2015 Fiscal Year Final Research Report
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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| Keywords | Postconditioning / mitoKATP channel / diazoxide / 5-HD / cerebral ischemia |
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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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| Free Research Field |
脳血管障害
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