Melatonin-Induced Postconditioning Suppresses NMDA Receptor through Opening of the Mitochondrial Permeability Transition Pore via Melatonin Receptor in Mouse Neurons. 3

• Material Type: 博士論文
• Title: Melatonin-Induced Postconditioning Suppresses NMDA Receptor through Opening of the Mitochondrial Permeability Transition Pore via Melatonin Receptor in Mouse Neurons.
• Volume: 23 3
• Author/Editor: Furuta, Takanori; Nakagawa, Ichiro; Yokoyama, Shohei; Morisaki, Yudai; Saito, Yasuhiko; Nakase, Hiroyuki
• Author Heading: Furuta, Takanori; Nakagawa, Ichiro; Yokoyama, Shohei; Morisaki, Yudai; Saito, Yasuhiko; Nakase, Hiroyuki
• Publication, Distribution, etc.: MDPI
• Publication Date: 2022-04; 23 3
• Publication Date (W3CDTF): 2022-04
• Alternative Title: メラトニンによるポストコンディショニングは、マウス神経細胞においてメラトニン受容体を介したミトコンドリア透過性遷移孔の開口を介してNMDA受容体の働きを抑制する
• Periodical title: International journal of molecular sciences
• Pages: Article No.3822-
• ISSN (Periodical Title): 14220067
• Degree Grantor: 奈良県立医科大学
• Date Granted: 2022-09-28
• Date Granted (W3CDTF): 2022-09-28
• Dissertation Number: 甲第847号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Subject Heading: ischemic postconditioning; melatonin receptor; NMDA receptor; mitochondrial permeability transition pore
• Target Audience: 一般
• Note (General): type:Thesis; Mitochondrial membrane potential regulation through the mitochondrial permeability transition pore (mPTP) is reportedly involved in the ischemic postconditioning (PostC) phenomenon. Melatonin is an endogenous hormone that regulates circadian rhythms. Its neuroprotective effects via mitochondrial melatonin receptors (MTs) have recently attracted attention. However, details of the neuroprotective mechanisms associated with PostC have not been clarified. Using hippocampal CA1 pyramidal cells from C57BL mice, we studied the involvement of MTs and the mPTP in melatonin-induced PostC mechanisms similar to those of ischemic PostC. We measured changes in spontaneous excitatory postsynaptic currents (sEPSCs), intracellular calcium concentration, mitochondrial membrane potential, and N-methyl-D-aspartate receptor (NMDAR) currents after ischemic challenge, using the whole-cell patch-clamp technique. Melatonin significantly suppressed increases in sEPSCs and intracellular calcium concentrations. The NMDAR currents were significantly suppressed by melatonin and the MT agonist, ramelteon. However, this suppressive effect was abolished by the mPTP inhibitor, cyclosporine A, and the MT antagonist, luzindole. Furthermore, both melatonin and ramelteon potentiated depolarization of mitochondrial membrane potentials, and luzindole suppressed depolarization of mitochondrial membrane potentials. This study suggests that melatonin-induced PostC via MTs suppressed the NMDAR that was induced by partial depolarization of mitochondrial membrane potential by opening the mPTP, reducing excessive release of glutamate and inducing neuroprotection against ischemia-reperfusion injury.; 博士（医学）・甲第847号・令和4年9月28日; Copyright: © 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).; identifier:International journal of molecular sciences Vol.23 No.3 Article No.3822 (2022 Apr); identifier:14220067; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/4074; identifier:International journal of molecular sciences, 23(3): Article No.3822
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• Date Accepted (W3CDTF): 2023-01-30T13:49:33+09:00
• Format (IMT): application/pdf
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• Related Material (URI): https://doi.org/10.3390/ijms23073822
• Periodical Title (URI): http://hdl.handle.net/10564/4074
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