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Loss of spinal substance P pain transmission under the condition of LPA1 receptor-mediated neuropathic pain

Academic Article
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Overview

authors

  • Inoue, M.
  • Yamaguchi, A.
  • Kawakami, M.
  • Chun, Jerold
  • Ueda, H.

publication date

  • 2006

journal

  • Molecular Pain  Journal

abstract

  • Among various machineries occurring in the experimental neuropathic pain model, there exists the loss of pain transmission through C-fiber neurons as well as the hypersensitivity through A-fibers. The current study reveals that molecular machineries underlying the latter hypersensitivity are derived from the events through LPA1 receptor and its downstream RhoA-activation following peripheral nerve injury. The loss of C-fiber responses, which are mediated by spinal substance P (SP) pain transmission was observed with the nociceptive flexor responses by intraplantar injection of SP in nerve-injured mice. The immunohistochemistry revealed that SP signal in the dorsal horn was markedly reduced in such mice. All these changes were completely abolished in LPA1-/- mice or by the pretreatment with BoNT/C3, a RhoA inhibitor. In addition, the loss of C-fiber responses and the down-regulation of spinal SP signal induced by single intrathecal LPA injection were also abolished in such treatments. All these results suggest that the loss of pain transmission through polymodal C-fiber neurons is also mediated by the LPA1 activation following nerve injury.

subject areas

  • Animals
  • Botulinum Toxins
  • Immunohistochemistry
  • Injections, Spinal
  • Lysophospholipids
  • Male
  • Mice
  • Mice, Knockout
  • Nerve Fibers, Unmyelinated
  • Neuralgia
  • Peripheral Nervous System
  • Posterior Horn Cells
  • Receptors, Lysophosphatidic Acid
  • Sciatic Nerve
  • Spinal Cord
  • Substance P
  • rhoA GTP-Binding Protein
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Identity

PubMed Central ID

  • PMC1562366

International Standard Serial Number (ISSN)

  • 1744-8069

Digital Object Identifier (DOI)

  • 10.1186/1744-8069-2-25

PubMed ID

  • 16914035
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Additional Document Info

start page

  • 25

volume

  • 2

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