期刊
NEUROCHEMISTRY INTERNATIONAL
卷 54, 期 3-4, 页码 215-221出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2008.11.004
关键词
Lysophosphatidic acid; Botulinum toxin C3; EphrinB1; Neuropathic pain; Dorsal root ganglion; Microarray
资金
- Japan Society for the Promotion of Science (JSPS) [17109015]
- Ministry of Education, Culture, Sports, Science and Technology (MEXT) [17025031, 18023028, 20023022]
- Ministry of Health, Labor and Welfare of Japan
- Grants-in-Aid for Scientific Research [17025031, 20023022, 18023028] Funding Source: KAKEN
Lysophosphatidic acid (LPA) signaling, through LPA(1) receptor and its downstream RhoA, has been reported to initiate nerve injury-induced neuropathic pain. In the present study, we performed gene expression profiling of the dorsal root ganglion (DRG) to identify genes induced by intrathecal injection of LPA in a botulinum toxin C3 (BoNT/C3)-reversible manner. We selected and functionally characterized ephrinB1 from 82 identified genes as a potential gene involved in pain transmission, since ephrinB1 is implicated to modulate N-methyl-D-aspartate (NMDA) receptor functions in spinal pain transmission. The LPA-induced and BoNT/C3-reversible ephrinB1 gene expression was confirmed by quantitative real-time PCR. Furthermore, treatments with an antisense oligodeoxynucleotide for ephrinB1 largely abolished the LPA-induced thermal hyperalgesia and allodynia in response to mechanical or A beta-fiber-mediated electrical stimuli on day 1 after the injection. In addition, intrathecal treatment with a soluble ligand, ephrinB1-Fc, caused similar neuropathic pain-like behaviors in a manner that was reversible by the NMDA receptor antagonist MK-801. These results suggest that ephrinB1 plays a crucial role in LPA-induced neuropathic pain. In addition, the present study may provide a new strategy to identify unique neuropathic pain-related genes. (C) 2008 Elsevier Ltd. All rights reserved.
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