ヤマウチ カヅヨ
YAMAUCHI Kadzuyo
山内 かづ代 所属 医学部 医学科 職種 評議員 |
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論文種別 | 原著 |
言語種別 | 英語 |
査読の有無 | 査読あり |
表題 | Low affinity NGF receptor (p75 neurotrophin receptor) inhibitory antibody reduces pain behavior and CGRP expression in DRG in the mouse sciatic nerve crush model. |
掲載誌名 | 正式名:Journal of orthopaedic research : official publication of the Orthopaedic Research Society 略 称:J Orthop Res ISSNコード:(1554-527X)0736-0266(Linking) |
掲載区分 | 国外 |
巻・号・頁 | 28(3),pp.279-83 |
著者・共著者 | Fukui Yu, Ohtori Seiji, Yamashita Masaomi, Yamauchi Kazuyo, Inoue Gen, Suzuki Munetaka, Orita Sumihisa, Eguchi Yawara, Ochiai Nobuyasu, Kishida Shunji, Takaso Masashi, Wakai Ken, Hayashi Yasushi, Aoki Yasuchika, Takahashi Kazuhisa |
発行年月 | 2010/03 |
概要 | Nerve growth factor (NGF) and its low-affinity receptor, p75 neurotrophin receptor (p75 NTR), are important mediators of pain. To explore further the mechanisms involved, we examined suppression of pain behavior and expression of neuropeptides such as calcitonin gene-related peptide (CGRP) using a p75 NTR inhibitory antibody, in a mouse sciatic nerve crush model. In the nerve-injured model, 150 microg of a p75 NTR inhibitory antibody or 10 microl of saline were applied. The sciatic nerve in the sham-operated group was uninjured. Mechanical allodynia was measured for 2 weeks. CGRP and p75 NTR expression in L5 dorsal root ganglions (DRGs) was examined immunohistochemically. Mechanical allodynia was found in the two nerve injured groups, but not in the sham-operated group (p < 0.05). However, the magnitude of the mechanical allodynia was significantly decreased after application of p75 NTR inhibitory antibody (p < 0.05). CGRP and p75 NTR immunoreactivity in the L5 DRG neurons was upregulated in the injured nerve groups compared with the sham-operated group; however, p75 NTR inhibitory antibody decreased the CGRP and p75 NTR expression (p < 0.01). Application of the p75 NTR inhibitory antibody to the pinched sciatic nerve suppressed CGRP and p75 NTR expression and pain behavior. |
DOI | 10.1002/jor.20986 |
PMID | 19824062 |