Lysophosphatidic acid precursor levels decrease and an arachidonic acid-containing phosphatidylcholine level increases in the dorsal root ganglion of mice after peripheral nerve injury.

Neurosci Lett

International Mass Imaging Center and Department of Cellular and Molecular Anatomy, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan; Preeminent Medical Photonics Education & Research Center, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka, 431-3192, Japan; Department of Anatomy, The University of Hong Kong, 6/F, William MW Mong Block 21 Sassoon Road, Pokfulam, Hong Kong SAR, China. Electronic address:

Published: April 2019

AI Article Synopsis

  • The study examined lipid changes in the dorsal root ganglion (DRG) after sciatic nerve transection (SNT) using MALDI-IMS.
  • It was found that arachidonic acid-containing phosphatidylcholine (AA-PC) increased significantly, while levels of certain other lipids decreased.
  • These changes are linked to neuropathic pain, suggesting that targeting lysophosphatidic acid (LPA) could be a potential treatment for this condition.

Article Abstract

In the current study, we aimed to analyze the lipid changes in the dorsal root ganglion (DRG) after sciatic nerve transection (SNT) using matrix-assisted laser desorption/ionization imaging mass spectrometry (MALDI-IMS). We found that the arachidonic acid-containing phosphatidylcholine (AA-PC), PC(16:0/20:4) largely increased, while PC(16:0/18:1), PC(18:0/18:1) and phosphatidic acid (PA)(36:2) levels largely decreased in the DRG following nerve injury. Previous studies show that the increase in PC(16:0/20:4) was associated with neuropathic pain and that decrease in PC(16:0/18:1), PC(18:0/18:1), and PA(36:2) were due to producing lysophosphatidic acid (LPA), an initiator for neuropathic pain. These results suggest that the lipid changes in DRG after SNT could be the result of changes for the cause of neuropathic pain. Thus, blocking of LPA could be potential for treatment of neuropathic pain.

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Source
http://dx.doi.org/10.1016/j.neulet.2018.12.035DOI Listing

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