Ischemic postconditioning prevents presynaptic glutamate release by activating mitoKATP channels.
| Project/Area Number |
25462230
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurosurgery
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| Research Institution | Nara Medical University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | Postconditioning / mitoKATP channel / diazoxide / 5-HD / cerebral ischemia / postconditioning / パッチクランプ法 / 脳虚血 / ischemic postconditining |
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| Outline of Final Research Achievements |
Ischemic postconditioning is a series of brief nonfatal ischemia and reperfusion cycles applied in the early phase of reperfusion of an ischemic organ, which induces tolerance of organ against long-term ischemic injury. We demonstrate the suppression of paradoxical increase of EPSCs after ischemic insult under ischemic postconditioning. Furthermore, Diazoxide, mitoKATP channel opener, produced same preventive effects and 5-HD, mitoKATP channel blocker, abolished these preventive effects on sEPSC frequencies. These results suggested that ischemic postconditioning acted on presynaptic terminals to prevent the paradoxical increase in glutamate release during ischemia through the activation of mito KATP channels.
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Report
(3 results)
Research Products
(5 results)
