Sertoli–Leydig cell communication via an LHRH-like factor

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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 suggested3,4. Indeed, follicle-stimulating hormone (FSH), which acts only on Sertoli cells5, can also cause profound changes in Leydig cell function6–8, 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 function10–13 and directly inhibit FSH-induced changes in Leydig cell function14 through specific membrane receptors15–17, 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.