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Loss of spinal substance P pain transmission under the condition of LPA1 receptor-mediated neuropathic pain
http://hdl.handle.net/10069/19214
http://hdl.handle.net/10069/19214c12a719c-88c3-42a0-8925-749fbdcdf585
名前 / ファイル | ライセンス | アクション |
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1744-8069-2-25.pdf (1.7 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2008-08-27 | |||||
タイトル | ||||||
タイトル | Loss of spinal substance P pain transmission under the condition of LPA1 receptor-mediated neuropathic pain | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Inoue, Makoto
× Inoue, Makoto× Yamaguchi, Asuka× Kawakami, Megumi× Chun, Jerold× Ueda, Hiroshi |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 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. | |||||
書誌情報 |
Molecular Pain 巻 2, 号 25, p. 1-5, 発行日 2006-08-16 |
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出版者 | ||||||
出版者 | BioMed Central | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 17448069 | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA12051230 | |||||
PubMed番号 | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | PMID | |||||
関連識別子 | 16914035 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1186/1744-8069-2-25 | |||||
権利 | ||||||
権利情報 | c 2006 Inoue et al; licensee BioMed Central Ltd. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | Molecular Pain 2006, 2:25 |