these gonadotropin-dependent PRL receptors are suppressed by direct action of LHRH-A upon the testes, and (3) there is a population of PRL receptors which is not affected by LHRH-A or gonadotropin.