| Project/Area Number |
25750207
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Rehabilitation science/Welfare engineering
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
Kikuchi Shin 札幌医科大学, 医学部, 助教 (20404585)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 末梢神経 / ミトコンドリア / 初代培養細胞 / コバルト / 軸索 / 培養神経細胞 / 疑似虚血 / 塩化コバルト / 神経 / 細胞内輸送 / タイムラプスイメージング |
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| Outline of Final Research Achievements |
In this study, we investigated that the effects of cobalt, considered to an inducer of hypoxia-inducible factor-1a (HIF-1a), on the axonal degeneration and mitochondrial dynamics in cultured peripheral nervous axons. Twenty-four hours exposure of cobalt decreased the rate of the motile mitochondria in the axons. Of particular note, the 800μM cobalt density suppressed the axonal mitochondria transport completely. The observation of microstructure with the transmission electron microscope found that high density cobalt destroyed the architecture of axonal mitochondria. In the axons treated with cobalt, the number of axonal swelling was associated with the increase of cobalt concentration. Although the mechanisms of neurotoxicity induced by cobalt are not clear, our results showed that high cobalt concentrations reduced mitochondria transport and induced axonal degeneration.
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