Navegando por Palavras-chave "Lateral hypothalamus"
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- ItemSomente MetadadadosAdrenalectomy abolishes the food-induced hypothalamic serotonin release in both normal and monosodium glutamate-obese rats(Elsevier B.V., 2002-08-15) Guimaraes, Regina Barros [UNIFESP]; Telles, Monica Marques [UNIFESP]; Coelho, Vivian Beatriz Orlandin [UNIFESP]; Mori, Rosana Cristina Tieko [UNIFESP]; Nascimento, Claudia Maria da Penha Oller do [UNIFESP]; Ribeiro, Eliane Beraldi [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Corticosteroids influence energy homeostasis through centrally-mediated stimulation of energy intake and inhibition of expenditure, while central serotonin (5-HT) has opposite effects. Both serotonergic dysfunction and high glucocorticoid levels may be relevant in obesity. the neurotoxin monosodium glutamate (MSG) induces a non-hyperphagic and hypometabolic obesity with hypercorticosteronemia. We investigated the influence of corticosterone levels on the serotonergic system of MSG-obese and control rats. Applying microdialysis, we found a similar feeding-induced stimulation of serotonin release in the lateral hypothalamus (LH) in sham-adrenalectomized control and MSG rats. the concomitant serum corticosterone variations were markedly distinct between them, in that an increase occurred in the control group, while the initially high levels of the MSG rats decreased with feeding. It is suggested that this lowering of corticosterone prevented a higher serotonergic activation, which would lead to a higher meal-induced thermogenesis and a better adequation of the,caloric intake to a low metabolism. Adrenalectomy completely abolished the feeding-evoked serotonergic stimulation in both groups. This observation demonstrates that glucocorticoids are necessary for food intake to acutely stimulate 5-HT release and indicates that serotonergic activity in the LH is not likely to participate in the adrenalectomy-induced attenuation of the MSG-obesity. (C) 2002 Elsevier Science Inc. All rights reserved.
- ItemSomente MetadadadosFeeding induced by increasing doses of neuropeptide Y: Dual effect on hypothalamic serotonin release in normal rats(Taylor & Francis Ltd, 2004-08-01) Mori, Rosana Cristina Tieko [UNIFESP]; Telles, Monica Marques [UNIFESP]; Guimaraes, Regina Barros [UNIFESP]; Novo, Neil Ferreira [UNIFESP]; Juliano, Yara [UNIFESP]; Nascimento, Claudia Maria da Penha Oller do [UNIFESP]; Ribeiro, Eliane Beraldi [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Endogenous neuropeptide Y (NPY) levels increase during fasting and before dark onset in rats. the feeding that follows these states elicits the release of serotonin in the lateral hypothalamus (LH), as part of the physiological mechanisms controlling satiety. With the hypothesis that exogenous NPY-induced feeding should also stimulate serotonin, we measured its release in the LH of non-fasted rats, which received a single intracerebroventricular injection of either 1.0, 2.0, or 5.0 mug of NPY. After 1.0 mug, the cumulative 2-h intake was of 13 g and serotonin release significantly increased (54% peak). These feeding and serotonergic responses were highly similar to the ones we observed in a previous study, in which feeding followed an overnight fast. Thus, the 1.0 mug NPY dose stimulated intake while preserving the normal serotonergic activation. Contrarily, as the NPY dose was increased to either 2.0 or 5.0 mug, the cumulative 2-h intakes were of 18 g, but the serotonergic stimulation was absent. It is suggested that this dual NPY effect relies on a finely tuned control mechanism, reflecting the existence of a narrow range of NPY levels within which the serotonergic stimulation resembles those seen in physiological states.
- ItemSomente MetadadadosLateral hypothalamic serotenergic responsiveness to food intake in rat obesity as measured by microdialysis(Natl Research Council Canada, 1999-04-01) Mori, Rosana Cristina Tieko [UNIFESP]; Guimaraes, Regina Barros [UNIFESP]; Nascimento, Claudia Maria da Penha Oller do [UNIFESP]; Ribeiro, Eliane Beraldi [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)The hypothalamic serotonergic system is involved in the regulation of food ingestion and energy metabolism. Since disturbances of both energy intake and expenditure can contribute to obesity, the objective of the present study was to evaluate the serotonergic response stimulated by food ingestion in two different models of obesity: the hyperphagic Zucker and the hypophagic and hypometabolic, monosodium glutamate (MSG) obese Wistar rat. for this we used microdialysis to examine the release of 5-hydroxytryptamine (serotonin, 5HT) and 5-hydroxyindoleacetic acid (5HIAA) in the lateral hypothalamus. Daily intake of MSG-obese rats was 40% lower while that of Zucker obese rats was 60% higher than that of the respective lean controls. in overnight-fasted animals, 20-min microdialysate samples were collected before (basal release) and during a 2-h period of access to a balanced palatable food mash. the animals began to eat during the first 20 min of food access, and food consumption was similar among the four groups in all six individual 20-min periods recorded. Ingestion of food increased 5HT release in all groups. in MSG-obese and lean Wistar rats, 5HT levels were similarly elevated during the whole experimental period. in the Zucker strain, 5HT increments of basal release tended to be higher in obese than in lean rats at 20 and 40 min, and a significantly higher increment was observed at 60 min after food access (40 and 135% for lean and obese, respectively). the area under the curve relating serotonin levels to the 120 min of food availability was significantly higher in Zucker obese (246.7 +/- 23.3) than MSG-obese (152.7 +/- 13.4), lean Wistar (151.9 +/- 11.1), and lean Zucker (173.5 +/- 24.0) rats. the present observation, of a food-induced serotonin release in the lateral hypothalamus of lean Wistar and Zucker rats, evidences that 5HT in the lateral hypothalamus is important in the normal response to feeding. in obese animals, the serotonin response was similar to (in the hypophagic-hypometabolic MSG model) or even higher than (in the hyperphagic Zucker model) that seen in the respective lean controls. This result indicates that the energy homeostasis disturbances of both these obesity models may not be ascribed to an impairment of the acute lateral hypothalamic serotonin response to a dietary stimulus.