| Project/Area Number |
20K16509
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 51030:Pathophysiologic neuroscience-related
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| Research Institution | Okinawa Institute of Science and Technology Graduate University |
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Principal Investigator |
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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| Project Period (FY) |
2020-04-01 – 2022-03-31
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| Project Status |
Discontinued (Fiscal Year 2021)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2022: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2021: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 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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| Outline of Research at the Start |
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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| Outline of Annual Research Achievements |
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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