Studies on temperature sensitivity and molecular identity of the acid-sensitive outwardly rectifying anion channel (ASOR) in neurons in relation to the mechanism of hypothermic neuroprotection
| Project/Area Number |
25670112
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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 |
General physiology
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| Research Institution | The Graduate University for Advanced Studies (2014)
National Institute for Physiological Sciences (2013) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NUMATA Kaori (SATO Kaori) 生理学研究所, 細胞器官研究系, 研究員 (60614196)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | アニオンチャネル / 温度感受性 / 酸毒性 / ニューロン / 低体温療法 / 酸毒性死 |
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| Outline of Final Research Achievements |
In the brain, strong acidosis is a common feature of ischemia, seizure, trauma and hyperglycemia, and it contributes to neuronal injury. On the other hand, the acid-sensitive outwardly rectifying anion channel (ASOR) has been found in non-neuronal cell types and to be involved in acidotoxic cell death. In the present study, we found that ASOR is expressed in mouse cortical neurons and involved in acidotoxic neuronal cell death. Also, it was found that the neuronal ASOR exhibits strong sensitiviry to temperature and that acidotoxic neuronal necrosis is largely protected by reduction of temperature to 25℃. Thus, it is suggested that this high temperature sensitivity provides a basis for hypothermic neuroprotection under acidotoxic conditions. Furthermore, we tried to identify the ASOR molecule. Using the gene-silencing technique, a number of the candidates were excluded from the molecular entity of ASOR.
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Report
(3 results)
Research Products
(13 results)
