| Project/Area Number |
24650198
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurochemistry/Neuropharmacology
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| Research Institution | Kyushu University (2013)
Nara Institute of Science and Technology (2012) |
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Principal Investigator |
NAKASHIMA Kinichi 九州大学, 医学(系)研究科(研究院), 教授 (80302892)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 成体ニューロン新生 / 神経幹細胞 / 自然免疫 / Toll様受容体 |
|---|
| Research Abstract |
It is known that the behavior of adult neural stem cells (aNSC) is strongly influenced by unique microenvironment surrounding aNSCs called niche. Acute epileptic seizures are classically know to be associated with aberrant augmentation of neurogenesis in the dentate gyrus (DG) in the adult hippocampus and migration of newly born neurons to ectopic locations. In this research, we found that TLR9, known as as innate immune receptor, suppress epilepsy-triggered aberrant neurogenesis in the adult mouse DG. Microglia are known to act as inflammatory cells in epileptic conditions. When we inhibited seizure-induced microglial activation in WT mice by minocycline administration, both aberrant augmentation of neurogenesis and ectopic localization of newly generated neurons in the DG were exacerbated. These findings imply that TLR9 signal activation in microglia plays a critical role in the attenuation of epilepsy-triggeres aberrant neurogenesis in the adult mouse DG.
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