title: Expression of Fos-like proteins in gonadotropin-releasing hormone neurons of Syrian hamsters: effects of estrous cycles and metabolic fuels.
abstract: In female mammals, reproduction is sensitive to the availability of metabolic fuels, and food deprivation has been shown to suppress pulsatile LH secretion, attenuate the preovulatory LH surge, and prevent ovulation. It has been suggested that food deprivation impairs fertility by reducing the secretion of GnRH by GnRH-producing neurons in the forebrain. A series of experiments tested this hypothesis by examining the effects of estrous cycles and manipulations of metabolic fuel availability on the expression of Fos-like proteins (Fos-IR) in GnRH-immunoreactive (GnRH-IR) neurons in the forebrain of Syrian hamsters. GnRH-IR neurons were detected in several areas, including the diagonal band of Broca (DBB), medial septum (MS), rostral medial preoptic area (mPOA), and caudal POA. In the more rostral regions (DBB and MS/mPOA), GnRH-IR neurons expressed Fos-IR almost exclusively on day 4 of the cycle, just after the preovulatory LH surge. However, in the caudal POA, GnRH-IR neurons expressed Fos-IR across the entire cycle, including days 1-3, when LH secretion is pulsatile. Food deprivation on days 1 and 2 of the cycle, which attenuates the LH surge and blocks ovulation in hamsters, significantly reduced the proportion of GnRH-IR neurons that expressed Fos-IR on days 2 and 4 (caudal POA) or only on day 4 (DBB and MS/mPOA). Suppression of fuel availability with insulin or 2-deoxy-D-glucose on day 1 of the cycle mimicked the effects of food deprivation and reduced the proportion of caudal POA GnRH-IR neurons that expressed Fos-IR. The results of these experiments suggest that in Syrian hamsters, there are separate populations of GnRH-IR neurons associated with pulsatile and surge modes of LH secretion. In addition, the fact that manipulations of metabolic fuel availability cause changes in the expression of Fos-IR in both populations of GnRH-IR neurons provides strong support for the hypothesis that nutritional infertility is due in part to decreased GnRH secretion.
authors.affiliation: Neuroscience and Behavior Program, University of Massachusetts, Amherst 01003.
authors.forename: S J
authors.initials: SJ
authors.lastname: Berriman
authors.forename: G N
authors.initials: GN
authors.lastname: Wade
authors.forename: J D
authors.initials: JD
authors.lastname: Blaustein
mesh_terms: D000818:Animals; D006224:Cricetinae; D003847:Deoxyglucose / Q000494:pharmacology; D004435:Eating / Q000502:physiology*; D004958:Estradiol / Q000494:pharmacology; D004971:Estrus / Q000502:physiology*; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000032:analysis*; D007150:Immunohistochemistry; D007328:Insulin / Q000494:pharmacology; D007986:Luteinizing Hormone / Q000378:metabolism; D008647:Mesocricetus; D009474:Neurons / Q000737:chemistry* / Q000378:metabolism / Q000502:physiology; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis*
chemical_list: D007328:Insulin; D016760:Proto-Oncogene Proteins c-fos; D007987:Gonadotropin-Releasing Hormone; D004958:Estradiol; D007986:Luteinizing Hormone; D003847:Deoxyglucose