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 fertility¹. This action of testosterone is mediated by the Sertoli cells which nourish and support the developing spermatozoa². 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^3,4. Indeed, follicle-stimulating hormone (FSH), which acts only on Sertoli cells⁵, can also cause profound changes in Leydig cell function^6–8, 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 cells⁹. As injected LHRH agonists cause impairment of gonadal function^10–13 and directly inhibit FSH-induced changes in Leydig cell function¹⁴ through specific membrane receptors^15–17, this ‘LHRH-like’ factor has all the correct credentials for the postulated messenger between the Sertoli and Leydig cells³. 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.