Papers

Peer-reviewed
Dec, 2003

Galectin-1 is involved in the potentiation of neuropathic pain in the dorsal horn

BRAIN RESEARCH
  • H Imbe
  • ,
  • K Okamoto
  • ,
  • T Kadoya
  • ,
  • H Horie
  • ,
  • E Senba

Volume
993
Number
1-2
First page
72
Last page
83
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1016/j.brainres.2003.08.064
Publisher
ELSEVIER SCIENCE BV

Galectin-1 is one of the endogenous-galactoside-binding lectins, suggested to be involved in a variety of functions, such as neurite outgrowth, synaptic connectivity, cell proliferation and apoptosis. This protein is expressed in the dorsal root ganglion (DRG) and the spinal cord in the developing and adult rats, especially intensely in small DRG neurons. In the present study, we examined whether galectin-1 is colocalized with TrkA or c-Ret mRNA in small DRG neurons and the effect of axotomy on the expression of galectin-1 in the spinal cord. About 20% of the DRG neurons showed intense galectin-l-immunoreactivity (IR). Of the intensely galectin-1-IR DRG neurons, 93.9% displayed c-Ret mRNA positive signals. On the other hand, only 6.8% displayed TrkA mRNA positive signals. Galectin-1-IR was increased in the dorsal horn at 1 to 2 weeks after axotomy. Intrathecal administration of anti-recombinant human galectin-1 antibody (anti-rhGAL-1 Ab) partially but significantly attenuated the upregulation of substance P receptor (SPR) in the spinal dorsal horn and the mechanical hypersensitivity induced by the peripheral nerve injury. These data suggest that endogenous galectin-1 may potentiate neuropathic pain after the peripheral nerve injury at least partly by increasing SPR in the dorsal horn. (C) 2003 Elsevier B.V. All rights reserved.

Link information
DOI
https://doi.org/10.1016/j.brainres.2003.08.064
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/14642832
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000187249400008&DestApp=WOS_CPL
ID information
  • DOI : 10.1016/j.brainres.2003.08.064
  • ISSN : 0006-8993
  • Pubmed ID : 14642832
  • Web of Science ID : WOS:000187249400008

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