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The bed nucleus is a neuroanatomical substrate for the anorectic effect of corticotropin-releasing factor and for its reversal by nociceptin/orphanin fq

Academic Article
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Overview

authors

  • Ciccocioppo, R.
  • Fedeli, A.
  • Economidou, D.
  • Policani, F.
  • Weiss, Friedbert
  • Massi, M.

publication date

  • October 2003

journal

  • Journal of Neuroscience  Journal

abstract

  • Nociceptin/orphanin FQ (N/OFQ), the endogenous ligand of the opioid N/OFQ receptor (NOP), possesses marked functional anti-stress and anti-corticotropin-releasing factor (CRF) actions. We have shown that intracerebroventricular injection of N/OFQ reverses the hypophagic effect induced by stress or by CRF given intracerebroventricularly. To shed new light on the mechanisms involved in the anti-CRF action of N/OFQ, we investigated the ability of N/OFQ to prevent CRF-induced anorexia after microinjection studies into brain areas of potential interest in the control of feeding behavior and coexpressing NOP and CRF receptors. These areas include the bed nucleus of the stria terminalis (BNST), the central amygdala (CeA), the locus ceruleus (LC), the ventromedial hypothalamus (VMH), the paraventricular nucleus (PVN), and the dorsal raphe (DR). The results demonstrated that the anorectic effect of 0.04 nmol of CRF per rat (200 ng per rat) given intracerebroventricularly is reversed by pretreatment with 0.01-0.21 nmol of N/OFQ per rat (25-500 ng per rat) injected into the BNST but not into the CeA, LC, VMH, PVN, or DR. Microinjection of 0.01-0.02 nmol of CRF per site (50-100 ng per site) into the BNST but not into the CeA or the LC induced marked anorexia in food-deprived rats. Pretreatment with 0.01-0.21 nmol of N/OFQ per site (25-500 ng per site) into the BNST also blocked the anorectic action of 0.02 nmol of CRF per site (100 ng per site) given in the same area. Finally, intra-BNST microinjection of 0.01-0.21 nmol of N/OFQ per site (25-500 ng per site) did not modify food intake in either food-sated or food-deprived rats. These data demonstrate that the BNST is involved in the modulation of CRF-induced anorexia, which is prevented by activation of N/OFQ receptors.

subject areas

  • Amygdala
  • Animals
  • Anorexia
  • Appetite Depressants
  • Corticotropin-Releasing Hormone
  • Drug Administration Routes
  • Eating
  • Locus Coeruleus
  • Male
  • Microinjections
  • Opioid Peptides
  • Paraventricular Hypothalamic Nucleus
  • Raphe Nuclei
  • Rats
  • Rats, Wistar
  • Septal Nuclei
  • Ventromedial Hypothalamic Nucleus
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Research

keywords

  • anorexia
  • bed nucleus of the stria terminalis
  • corticotropin-releasing factor
  • nociceptin
  • orphanin FQ
  • stress
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Identity

PubMed Central ID

  • PMC3035815

International Standard Serial Number (ISSN)

  • 0270-6474

PubMed ID

  • 14561874
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Additional Document Info

start page

  • 9445

end page

  • 9451

volume

  • 23

issue

  • 28

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