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

• Material Type: 博士論文
• ISSN: 0272-4340
• Title: Ischemic Postconditioning Reduces NMDA Receptor Currents Through the Opening of the Mitochondrial Permeability Transition Pore and K ATP Channel in Mouse Neurons.
• Volume: 42 4
• Author/Editor: Morisaki, Yudai; Nakagawa, Ichiro; Ogawa, Yoichi; Yokoyama, Shohei; Furuta, Takanori; Saito, Yoshihiko; Nakase, Hiroyuki
• Author Heading: Morisaki, Yudai; Nakagawa, Ichiro; Ogawa, Yoichi; Yokoyama, Shohei; Furuta, Takanori; Saito, Yoshihiko; Nakase, Hiroyuki
• Publication, Distribution, etc.: Springer Nature
• Publication Date: 2020-11-07; 42 4
• Publication Date (W3CDTF): 2020-11-07
• Alternative Title: 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。
• Periodical title: Cellular and molecular neurobiology
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2021-03-15
• Date Granted (W3CDTF): 2021-03-15
• Dissertation Number: 甲第781号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第781号
• Text Language Code: eng
• Subject Heading: Ischemic postconditioning; NMDA receptor; Mitochondrial KATP channel; Mitochondrial permeability transition pore; Ca²⁺
• Target Audience: 一般
• Note (General): 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
• Persistent ID (NDL): info:ndljp/pid/12070980; https://dl.ndl.go.jp/pid/12070980
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 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
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2022-02-06T04:33:19+09:00
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://hdl.handle.net/10564/3905
• Data Provider (Database): 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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