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Phosphorylation of TRPV1 by neurokinin-1 receptor agonist exaggerates the capsaicin-mediated substance P release from cultured rat dorsal root ganglion neurons

https://hiroshima.repo.nii.ac.jp/records/2007773
https://hiroshima.repo.nii.ac.jp/records/2007773
88c0fed8-3b7c-4062-bc3d-6b1d9bb8ec3e
名前 / ファイル ライセンス アクション
Neuropharmacology_55_1405.pdf Neuropharmacology_55_1405.pdf (225.4 KB)
Item type デフォルトアイテムタイプ_(フル)(1)
公開日 2023-03-18
タイトル
タイトル Phosphorylation of TRPV1 by neurokinin-1 receptor agonist exaggerates the capsaicin-mediated substance P release from cultured rat dorsal root ganglion neurons
言語 en
作成者 Tang, He-Bin

× Tang, He-Bin

en Tang, He-Bin

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Li, Yu-Sang

× Li, Yu-Sang

en Li, Yu-Sang

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Miyano, Kanako

× Miyano, Kanako

en Miyano, Kanako

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Nakata, Yoshihiro

× Nakata, Yoshihiro

en Nakata, Yoshihiro

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アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
権利情報
権利情報 Copyright (c) 2009 Elsevier B.V.
主題
主題Scheme Other
主題 Dorsal root ganglion neuron
主題
主題Scheme Other
主題 Neurokinin-1 receptor
主題
主題Scheme Other
主題 Phosphorylation of transient receptor potential vanilloid receptor subtype 1
主題
主題Scheme Other
主題 Substance P release
主題
主題Scheme NDC
主題 490
内容記述
内容記述 The present study was conducted to determine whether the activation of neurokinin-1 receptor (NK-1R) by its agonist (GR73632) enhances the capsaicin-evoked substance P (SP) release using a radioimmunoassay. A pre-exposure to GR73632 enhanced the capsaicin-evoked SP release in a time- and dose-dependent manner. The augmentation of capsaicin-evoked SP release by GR73632 was completely inhibited by pharmacological blockade of NK-1R or transient receptor potential vanilloid receptor subtype 1 (TRPV1), and was partially attenuated by the inhibition of either protein kinase C (PKC), cyclooxygenase (COX) or phospholipase C (PLC), p38 or p42/44 mitogen-activated protein (MAP) kinase, but not protein kinase A. This augmentation of SP release was further increased by inhibition of c-Jun NH2-terminal kinase. A short-term (10 min) exposure to GR73632 resulted in an increase in the TRPV1 phosphorylation. The increase in the TRPV1 phosphorylated forms induced by a 60-min exposure to GR73632 was completely abolished by the inhibition of either PKC, COX or PLC, p38 or p42/44 MAP kinases. Immunocytochemistry study demonstrated that the NK-1R and TRPV1 were mainly co-expressed in the small-sized neurons. These findings suggest that the activation of NK-1R by its agonist, by sensitizing the TRPV1 through the PKC phosphorylation of TRPV1, may play a role in the enhancement of the capsaicin-evoked SP release from cultured rat DRG neurons.
言語 en
出版者
出版者 Pergamon-Elsevier Science Ltd.
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
出版タイプ
出版タイプ AO
出版タイプResource http://purl.org/coar/version/c_b1a7d7d4d402bcce
関連情報
識別子タイプ DOI
関連識別子 10.1016/j.neuropharm.2008.08.037
関連情報
識別子タイプ DOI
関連識別子 http://dx.doi.org/10.1016/j.neuropharm.2008.08.037
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 0028-3908
収録物識別子
収録物識別子タイプ NCID
収録物識別子 AA00754812
開始ページ
開始ページ 1405
書誌情報 Neuropharmacology
Neuropharmacology

巻 55, 号 8, p. 1405-1411, 発行日 2008-12
旧ID 25915
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