title: Seasonal differences in testicular receptors and steroidogenesis.
abstract: Gonadal function in most animal species exhibits considerable annual fluctuations, with gametogenesis and fertility often being confined to a short and rigidly controlled breeding season. In males, production of androgenic steroids by the testis is usually maximal immediately before and during the breeding season. In the golden hamster, seasonal regression of the testes is associated with decrease in the total content of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) receptors, and similar findings have been reported for other mammalian species. However, the concentration of LH and FSH receptors per unit of testis weight is typically elevated rather than suppressed during testicular regression. Reduction in the number of testicular LH and PRL receptors in adult golden hamsters exposed to short photoperiod is due primarily to suppression of pituitary PRL release under these circumstances. Regulation of seasonal changes in testicular FSH binding, as well as regulation of the levels of LH, PRL and FSH receptors in other seasonally breeding species remain to be elucidated. Reduction in the content of LH receptors in the testes is accompanied by reduced capacity to produce androgens in response to LH stimulation. Although these events are likely to be causally related, other mechanisms are also involved. In particular, seasonal regression is accompanied by reduced capacity of the testes to convert C21 steroid precursors into biologically active androgens. Seasonal loss of FSH receptors was reported to be accompanied by increased rather than reduced responsiveness of the Sertoli cells to FSH, thus resembling the situation in immature animals. It can be concluded that alterations in the ability of the testes to bind pituitary gonadotropins and to respond to gonadotropic stimulation are among the mechanisms responsible for seasonal shifts between gonadal activity and quiescence.
authors.affiliation: Department of Physiology, Southern Illinois University School of Medicine, Carbondale 62901.
authors.forename: A
authors.initials: A
authors.lastname: Bartke
authors.forename: A G
authors.initials: AG
authors.lastname: Amador
authors.forename: V
authors.initials: V
authors.lastname: Chandrashekar
authors.forename: H G
authors.initials: HG
authors.lastname: Klemcke
mesh_terms: D000818:Animals; D003411:Arvicolinae / Q000502:physiology; D006224:Cricetinae / Q000502:physiology*; D012739:Gonadal Steroid Hormones / Q000096:biosynthesis*; D006065:Gonadotropins, Pituitary / Q000494:pharmacology*; D008988:Herpestidae / Q000502:physiology; D008027:Light; D008297:Male; D008647:Mesocricetus / Q000502:physiology*; D010507:Periodicity / Q000528:radiation effects; D051381:Rats / Q000502:physiology; D011967:Receptors, Gonadotropin / Q000378:metabolism*; D012621:Seasons; D012708:Sertoli Cells / Q000502:physiology / Q000528:radiation effects; D012756:Sheep / Q000502:physiology; D013737:Testis / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*
chemical_list: D012739:Gonadal Steroid Hormones; D006065:Gonadotropins, Pituitary; D011967:Receptors, Gonadotropin