PMID- 24361264
OWN - NLM
STAT- MEDLINE
DCOM- 20141101
LR  - 20141120
IS  - 1872-8111 (Electronic)
IS  - 0168-0102 (Linking)
VI  - 79
DP  - 2014 Feb
TI  - Involvement of Wnt/beta-catenin signaling in the development of neuropathic pain.
PG  - 34-40
LID - S0168-0102(13)00265-4 [pii]
LID - 10.1016/j.neures.2013.12.002 [doi]
AB  - Despite tremendous research effort in the field, our current understanding of the 
      molecular mechanisms underlying neuropathic pain is still incomplete. In the 
      present study, our objective was to elucidate the involvement of the 
      Wnt/beta-catenin signaling pathway in the development of neuropathic pain. We showed 
      that Wnt/beta-catenin signaling is activated in the spinal cord dorsal horn after 
      partial sciatic nerve ligation (PSL). Expression of Wnt3a, a prototypic Wnt 
      ligand that activates the Wnt/beta-catenin pathway, was also upregulated in the 
      dorsal horn. We then tested the effect of intrathecal administration of XAV939, a 
      Wnt/beta-catenin signaling inhibitor, and found that this treatment effectively 
      attenuated the induction of neuropathic pain. Conversely, intrathecal 
      administration of Wnt3a to the lumbar spinal cord of naive animals triggered the 
      development of allodynia. These results suggest a critical involvement of the 
      Wnt/beta-catenin pathway in the development of neuropathic pain. Moreover, we also 
      found that PSL-induced microglial activation was significantly suppressed by 
      intrathecal administration of XAV939 treatment. Because it was revealed that 
      Wnt3a treatment triggered brain-derived neurotrophic factor (BDNF) release from 
      microglial cells in vitro, it is possible that Wnt3a upregulation in the dorsal 
      horn leads to the activation of microglial cells, then triggers BDNF secretion 
      that is responsible for the establishment of neuropathic pain. Further studies 
      will be needed for the comprehensive understanding of the roles of Wnt/beta-catenin 
      signaling in the development of neuropathic pain.
CI  - Copyright (c) 2013 Elsevier Ireland Ltd and the Japan Neuroscience Society. All 
      rights reserved.
FAU - Itokazu, Takahide
AU  - Itokazu T
AD  - Department of Molecular Neuroscience, Graduate School of Medicine, Osaka 
      University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan; Department of Neurology, 
      Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.
FAU - Hayano, Yasufumi
AU  - Hayano Y
AD  - Department of Molecular Neuroscience, Graduate School of Medicine, Osaka 
      University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
FAU - Takahashi, Ryosuke
AU  - Takahashi R
AD  - Department of Neurology, Graduate School of Medicine, Kyoto University, Sakyo-ku, 
      Kyoto 606-8501, Japan.
FAU - Yamashita, Toshihide
AU  - Yamashita T
AD  - Department of Molecular Neuroscience, Graduate School of Medicine, Osaka 
      University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. Electronic address: 
      yamashita@molneu.med.osaka-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131217
PL  - Ireland
TA  - Neurosci Res
JT  - Neuroscience research
JID - 8500749
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (CTNNB1 protein, mouse)
RN  - 0 (Wnt3 Protein)
RN  - 0 (Wnt3 protein, mouse)
RN  - 0 (beta Catenin)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/analysis
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Microglia/metabolism
MH  - Neuralgia/*metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Spinal Cord/*metabolism
MH  - Wnt Signaling Pathway/*physiology
MH  - Wnt3 Protein/metabolism
MH  - beta Catenin/metabolism
OTO - NOTNLM
OT  - Brain-derived neurotrophic factor
OT  - Microglia
OT  - Neuropathic pain
OT  - Wnt signaling
EDAT- 2013/12/24 06:00
MHDA- 2014/11/02 06:00
CRDT- 2013/12/24 06:00
PHST- 2013/10/23 00:00 [received]
PHST- 2013/12/10 00:00 [revised]
PHST- 2013/12/10 00:00 [accepted]
PHST- 2013/12/24 06:00 [entrez]
PHST- 2013/12/24 06:00 [pubmed]
PHST- 2014/11/02 06:00 [medline]
AID - S0168-0102(13)00265-4 [pii]
AID - 10.1016/j.neures.2013.12.002 [doi]
PST - ppublish
SO  - Neurosci Res. 2014 Feb;79:34-40. doi: 10.1016/j.neures.2013.12.002. Epub 2013 Dec 
      17.