| Project/Area Number |
21591086
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Hiroshima University |
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Principal Investigator |
TANAKA Shigeru 広島大学, 医歯薬学総合研究科, 助教 (20512651)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MATSUMOTO Masayasu 広島大学, 医歯薬学総合研究科, 教授 (20192346)
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| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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|---|
| Keywords | GPCR / G蛋白質共役型受容体 / 脳虚血 / アポトーシス / 低酸素 / cAMP / GPR3 / GPR6 / GPR12 |
|---|
| Research Abstract |
G-protein coupled receptor(GPR) 3, GPR6, and GPR12 are predominantly expressed in the mammalian central nervous system and make up a subfamily of GPRs that constitutively activate adenylate cyclases. In the current study, principal investigator has clarified that expression of GPR3, GPR6, and GPR12 in rat primary neurons facilitates neuronal survival. In addition, GPR3 provides a survival advantage to cerebellar granular neurons under the hypoxic condition. Furthermore, GPR3 knockout mice exhibit a larger infarct area after transient middle cerebral artery occlusion.
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