| Project/Area Number |
22510056
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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 |
Risk sciences of radiation/Chemicals
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| Research Institution | The University of Tokyo |
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Principal Investigator |
YASUDA Takako 東京大学, 大学院・新領域創成科学研究科, 特任研究員 (40450431)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2010: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 神経細胞傷害 / ミクログリア / アポトーシス / メダカ / 放射線 / 放射線傷害 / 発達神経毒性 / 貪食 / p53 / whole-mount in situハイブリダイゼーション |
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| Research Abstract |
The developing central nervous system (CNS) of vertebrate embryos is highly susceptible to various hazardous factors, such as chemical toxicants and ionizing radiation (IR), and the injured neurons in embryonic brain are eliminated by apoptosis. Here, we induced neural injury by IR irradiation in developing brain of medaka embryo for investigating the neuronal damage by light and electron microscopy, and the microglial activity for disposal of damaged neurons by whole-mount in situ hybridization using Apolipoprotein E (ApoE) probe.IR irradiation induced apoptotic neural cells in medaka embryonic brain and the activated microglia continued to express ApoE even after finishing digestion of phagocytosed apoptotic neurons. This microglial activation was induced in the same manner in the absence of p53 functions, although the number of IR-induced apoptotic neurons was remarkably less in p53 deficient embryonic brain. These results strongly suggest that the microglial activation in the developing medaka brain is induced by the presence of apoptotic neurons in the all or none mannerthrough the p53 independent pathway.
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