| 研究課題/領域番号 |
20K16509
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| 研究種目 |
若手研究
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| 配分区分 | 基金 |
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| 審査区分 |
小区分51030:病態神経科学関連
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| 研究機関 | 沖縄科学技術大学院大学 |
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研究代表者 |
WANG Han・Ying 沖縄科学技術大学院大学, 細胞分子シナプス機能ユニット, ポストドクトラルスカラー (70814333)
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| 研究期間 (年度) |
2020-04-01 – 2022-03-31
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| 研究課題ステータス |
中途終了 (2021年度)
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| 配分額 *注記 |
4,160千円 (直接経費: 3,200千円、間接経費: 960千円)
2022年度: 910千円 (直接経費: 700千円、間接経費: 210千円)
2021年度: 1,690千円 (直接経費: 1,300千円、間接経費: 390千円)
2020年度: 1,560千円 (直接経費: 1,200千円、間接経費: 360千円)
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| キーワード | Anoxia / LTP / Glutamate / NO / Hippocampus / anoxia / aLTP / Nitric oxide / positive feedback loop / memory / ischemia / Nitric Oxide / long-term potentiatino / retrograde modulation / PKG |
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| 研究開始時の研究の概要 |
A transient OGD induces iLTP in the hippocampal CA1 area in slices is modeled for glutamate-induced neuronal damage in brain anoxia. I will clarify whether iLTP is initiated in astrocytes by a Ca2+-calmodulin kinase II dependent NO synthesis, via glial type NMDA receptors.
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| 研究実績の概要 |
A transient anoxia can be mimicked in slices as anoxia-induced long-term potentiation (aLTP) of glutamate release. Although nitric oxide (NO) is responsible for aLTP induction, the site of NO production is unclear as well as the mechanism by which aLTP is expressed and maintained for a long period.
We identified that NO is released from both pyramidal neurons and nearby astrocytes. We also found that elevated NO switches on a positive feedback loop for its regenerative production. Once aLTP is expressed, it occludes activity-dependent LTP, which however can be rescued by blocking the regenerative loop of NO production.
These results offer a therapeutic possibility of rescuing patients from memory deficit after exposure to anoxia.
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