| Project/Area Number |
21500357
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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 |
Neurochemistry/Neuropharmacology
|
|---|
| Research Institution | Soka University |
|---|
Principal Investigator |
|
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| Research Collaborator |
YAMAMOTO Shinichi 創価大学, 大学院・工学研究科, 大学院生
MAEDA Shyuichi 創価大学, 大学院・工学研究科, 大学院生
YOSHINO Yukihisa 創価大学, 大学院・工学研究科, 大学院生
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| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 神経科学 / 脳・神経 / グリア細胞 / 免疫 / ミクログリア / 貪食細胞 / 運動ニューロン死 / CD68 / スーパーオキシドアニオン / TNFα / 貪食 / M-CSF / MHC claa II |
|---|
| Research Abstract |
The ability of microglia to proliferate, produce harmful factors, express phagocytic properties and present antigens has been considered to be switched on/off by intracellular signal transduction mechanism. However, the experiments using rat facial nerve transection model and in vitro model revealed that the abilities of microglia were suggested to be switched on/off by specific factors present in extracellular space, but not by intracellular signal transduction mechanism.
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