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.
journal_name
Proc Natl Acad Sci U S Aauthors
Kelly MA,Beuckmann CT,Williams SC,Sinton CM,Motoike T,Richardson JA,Hammer RE,Garry MG,Yanagisawa Mdoi
10.1073/pnas.0503795102keywords:
subject
Has Abstractpub_date
2005-07-12 00:00:00pages
9942-7issue
28eissn
0027-8424issn
1091-6490pii
0503795102journal_volume
102pub_type
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