Cell response of glutamate transporter against rotenone
| Project/Area Number |
26670063
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Environmental and hygienic pharmacy
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| Research Institution | Hiroshima University |
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Principal Investigator |
Kotake Yaichiro 広島大学, 大学院医歯薬保健学研究院(薬), 准教授 (20335649)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | ロテノン / グルタミン酸 / グルタミン酸トランスポーター / 細胞応答 |
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| Outline of Final Research Achievements |
Glutamate causes neurotoxicity by releasing into the extracellular space in excess and activating glutamate receptors. Glutamate transporter EAAT3, an excitatory amino acid transporter, plays an important role in regulating extracellular glutamate concentration. In this study, we investigated the expression of EAAT3 protein induced by rotenone in rat C6 cells. We found that EAAT3 protein was increased by 50 nM rotenone. However, EAAT3 mRNA was not increased by rotenone. These results suggest the possibility that increased expression of EAAT3 protein is caused by the suppression of protein degradation. Combination of rotenone and an EAAT inhibitor dramatically increased extracellular glutamate concentration, before cell death occurs. These findings suggest that increased expression of EAAT3 protein by rotenone is one of the biological defense responses against glutamate neurotoxicity and that the rupture of this system leads to neuronal cell death.
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Report
(3 results)
Research Products
(2 results)
