4.4 Article

The anorexigenic effect of cholecystokinin octapeptide in a goldfish model is mediated by the vagal afferent and subsequently through the melanocortin- and corticotropin-releasing hormone-signaling pathways

期刊

PEPTIDES
卷 31, 期 11, 页码 2130-2134

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.peptides.2010.07.019

关键词

Feeding behavior; Sulfated cholecystokinin octapeptide; Vagal afferent; Corticotropin-releasing hormone; Proopiomelanocortin; Anorexigenic action; Goldfish

资金

  1. Japan Society for the Promotion of Science
  2. University of Toyama
  3. Yamazaki Spice Foundation

向作者/读者索取更多资源

We have been extensively investigating the mechanisms by which neuropeptides regulate feeding behavior by using a goldfish (Carassius auratus) model In this species the anorexigenic action of melanocortin peptide is centrally mediated via the corticotropin-releasing hormone (CRH)/CRH receptor neuronal system whereas sulfated cholecystokinin octapeptide (CCK-8s) is Involved in the appetite regulation as a peripheral anorexigenic factor The aim of the present study was to identify the mechanism of the anorexigenic effect of peripherally injected CCK-8s which has not yet been identified in goldfish Co-administration of capsaicin a neurotoxin that destroys primary sensory afferents at 100 nmol/g BW blocked the anorexigenic action of intraperitoneally injected CCK-8s (100 pmol/g BW) whereas the anorexigenic action of intracerebroventricularly injected CCK-8s (5 pmol/g BW) was not blocked by co-administration of capsaicin Pre-treatment with a specific CRH receptor antagonist alpha-helical CRH(9-41) attenuated the anorexigenic action of CCK-8s The expression level of CRH mRNA in the diencephalic tissue of the CCK-8s-injected group was not changed but the level of proopiomelanocortin mRNA was significantly Increased at 1 h after treatment Therefore we have identified for the first time that the reduction of appetite induced by peripherally injected CCK-8s in goldfish appears to be mediated by the vagal afferent and subsequently through the melanocortin- and corticotropin-releasing hormone-signaling pathways (C) 2010 Elsevier Inc All rights reserved

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