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

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

Research output: Contribution to journalArticlepeer-review


Lysophosphatidic acid receptor (LPA1) 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 LPA1 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 LPA1 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 LPA1 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 LPA1 receptor to initiate neuropathic pain.

Original languageEnglish (US)
Pages (from-to)296-298
Number of pages3
Issue number2
StatePublished - Mar 18 2008
Externally publishedYes


  • LPA
  • LPA receptor
  • LPC
  • autotaxin
  • biosynthesis
  • neuropathic pain

ASJC Scopus subject areas

  • General Neuroscience


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