Regulation of testicular function in the stallion: an intricate network of endocrine, paracrine and autocrine systems.
It is well established in many mammalian species, including the horse that normal testicular function is dependent upon a functional hypothalamic-pituitary-testicular (HPT) axis, which involves classic feedback mechanisms. The major HPT hormones involved in the stallion are gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone (T), estrogens (Es) and inhibin (INH). Although prolactin (PRL) fluctuates with season in the stallion and both PRL and thyroid hormone (TH) affect reproduction in other male species, their effects on stallion reproduction have not been elucidated. Growth hormone (GH) in the stallion may be involved in sperm motility, production and secretion of insulin-like growth factor-1 (IGF-1) and LH-induced testosterone release. The action of these hormones and the products involved for normal spermatogenesis require cell to cell communication within the testis. The somatic cell types, Leydig, Sertoli and peritubular myoid cells, all support germ cell development, maturation and release into the seminiferous tubule lumen. The cell to cell crosstalk involves an intricate network of paracrine-autocrine systems that support the endocrine input to modulate cell function. In other male species, researchers have demonstrated the reproductive effects of such paracrine-autocrine factors as IGF-1, transferrin, androgens, estrogens, inhibin, insulin like peptide 3 (INSL3), beta-endorphin and oxytocin. The specific nature and relative contribution of these various factors on testicular function in fertile and subfertile stallions are under investigation. This review summarizes current information regarding the nature of the multiple endocrine-paracrine-autocrine systems that may be necessary for normal testicular function in the stallion.
Roser
Janet F
JF
Department of Animal Science, University of California, Davis, CA 95616, United States. jfroser@ucdavis.edu
D000818:Animals; D019898:Autocrine Communication / Q000502:physiology*; D004703:Endocrine System / Q000502:physiology*; D005298:Fertility / Q000502:physiology; D006706:Homeostasis / Q000502:physiology; D006736:Horses / Q000502:physiology*; D008297:Male; D008954:Models, Biological; D019899:Paracrine Communication / Q000502:physiology*; D013737:Testis / Q000502:physiology*