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Lysophosphatidylcholine induces neuropathic pain through an action of autotaxin to generate lysophosphatidic acid

Academic Article
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Overview

authors

  • Inoue, M.
  • Xie, W.
  • Matsushita, Y.
  • Chun, Jerold
  • Aoki, J.
  • Ueda, H.

publication date

  • March 2008

journal

  • Neuroscience  Journal

abstract

  • Lysophosphatidic acid receptor (LPA(1)) signaling initiates neuropathic pain and several pathological events in a partial sciatic nerve injury model. Recently, we reported that lysophosphatidic acid (LPA) induces neuropathic pain as well as demyelination and pain-related protein expression changes via LPA(1) receptor signaling. Lysophosphatidylcholine (LPC), also known as lysolecithin, which is hydrolyzed by autotaxin/ATX into LPA, induces similar plastic changes. Here, we attempted to clarify whether ATX and LPA(1) receptor signaling is involved in the LPC-induced neuropathic pain. In wild-type mice, a single intrathecal (i.t.) injection of LPC induced mechanical allodynia and thermal hyperalgesia 2 days after injection; this persisted for 7 days at least. On the other hand, LPC-induced mechanical allodynia and thermal hyperalgesia were completely abolished in mice lacking an LPA(1) receptor gene. Furthermore, the LPC-induced response was also significantly, but partially reduced in heterozygous mutant mice for the ATX gene. These findings suggest that intrathecally-injected LPC is converted to LPA by ATX, and this LPA activates the LPA(1) receptor to initiate neuropathic pain.

subject areas

  • Animals
  • Dose-Response Relationship, Drug
  • Hyperalgesia
  • Lysophosphatidylcholines
  • Lysophospholipids
  • Male
  • Mice
  • Mice, Knockout
  • Multienzyme Complexes
  • Pain Measurement
  • Phosphodiesterase I
  • Phosphoric Diester Hydrolases
  • Pyrophosphatases
  • Reaction Time
  • Receptors, Lysophosphatidic Acid
  • Time Factors
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Research

keywords

  • LPA
  • LPA(1) receptor
  • LPC
  • autotaxin
  • biosynthesis
  • neuropathic pain
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Identity

International Standard Serial Number (ISSN)

  • 0306-4522

Digital Object Identifier (DOI)

  • 10.1016/j.neuroscience.2007.12.041

PubMed ID

  • 18280050
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Additional Document Info

start page

  • 296

end page

  • 298

volume

  • 152

issue

  • 2

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