| Project/Area Number |
22890130
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
General anatomy (including Histology/Embryology)
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| Research Institution | Kyushu University |
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Principal Investigator |
YAMADA Jun 九州大学, 医学研究院, 助教 (70582708)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥3,146,000 (Direct Cost: ¥2,420,000、Indirect Cost: ¥726,000)
Fiscal Year 2011: ¥1,508,000 (Direct Cost: ¥1,160,000、Indirect Cost: ¥348,000)
Fiscal Year 2010: ¥1,638,000 (Direct Cost: ¥1,260,000、Indirect Cost: ¥378,000)
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| Keywords | Kv 1. 3 / Kv1. 5 / カリウムチャネルミ / クログリア / ミノサイクリン / Kv1.3 / Kv1.5 / カリウムチャネル / ミクログリア |
|---|
| Research Abstract |
Immunoreactivity for voltage dependent potassium channels Kv1. 3 and Kv1. 5 was not observed in the mouse hippocampus. On the other hand, Kvl. 3 and Kv1. 5 were most highly expressed in microglia after neuronal injuries. Proliferating microglia were not labeled by Kv1. 3/Kv1. 5, but microglia expressing phosphorylated p38 mitogenactivated protein kinase(p-p38 MAPK), markers for neurotoxicity, were Kv1. 3/Kv1. 5positive. Minocyclinetreatment suppressed expression of Kv1. 3/1. 5 and p-p38 MAPK in microglia. These findings suggest that microglia expressing Kv1. 3/1. 5 and p-p38 MAPK can be a potential therapeutic target against neuronal death.
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