Hindbrain noradrenergic input to the hypothalamic PVN mediates the activation of oxytocinergic neurons induced by the satiety factor oleoylethanolamide
| Autor: | Bianca Tempesta, Catarina Soares Potes, Tommaso Cassano, Vincenzo Cuomo, Thomas A. Lutz, Adele Romano, Silvana Gaetani |
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| Přispěvatelé: | University of Zurich, Gaetani, Silvana |
| Rok vydání: | 2013 |
| Předmět: |
Adrenergic Neurons
Male Saporin Physiology Endocrinology Diabetes and Metabolism Oleic Acids Dopamine beta-Hydroxylase Oxytocin Oleoylethanolamide chemistry.chemical_compound 0302 clinical medicine 2737 Physiology (medical) Neurons 2. Zero hunger 0303 health sciences biology Immunotoxins digestive oral and skin physiology Solitary tract Receptor antagonist 10081 Institute of Veterinary Physiology 2712 Endocrinology Diabetes and Metabolism medicine.anatomical_structure 10076 Center for Integrative Human Physiology Ribosome Inactivating Proteins Type 1 hormones hormone substitutes and hormone antagonists medicine.drug medicine.medical_specialty medicine.drug_class Neuropeptide Hindbrain 610 Medicine & health Satiation 03 medical and health sciences Posterior pituitary Physiology (medical) Internal medicine medicine Animals Rats Wistar 030304 developmental biology acylethanolamides gut-brain axis neuropeptides noradrenergic projections nucleus of solitary tract paraventricular nucleus 1314 Physiology Saporins Rats Rhombencephalon Endocrinology chemistry nervous system biology.protein 570 Life sciences 030217 neurology & neurosurgery Endocannabinoids Paraventricular Hypothalamic Nucleus |
| Zdroj: | American journal of physiology. Endocrinology and metabolism |
| DOI: | 10.1152/ajpendo.00411.2013 |
| Popis: | Oleoylethanolamide (OEA) is a gut-derived endogenous lipid that stimulates vagal fibers to induce satiety. Our previous work has shown that peripherally administered OEA activates c-fos transcription in the nucleus of the solitary tract (NST) and in the paraventricular nucleus (PVN), where it enhances oxytocin (OXY) expression. The anorexigenic action of OEA is prevented by the intracerebroventricular administration of a selective OXY receptor antagonist, suggesting a necessary role of OXYergic mediation of OEA's effect. The NST is the source of direct noradrenergic afferent input to hypothalamic OXY neurons, and therefore, we hypothesized that the activation of this pathway might mediate OEA effects on PVN neurons. To test this hypothesis, we subjected rats to intra-PVN administration of the toxin saporin (DSAP) conjugated to an antibody against dopamine-β-hydroxylase (DBH) to destroy hindbrain noradrenergic neurons. In these rats we evaluated the effects of OEA (10 mg/kg, ip) on feeding behavior, on c-Fos and OXY immunoreactivity in the PVN, and on OXY immunoreactivity in the posterior pituitary gland. We found that the DSAP lesion completely prevented OEA's effects on food intake, on Fos and OXY expression in the PVN, and on OXY immunoreactivity of the posterior pituitary gland; all effects were maintained in sham-operated rats. These results support the hypothesis that noradrenergic NST-PVN projections are involved in the activation of the hypothalamic OXY system, which mediates OEA's prosatiety action. |
| Databáze: | OpenAIRE |
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