Neuropeptide B-deficient mice demonstrate hyperalgesia in response to inflammatory pain

Michele A. Kelly, Carsten T. Beuckmann, S. Clay Williams, Christopher M. Sinton, Toshiyuki Motoike, James A Richardson, Robert E Hammer, Mary G. Garry, Masashi Yanagisawa

Research output: Contribution to journalArticle

45 Scopus citations

Abstract

Neuropeptide B (NPB) and neuropeptide W (NPW) have been recently identified as ligands for the G protein-coupled receptor (GPR) 7 and GPR8. The precise in vivo role of this neuropeptide-receptor pathway has not been fully demonstrated. In this paper, we report that NPB-deficient mice manifest a mild adult-onset obesity, similar to that reported in GPR7-null mice. NPB-deficient mice also exhibit hyperalgesia in response to inflammatory pain. Hyperalgesia was not observed in response to chemical pain, thermal pain, or electrical stimulation. NPB-deficient mice demonstrated intact behavioral responses to pain, and learning from the negative reinforcement of electrical stimulation was unaltered. Baseline anxiety was also unchanged as measured in both the elevated plus maze and time spent immobile in a novel environment. These data support the idea that NPB is a factor in the modulation of responses to inflammatory pain and body weight homeostasis.

Original languageEnglish (US)
Pages (from-to)9942-9947
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume102
Issue number28
DOIs
StatePublished - Jul 12 2005

Keywords

  • Body weight
  • G protein-coupled receptor 7
  • Neuropeptide W
  • Obesity

ASJC Scopus subject areas

  • General

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