Neuropeptide B-deficient mice demonstrate hyperalgesia in response to inflammatory pain.
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.
Howard Hughes Medical Institute and Departments of Molecular Genetics, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA.
Michele A
MA
Kelly
Carsten T
CT
Beuckmann
S Clay
SC
Williams
Christopher M
CM
Sinton
Toshiyuki
T
Motoike
James A
JA
Richardson
Robert E
RE
Hammer
Mary G
MG
Garry
Masashi
M
Yanagisawa
D000704:Analysis of Variance; D000818:Animals; D001835:Body Weight / Q000235:genetics; D005557:Formaldehyde; D006930:Hyperalgesia / Q000209:etiology / Q000235:genetics*; D017403:In Situ Hybridization; D007249:Inflammation / Q000150:complications*; D051379:Mice; D018345:Mice, Knockout; D009479:Neuropeptides / Q000235:genetics*; D010146:Pain / Q000209:etiology / Q000503:physiopathology*
D009479:Neuropeptides; C495188:neuropeptide B; D005557:Formaldehyde