Ischemic Postconditioning Reduces NMDA Receptor Currents Through the Opening of the Mitochondrial Permeability Transition Pore and K ATP Channel in Mouse Neurons.

• 資料種別: 博士論文
• ISSN: 0272-4340
• タイトル: Ischemic Postconditioning Reduces NMDA Receptor Currents Through the Opening of the Mitochondrial Permeability Transition Pore and K ATP Channel in Mouse Neurons.
• 巻次・部編番号: 42 4
• 著者・編者: Morisaki, Yudai; Nakagawa, Ichiro; Ogawa, Yoichi; Yokoyama, Shohei; Furuta, Takanori; Saito, Yoshihiko; Nakase, Hiroyuki
• 著者標目: Morisaki, Yudai; Nakagawa, Ichiro; Ogawa, Yoichi; Yokoyama, Shohei; Furuta, Takanori; Saito, Yoshihiko; Nakase, Hiroyuki
• 出版事項: Springer Nature
• 出版年月日等: 2020-11-07; 42 4
• 出版年（W3CDTF）: 2020-11-07
• 並列タイトル等: マウスの神経細胞において、Ischemic postconditioningはmitochondrial permeability transition poreとKATPチャネルの開口を介してNMDA受容体電流を低下させる。
• タイトル（掲載誌）: Cellular and molecular neurobiology
• 授与機関名: 奈良県立医科大学
• 授与年月日: 2021-03-15
• 授与年月日（W3CDTF）: 2021-03-15
• 報告番号: 甲第781号
• 学位: 博士（医学）
• 博論授与番号: 甲第781号
• 本文の言語コード: eng
• 件名標目: Ischemic postconditioning; NMDA receptor; Mitochondrial KATP channel; Mitochondrial permeability transition pore; Ca²⁺
• 対象利用者: 一般
• 一般注記: type:Thesis; Ischemic postconditioning (PostC) is known to reduce cerebral ischemia/reperfusion (I/R) injury; however, whether the opening of mitochondrial ATP-dependent potassium (mito-KATP) channels and mitochondrial permeability transition pore (mPTP) cause the depolarization of the mitochondrial membrane that remains unknown. We examined the involvement of the mito-KATP channel and the mPTP in the PostC mechanism. Ischemic PostC consisted of three cycles of 15 s reperfusion and 15 s re-ischemia, and was started 30 s after the 7.5 min ischemic load. We recorded N-methyl-D-aspartate receptors (NMDAR)-mediated currents and measured cytosolic Ca²⁺ concentrations, and mitochondrial membrane potentials in mouse hippocampal pyramidal neurons. Both ischemic PostC and the application of a mito-KATP channel opener, diazoxide, reduced NMDAR-mediated currents, and suppressed cytosolic Ca2+ elevations during the early reperfusion period. An mPTP blocker, cyclosporine A, abolished the reducing effect of PostC on NMDAR currents. Furthermore, both ischemic PostC and the application of diazoxide potentiated the depolarization of the mitochondrial membrane potential. These results indicate that ischemic PostC suppresses Ca²⁺ influx into the cytoplasm by reducing NMDAR-mediated currents through mPTP opening. The present study suggests that depolarization of the mitochondrial membrane potential by opening of the mito-KATP channel is essential to the mechanism of PostC in neuroprotection against anoxic injury.; 博士（医学）・甲第781号・令和3年3月15日; © Springer Science+Business Media, LLC, part of Springer Nature 2020; This is a post-peer-review, pre-copyedit version of an article published in Cellular and molecular neurobiology. The final authenticated version is available online at: http://dx.doi.org/10.1007/s10571-020-00996-y.; identifier:Cellular and molecular neurobiology Vol.42 No.4 p.1079-1089 (2022 May); identifier:02724340; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/3905; identifier:Cellular and molecular neurobiology, 42(4): 1079-1089
• DOI: info:doi/10.1007/s10571-020-00996-y; https://doi.org/info:doi/10.1007/s10571-020-00996-y
• 国立国会図書館永続的識別子: info:ndljp/pid/12070980; https://dl.ndl.go.jp/pid/12070980
• コレクション（共通）: 障害者向け資料
• コレクション（障害者向け資料：レベル1）: テキストデータ
• コレクション（個別）: 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• 収集根拠: 博士論文（自動収集）
• 受理日（W3CDTF）: 2022-02-06T04:33:19+09:00
• 記録形式（IMT）: application/pdf
• オンライン閲覧公開範囲: 国立国会図書館内限定公開
• デジタル化資料送信: 図書館・個人送信対象外
• 遠隔複写可否（NDL）: 可
• 掲載誌（URI）: http://hdl.handle.net/10564/3905
• 連携機関・データベース: 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

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