Localization of Luteinizing Hormone, Follicle-Stimulating Hormone, Prolactin, and Their Receptors in Human and Rat Testis Using Immunohistochemistry and Radioreceptor Assay*

Abstract

Immunoperoxidase staining and radioreceptor assay were used to study the localization of LH, FSH, and PRL and their receptors in the human and rat testis. In immunohistochemical staining, the Leydig cells of both species were invariably LH positive and generally FSH negative, but there were some FSH positive cells which were morphologically indistinguishable from the Leydig cells. The tubules were LH negative. The Sertoli cells of both species were FSH positive, whereas the spermatogonia and other germ cells were negative. Positive staining for PRL was seen in rat Leydig cells, whereas the human testes were negative. In keeping with the immunohistochemical findings, LH and FSH receptors were found in the testis of both species, but PRL receptors only in the rat. The finding of FSH positive cells in the interstitial tissue may explain why FSH increases the number of Leydig cell LH receptors and increases the sensitivity and maximum response to LH stimulation. Failure to demonstrate PRL and PRL receptors in the human testis indicates either that very low receptor concentrations are needed to bring about PRL action or that the established testicular effects of PRL are indirect.

Mutations of follicle-stimulating hormone and its receptor: effects on gonadal function

“…In accordance, the cells expressing the mutant receptor bound 125 I-labeled rhFSH at only 3% of that measured in cells expressing the wild-type FSHR. The affinity of binding (K a ) was in both cases similar ((4.8-6.7) × 10 9 liter/mol) and in good agreement with the affinity of human testicular FSHR (34). We have recently observed that the mutation mainly affects the folding and trafficking of the receptor protein to the cell membrane (A Rannikko, K Aittomäki, P Pakarinen & I Huhtaniemi, unpublished observations).…”

Hormonal regulation of male germ cell development

“…These pathways eventually activate cAMPresponsive element (CRE)-binding protein (CREB), and then transcribe downstream target genes of spermatogenesis. Testosterone is synthesized by Leydig cells upon LH stimulation (de Kretser et al 1971, Wahlstrom et al 1983. Testosterone exerts its biological effects on spermatogenesis via androgen receptors (ARs) that are localized in the Sertoli cells (reviewed in Silva et al (2002)).…”

Violation of spermatogenesis and outcomesof assisted reproductive technologies in various forms of hypogonadism

“…Клетки Лейдига вырабатывают тестостерон под действием ЛГ, последний оказывает биоло-гическое действие на сперматогенез через андро-геновые рецепторы, расположенные на клетках Сертоли [6]. ФСГ оказывает свое действие через G-ассоциированные рецепторы к ФСГ, находящи-еся на мембране клеток Сертоли.…”