A study was conducted with hypophysectomized hamsters to determine effects of administration of prolactin (PRL), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) - alone or in combination - on testicular PRL receptors and in vitro testosterone production. Hormonal injections commenced the second day after hypophysectomy, and hamsters were killed on Day 5, approximately 13 h after the last hormonal injection. PRL receptor numbers were reduced by hypophysectomy, and PRL administration alone lessened the extent of this decrease. By themselves, neither LH nor FSH affected PRL receptors, but a combination of PRL + FSH + LH produced the greatest effect on these receptors. Receptor affinity was only modestly affected by any treatments. In vitro testosterone synthesis was measured after addition of 0, 2, 10, and 50 mIU of human chorionic gonadotropin (hCG) to incubations of testicular tissue. Neither PRL nor FSH by themselves in vivo affected basal or hCG-stimulated testosterone production. However, PRL + FSH increased (p < 0.05) the magnitude of the in vitro testosterone response to hCG, as well as the sensitivity of that response (slope of the dose-response curve). LH alone increased both basal and hCG-stimulated testosterone production. PRL + LH provided no additional increase in the magnitude of the testosterone response, but increased (p < 0.05) the sensitivity. PRL + FSH + LH in vivo provided for the greatest sensitivity of the in vitro testosterone response to hCG. These data strongly support the importance of PRL in the maintenance of testicular PRL recptors, and indicate a modest but significant trophic effect of LH and FSH. The data also indicate that PRL by itself is incapable of supporting steroidogenesis in the absence of either LH or FSH.
Mendeley helps you to discover research relevant for your work.
CITATION STYLE
Klemcke, H. G., Amador, A. G., & Bartke, A. (1990). Hormonal regulation of testicular prolactin receptors and testosterone synthesis in golden hamsters. Biology of Reproduction, 43(1), 162–168. https://doi.org/10.1095/biolreprod43.1.162