Paracrine control of the testis.
The mammalian testis is under the overall control of pituitary gonadotropins but the utilization of these signals to achieve normal testicular function involves complex local interactions between the Sertoli and germ cells, the Sertoli and peritubular cells, and the Sertoli and Leydig cells as well as local control of the testicular vasculature. These interactions serve two purposes: (1) to coordinate the functions of the three testicular compartments (seminiferous tubules, interstitium and the vasculature); and (2) to control the complex but orderly sequence of events that constitutes the spermatogenic cycle. This process, which involves multiplication, differentiation and translocation of the germ cells is organized into a sequence of stages, each of which is composed of a constant association of germ cells at four or five different stages of development. At each stage of the spermatogenic cycle, different events occur and the function of the Sertoli cells alters, probably in accordance with the changing requirements of the associated germ cells. As yet, our understanding of these many local events is extremely limited, particularly with respect to the identity of the hormones/factors involved in controlling the various processes. Our knowledge of paracrine control mechanisms in the testis is derived mainly from studies of the rat, but as the process of spermatogenesis is essentially the same in most mammals and involves the same sequence of events, then findings in the rat can probably be applied in general, if not in detail, to the human testis; the limited direct information available on the human testis supports this view. As most cases of infertility in men occur despite normal or raised serum gonadotropin levels and are characterized by the production of reduced or normal numbers of sperm, then it seems likely that malfunction of one or more of the intricate paracrine processes within the testis may be involved in the aetiology of idiopathic oligospermia. It is therefore argued that advances in our knowledge of the paracrine control of the testis should have major repercussions on our ability to understand, and eventually treat, idiopathic infertility in men, and also to induce infertility for contraceptive purposes.
D000818:Animals; D002450:Cell Communication; D004702:Endocrine Glands / Q000502:physiology*; D005298:Fertility; D007987:Gonadotropin-Releasing Hormone / Q000502:physiology; D006801:Humans; D007248:Infertility, Male / Q000209:etiology; D007985:Leydig Cells / Q000502:physiology; D008297:Male; D051381:Rats; D012671:Seminiferous Tubules / Q000502:physiology; D012708:Sertoli Cells / Q000502:physiology; D013091:Spermatogenesis; D013094:Spermatozoa / Q000502:physiology; D013737:Testis / Q000098:blood supply / Q000502:physiology*; D013739:Testosterone / Q000502:physiology
D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone