Study on the glutamate-induced spinal neurodysfunction.
| Project/Area Number |
23590113
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Keio University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KWAK Shin 東京大学, 医学部付属病院, 准教授 (40160981)
SATO Kaoru 国立医薬品食品研究所, 薬理部, 第一室長 (10311391)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 薬理学 / グルタミン酸 / 情報伝達 / 神経変性疾患 / 興奮毒性 / 神経炎症 / ATP / ミクログリア / パロキセチン / 脊髄 |
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| Research Abstract |
In this study, we investigated mechanisms underlying the dysfunction of glutamate transmission under the inflammatory condition in the spinal cord. We also examined effects of drugs acting on CNS functions. We made in vitro inflammation model using co-culture comprised of astrocytes, microglia and neurons obtained from newborn rat brains. Inflammation decreased glutamate transport by down-regulation of GLAST induced by high-concentration of extracellular glutamate released from activated microglia in this co-culture. Among centrally acting drugs including antidepressants we tested, only paroxetine inhibited the inflammation-induced glutamate release from activated microglia and prevented the decrease in the glutamate transport. We also demonstrated that ATP is one of the factor that made the neural inflammation worse.
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Report
(4 results)
Research Products
(16 results)
