Involvement of Nitric Oxide In Simulated Retinal Ischemia

Material type: 博士論文

Author: 神, 大介ほか

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Publication date: 2014-06-01

Material Format: Digital

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Name of awarding university/degree: 秋田大学,博士（医学）

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Note (General)：: Purpose. To examine the involvement of nitric oxide (NO) in the development of ischemic retinal degeneration using glutamate receptor antagonists, inh...

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http://hdl.handle.net/10295/2503

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Material Type: 博士論文
Title: Involvement of Nitric Oxide In Simulated Retinal Ischemia
Author/Editor: 神, 大介
Jin, Daisuke
Author Heading: 神, 大介
Jin, Daisuke
Publication Date: 2014-06-01
Publication Date (W3CDTF): 2014-06-01
Alternative Title: 疑似虚血を誘導した網膜における一酸化窒素の役割の解明
Degree grantor/type: 秋田大学
Date Granted: 2014-03-27
Dissertation Number: 乙第630号
Degree Type: 博士（医学）
Text Language Code: eng
Subject Heading: Retina
simulated ischemia
glutamate receptor antagonist
nitric oxide synthetase inhibitors
nitric oxide donor
Target Audience: 一般
Note (General): Purpose. To examine the involvement of nitric oxide (NO) in the development of ischemic retinal degeneration using glutamate receptor antagonists, inhibitors of nitric oxide syntheses (NOS), and NO donors. Methods. Simulated ischemia was induced in the rat ex vivo retinal preparations by deprivation of oxygen and glucose from the incubation medium. The NMDA receptor antagonist (MK-801) and non-NMDA receptor antagonist (GYKI) were applied to the ischemic retinal preparations in combination with different types of NOS inhibitors. The neuroprotective effects of these agents were evaluated by morphologically and biochemically. In addition, the deteriorating actions of NO donors to the control and ischemic retina were also examined. Results. Simulated ischemia produced severe acute neurodegeneration. This neurodegeneration was prevented by the combination of GYKI and MK-801. However, the NO donor induced severe retinal degeneration under the simulated ischemia, in spite of the co-administration of GYKI and MK-801. A neuronal NOS inhibitor offered substantial protection against neuronal damage combined with GYKI. Administration of NO donors invalidated the neuroprotective effects of MK-801and GYKI against the simulated ischemia. Conclusions. The present study revealed that the NO release after activation of glutamate receptors seems to play an important role in the neuronal cell death induced by ischemia.
Access Restrictions: インターネット公開
Related Material: http://hdl.handle.net/10295/2503
http://hdl.handle.net/10295/2503
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 秋田大学 : 秋田大学学術情報リポジトリ