Involvement of LPA<sub>1 </sub>receptor signaling in the reorganization of spinal input through Abeta-fibers in mice with partial sciatic nerve injury
<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 (...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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SAGE Publishing
2008-10-01
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| Series: | Molecular Pain |
| Online Access: | http://www.molecularpain.com/content/4/1/46 |
| _version_ | 1818788107371151360 |
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| author | Chun Jerold Matsumoto Misaki Xie Weijiao Ueda Hiroshi |
| author_facet | Chun Jerold Matsumoto Misaki Xie Weijiao Ueda Hiroshi |
| author_sort | Chun Jerold |
| collection | DOAJ |
| description | <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> |
| first_indexed | 2024-12-18T14:18:24Z |
| format | Article |
| id | doaj.art-6bfa60f690ff466b8e587fb76ee85bb5 |
| institution | Directory Open Access Journal |
| issn | 1744-8069 |
| language | English |
| last_indexed | 2024-12-18T14:18:24Z |
| publishDate | 2008-10-01 |
| publisher | SAGE Publishing |
| record_format | Article |
| series | Molecular Pain |
| spelling | doaj.art-6bfa60f690ff466b8e587fb76ee85bb52022-12-21T21:04:56ZengSAGE PublishingMolecular Pain1744-80692008-10-01414610.1186/1744-8069-4-46Involvement of LPA<sub>1 </sub>receptor signaling in the reorganization of spinal input through Abeta-fibers in mice with partial sciatic nerve injuryChun JeroldMatsumoto MisakiXie WeijiaoUeda Hiroshi<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>http://www.molecularpain.com/content/4/1/46 |
| spellingShingle | Chun Jerold Matsumoto Misaki Xie Weijiao Ueda Hiroshi Involvement of LPA<sub>1 </sub>receptor signaling in the reorganization of spinal input through Abeta-fibers in mice with partial sciatic nerve injury Molecular Pain |
| title | Involvement of LPA<sub>1 </sub>receptor signaling in the reorganization of spinal input through Abeta-fibers in mice with partial sciatic nerve injury |
| title_full | Involvement of LPA<sub>1 </sub>receptor signaling in the reorganization of spinal input through Abeta-fibers in mice with partial sciatic nerve injury |
| title_fullStr | Involvement of LPA<sub>1 </sub>receptor signaling in the reorganization of spinal input through Abeta-fibers in mice with partial sciatic nerve injury |
| title_full_unstemmed | Involvement of LPA<sub>1 </sub>receptor signaling in the reorganization of spinal input through Abeta-fibers in mice with partial sciatic nerve injury |
| title_short | Involvement of LPA<sub>1 </sub>receptor signaling in the reorganization of spinal input through Abeta-fibers in mice with partial sciatic nerve injury |
| title_sort | involvement of lpa sub 1 sub receptor signaling in the reorganization of spinal input through abeta fibers in mice with partial sciatic nerve injury |
| url | http://www.molecularpain.com/content/4/1/46 |
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