title: Glucoprivic treatments that induce anestrus, but do not affect food intake, increase FOS-like immunoreactivity in the area postrema and nucleus of the solitary tract in Syrian hamsters.
abstract: Animals make a wide variety of physiological and behavioral adjustments in order to maintain caloric homeostasis. For example, most animals increase food intake when the availability of cellular metabolic fuels is low. The area postrema (AP) and adjacent, reciprocally-innervated nucleus of the solitary tract (NTS) are important brain areas for metabolic control of food intake in rats. However, in Syrian hamsters, food intake is not affected by decreases in metabolic fuel availability such as those that occur with food deprivation or with pharmacological inhibitors of metabolic fuels. Hamsters make other adjustments that conserve energy when the availability of metabolic fuels is low. Estrous cycles are inhibited by treatment with a high dose of 2-deoxy-D-glucose (2DG), a drug that inhibits cellular glucose utilization, but not by treatment with methyl palmoxirate (MP) a drug that inhibits fatty acid utilization. Recent data suggest that the AP/NTS is critical for the effects of glucoprivation on estrous cycles. Lesions of the AP/NTS prevent 2DG-induced anestrus. If the AP/NTS is involved in anestrus induced by glucoprivation, it might be predicted that glucoprivic treatments that induce anestrus would change patterns of neural activation, as measured by FOS-like immunoreactivity (FOS-li), in the AP/NTS. We examined FOS-li in females that were either food deprived or fed ad libitum, and in females treated with 2DG, MP or the appropriate vehicle. FOS-li was increased in the AP/NTS only in hamsters food deprived or treated with 2DG, the two treatments that induce anestrus but have no effect on food intake. These results are consistent with the notion that metabolic control of estrous cycles involves detection of decreases in the availability of metabolic fuels in the AP/NTS.
authors.affiliation: Department of Biological Sciences, Lehigh University, Bethlehem, PA 18015, USA.
authors.forename: J E
authors.initials: JE
authors.lastname: Schneider
authors.forename: B C
authors.initials: BC
authors.lastname: Finnerty
authors.forename: J M
authors.initials: JM
authors.lastname: Swann
authors.forename: J M
authors.initials: JM
authors.lastname: Gabriel
mesh_terms: D000780:Anestrus / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D002552:Cerebral Ventricles / Q000378:metabolism*; D006224:Cricetinae; D003847:Deoxyglucose / Q000494:pharmacology; D004852:Epoxy Compounds / Q000494:pharmacology; D005247:Feeding Behavior / Q000187:drug effects / Q000502:physiology; D005260:Female; D005508:Food Deprivation / Q000502:physiology*; D005947:Glucose / Q000172:deficiency*; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007150:Immunohistochemistry; D008647:Mesocricetus; D011422:Propionates / Q000494:pharmacology; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D017552:Solitary Nucleus / Q000378:metabolism*
chemical_list: D004852:Epoxy Compounds; D007004:Hypoglycemic Agents; D011422:Propionates; D016760:Proto-Oncogene Proteins c-fos; D003847:Deoxyglucose; D005947:Glucose; C017522:methyl 2-tetradecylglycidate