{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,3]],"date-time":"2025-11-03T04:34:49Z","timestamp":1762144489636,"version":"3.41.2"},"reference-count":24,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2006,1,1]],"date-time":"2006-01-01T00:00:00Z","timestamp":1136073600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mol Pain"],"published-print":{"date-parts":[[2006,1,1]]},"abstract":"<jats:p> 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 LPA<jats:sub>1<\/jats:sub> 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 LPA<jats:sub>1<\/jats:sub>\u2212\/\u2212 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 LPA<jats:sub>1<\/jats:sub> activation following nerve injury. <\/jats:p>","DOI":"10.1186\/1744-8069-2-25","type":"journal-article","created":{"date-parts":[[2006,8,16]],"date-time":"2006-08-16T18:14:44Z","timestamp":1155752084000},"source":"Crossref","is-referenced-by-count":37,"title":["Loss of Spinal Substance P Pain Transmission under the Condition of LPA<sub>I<\/sub> Receptor-Mediated Neuropathic Pain"],"prefix":"10.1177","volume":"2","author":[{"given":"Makoto","family":"Inoue","sequence":"first","affiliation":[{"name":"Division of Molecular Pharmacology and Neuroscience, Nagasaki University Graduate School of Biomedical Sciences, 1\u201314 Bunkyomachi, Nagasaki 852-8521, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Asuka","family":"Yamaguchi","sequence":"additional","affiliation":[{"name":"Division of Molecular Pharmacology and Neuroscience, Nagasaki University Graduate School of Biomedical Sciences, 1\u201314 Bunkyomachi, Nagasaki 852-8521, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Megumi","family":"Kawakami","sequence":"additional","affiliation":[{"name":"Division of Molecular Pharmacology and Neuroscience, Nagasaki University Graduate School of Biomedical Sciences, 1\u201314 Bunkyomachi, Nagasaki 852-8521, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jerold","family":"Chun","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, Helen L. Dorris Child and Adolescent Neuropsychiatric Disorder Institute, The Scripps Research Institute, 10550 N. Torrey Pines Road, La Jolla, CA 92037, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroshi","family":"Ueda","sequence":"additional","affiliation":[{"name":"Division of Molecular Pharmacology and Neuroscience, Nagasaki University Graduate School of Biomedical Sciences, 1\u201314 Bunkyomachi, Nagasaki 852-8521, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2006,1,1]]},"reference":[{"key":"bibr1-1744-8069-2-25","unstructured":"1. Dubner R: Neuronal plasticity in the spinal cord medullary dorsal horn: a possible role in central pain mechanisms. 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