| Summary: | <p>Abstract</p> <p>Lysophosphatidic acid receptor subtype LPA<sub>1 </sub>is crucial for the initiation of neuropathic pain and underlying changes, such as up-regulation of Ca<sup>2</sup>+ channel α<sub>2</sub>δ-1 subunit in dorsal root ganglia (DRG), up-regulation of PKCγ in the spinal dorsal horn, and demyelination of dorsal root fibers. In the present study, we further examined the involvement of LPA<sub>1 </sub>signaling in the reorganization of Aβ-fiber-mediated spinal transmission, which is presumed to underlie neuropathic allodynia. Following nerve injury, the phosphorylation of extracellular-signal regulated kinase (pERK) by Aβ-fiber stimulation was observed in the superficial layer of spinal dorsal horn, where nociceptive C- or Aδ-fibers are innervated, but not in sham-operated wild-type mice. However, the pERK signals were largely abolished in LPA<sub>1 </sub>receptor knock-out (<it>Lpar1</it><sup>-/-</sup>) mice, further supported by quantitative analyses of pERK-positive cells. These results suggest that LPA<sub>1 </sub>receptor-mediated signaling mechanisms also participate in functional cross-talk between Aβ- and C- or Aδ-fibers.</p>
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