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Dexamethasone blocks the refeeding-induced phosphorylation of cAMP response element-binding protein in the rat hypothalamus

Authors
Journal
Neuroscience Letters
0304-3940
Publisher
Elsevier
Publication Date
Volume
344
Issue
2
Identifiers
DOI: 10.1016/s0304-3940(03)00299-4
Keywords
  • Neuronal Nitric Oxide Synthase
  • Phosphorylated Camp Response Element-Binding Protein
  • Food Deprivation
  • Refeeding
  • Glucocorticoid
  • Hypothalamus
Disciplines
  • Biology
  • Medicine

Abstract

Abstract We previously reported that dexamethasone pretreatment abolishes the refeeding-induced neuronal nitric oxide synthase (nNOS) expression in the rat paraventricular nucleus (PVN). It was reported that nNOS upstream carries cAMP response element (CRE) and nNOS expression is mediated by a CRE-binding protein (CREB)-dependent mechanism. In this study, CREB phosphorylation was co-localized in the nNOS neurons of the rat PVN regardless of feeding conditions. The relative amount of phosphorylated CREB in the hypothalamic tissue lysates increased by 1 h of refeeding following 48 h of food deprivation, and interestingly, this increase was blocked by dexamethasone administration before the food onset. These results suggest that glucocorticoids exert an inhibitory role in CREB phosphorylation directed by nutritional stimuli in the rat hypothalamus, and this inhibition may be related to nNOS gene expression in this brain region.

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