Sertoli–Leydig cell communication via an LHRH-like factor

Abstract

The primary function of the testosterone secreted by Leydig cells is the maintenance of spermatogenesis and hence fertility. This action of testosterone is mediated by the Sertoli cells which nourish and support the developing spermatozoa. As normal Sertoli cell function is so critically dependent on normal Leydig cell function, a regulatory influence of the Sertoli cells on the Leydig cells has been suggested. Indeed, follicle-stimulating hormone (FSH), which acts only on Sertoli cells, can also cause profound changes in Leydig cell function, although how this is effected is unknown. We recently hypothesized that the Sertoli cell might be the source of a luteinizing hormone releasing hormone (LHRH)-like factor which we detected in the interstitial fluid surrounding the Leydig cells. As injected LHRH agonists cause impairment of gonadal function and directly inhibit FSH-induced changes in Leydig cell function through specific membrane receptors, this 'LHRH-like' factor has all the correct credentials for the postulated messenger between the Sertoli and Leydig cells. Here, we strengthen this case by demonstrating that seminiferous tubules from both the rat and the stumptailed macaque (Macaca arctoides) contain a factor which has LHRH-like receptor-binding and biological activity in vitro, but which is immunologically distinct from native LHRH. We have also shown that this factor is secreted in vitro by cultured rat Sertoli cells.

Effect of scrotal insulation on the pituitary--testicular axis of the ram

“…This aggregation effect will be less pronounced in the perfused tissue used in the present study as space left after shrinkage of the seminiferous epithelium is partly accounted for by the dilated lymphatics. Kerr, Rich & de Kretser (1979) have confirmed the impressions of earlier workers (Hanes, 1911;Lynch & Scott, 1951) (Chemes, Ri varóla & Bergada, 1976;Christensen & Peacock, 1980 (Schanbacher, 1979a;1980 (Schanbacher, 1979b;D'Occhio, Schanbacher & Kinder, 1982 (Catt et al, 1980) and an LHRH-like factor produced by the seminiferous tubule (Sharpe, Fraser, Cooper & Rommerts, 1981) have been shown to exert an intratesticular control of Leydig cell steroidogenesis, the relationship between these substances and Leydig cell structure and function has not yet been investigated. The role of the seminiferous epithelium in exerting some control of Leydig cell activity has been emphasized by Ucci (1982), who showed that there was an inverse relationship between Leydig cell size and activity, and germ cell maturation in the normal urodele testis.…”

Local Control of Testicular Function

“…Sharpe & Fraser, 1980b) and in most respects these receptors are identical to LHRH receptors on the anterior pituitary (Clayton & Catt, 1981). Low levels of LHRH-like activity have been demonstrated in extracts of whole testis, seminiferous tubules and spent media from Sertoli cell cultures using a variety of assay techniques (Dutlow & Millar, 1981;Sharpe, Fraser, Cooper & Rommerts, 1981;reviewed by Sharpe & Harmar, 1983) and activity has also been demonstrated in vivo in testicular interstitial fluid from hCG-treated rats (Sharpe & Fraser, 1980a;. However, there is no definitive evidence that the Sertoli cell is the only or even the most important source of 'LHRH' within the testis, and attempts to purify this compound have made poor progress (Sharpe & Harmar, 1983).…”

Antifertility effects of GnRH

“…This concept received further support from the demonstration of receptor sites for GnRH on the Leydig cell (Sharpe & Fraser, 1980a). The stimulation of a GnRH-like factor by the testes after administration of hCG indicated that high doses of GnRH and its agonists might mimic the action of a naturally produced intra-gonadal regulator, the normal function of which was to reduce the responsiveness of the Leydig cells (Sharpe & Fraser, 1980b;Sharpe, Fraser, Cooper & Rommerts, 1981;Sharpe, 1982 (Fraser, 1980a).…”