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  1. 0 資料タイプ別
  2. 02 学位論文
  1. 250 大学院医歯学総合研究科(医)
  2. 60 博士学位論文
  3. 10 博士学位論文

Spinal mechanisms underlying potentiation of hindpaw responses observed after transient hindpaw ischemia in mice

http://hdl.handle.net/10191/35558
http://hdl.handle.net/10191/35558
22e3c9d6-812a-4bb2-9d72-045eee5b24b5
名前 / ファイル ライセンス アクション
h27nmk655.pdf 本文 (3.4 MB)
h27nmk655_a.pdf 要旨 (225.8 kB)
Item type 学位論文 / Thesis or Dissertation(1)
公開日 2015-12-14
タイトル
タイトル Spinal mechanisms underlying potentiation of hindpaw responses observed after transient hindpaw ischemia in mice
タイトル
言語 en
タイトル Spinal mechanisms underlying potentiation of hindpaw responses observed after transient hindpaw ischemia in mice
言語
言語 eng
資源タイプ
資源 http://purl.org/coar/resource_type/c_46ec
タイプ thesis
その他のタイトル
その他のタイトル 一過性血流遮断後のしびれのマウスモデルにおける脊髄機序
著者 Watanabe, Tatsunori

× Watanabe, Tatsunori

WEKO 50655

Watanabe, Tatsunori

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著者別名
識別子 50656
識別子Scheme WEKO
姓名 渡部, 達範
抄録
内容記述タイプ Abstract
内容記述 Transient ischemia produces postischemic tingling sensation. Ischemia also produces nerve conduction block that may modulate spinal neural circuits. In the present study, reduced mechanical thresholds for hindpaw-withdrawal reflex were found in mice after transient hindpaw ischemia, which was produced by a high pressure applied around the hindpaw for 30 min. The reduction in the threshold was blocked by spinal application of LY354740, a specific agonist of group II metabotropic glutamate receptors. Neural activities in the spinal cord and the primary somatosensory cortex (S1) were investigated using activity-dependent changes in endogenous fluorescence derived from mitochondrial flavoproteins. Ischemic treatment induced potentiation of the ipsilateral spinal and contralateral S1 responses to hindpaw stimulation. Both types of potentiation were blocked by spinal application of LY354740. The contralateral S1 responses, abolished by lesioning the ipsilateral dorsal column, reappeared after ischemic treatment, indicating that postischemic tingling sensation reflects a sensory modality shift from tactile sensation to nociception in the spinal cord. Changes in neural responses were investigated during ischemic treatment in the contralateral spinal cord and the ipsilateral S1. Potentiation already appeared during ischemic treatment for 30 min. The present findings suggest that the postischemic potentiation shares spinal mechanisms, at least in part, with neuropathic pain.
内容記述
内容記述タイプ Other
内容記述 学位の種類: 博士(医学). 報告番号: 甲第4066号. 学位記番号: 新大院博(医)甲第655号. 学位授与年月日: 平成27年9月24日
内容記述
内容記述タイプ Other
内容記述 Scientific Reports. 2015, 5, 11191.
書誌情報 発行日 2015-09-24
出版者
出版者 新潟大学
DOI
識別子タイプ DOI
関連識別子 info:doi/10.1038/srep11191
著者版フラグ
値 ETD
学位名
学位名 博士(医学)
学位授与機関
学位授与機関名 新潟大学
学位授与年月日
学位授与年月日 2015-09-24
学位授与番号
学位授与番号 13101甲第4066号
学位記番号
内容記述タイプ Other
内容記述 新大院博(医)甲第655号
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