@article{oai:nagasaki-u.repo.nii.ac.jp:00018208,
 author = {Inoue, Makoto and Yamaguchi, Asuka and Kawakami, Megumi and Chun, Jerold and Ueda, Hiroshi},
 issue = {25},
 journal = {Molecular Pain},
 month = {Aug},
 note = {Among various machineries occurring in the experimental neuropathic pain model, there exists the loss of pain transmission through C-fiber neurons as well as the hypersensitivity through A-fibers. The current study reveals that molecular machineries underlying the latter hypersensitivity are derived from the events through LPA1 receptor and its downstream RhoA-activation following peripheral nerve injury. The loss of C-fiber responses, which are mediated by spinal substance P (SP) pain transmission was observed with the nociceptive flexor responses by intraplantar injection of SP in nerve-injured mice. The immunohistochemistry revealed that SP signal in the dorsal horn was markedly reduced in such mice. All these changes were completely abolished in LPA1-/- mice or by the pretreatment with BoNT/C3, a RhoA inhibitor. In addition, the loss of C-fiber responses and the down-regulation of spinal SP signal induced by single intrathecal LPA injection were also abolished in such treatments. All these results suggest that the loss of pain transmission through polymodal C-fiber neurons is also mediated by the LPA1 activation following nerve injury., Molecular Pain 2006, 2:25},
 pages = {1--5},
 title = {Loss of spinal substance P pain transmission under the condition of LPA1 receptor-mediated neuropathic pain},
 volume = {2},
 year = {2006}
}