| Project/Area Number |
25670617
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurosurgery
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| Research Institution | Gunma University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | プロトン / 虚血再灌流 / 脳梗塞 / ミクログリア / 神経細胞死 / GPCR / TDAG8 / OGR1 / 中枢神経 |
|---|
| Outline of Final Research Achievements |
It is well known that acidification takes place in the ischemia region. However, how acidic pH regulates neuronal cell functions remains uncharacterized yet. In the present study, we characterized the roles of OGR1 family GPCRs, which have been recently identified as extracellular proton-sensing receptors, in ischemia reperfusion model in vivo and in mouse microglia and cultured N1E115 cells as neuronal cell model in vitro. We found that TDAG8 is functioning as protective for brain damage after the ischemia reperfusion. TDAG8 in microglia might be involved in the protective effects. We also found that acidic pH activates nNOS/cGMP signaling through OGR1 in N1E115 cells. Thus, OGR1 family GPCRs are involved in the regulation of brain functions.
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