| Project/Area Number |
15590202
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
HAZAMA Akihiro Fukushima Medical University, Physiology, Professor (60218394)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2003: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | glutamamic acid / aquanorin / glia / Cl-channel / cell swelling / グリオーマ / C6 / CL-チャンネル / グルコース / アミノ酸 / 低浸透圧 |
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| Research Abstract |
We investigate the mechanism of amino acid release from swollen cells induced by the metabolic inhibition. Among the amino acids, we focused on the glutamate because of the importance in the brain anoxia. First we developed the method of detecting glutamate. We used the tetrazolium salts (WST-8, DOJIN) and glutamate dehydrogenase to form the formazan. With this combination, we could measure the concentration of glutamate using the plate reader. We applied the NaN3 to the glioma cell line (C6) and measured the glutamate in the extracellular solution. Extracellular gutamate increased from 3μM in the initial condition to 10μM after 30min. The rise of glutamate could not be suppressed by chloride channel blockers. We also tested HgC12 which could block aquaporin water pathway. By the application of HgC12, we could observed the rise of glutamate even without the metabolic inhibitor. This effect might be explained by the damage of cell membrane by HgC12. During this project, we also found the glutamate released form C6 cells by the application of extracellular glucose. This finding might contribute the investigation of mechanism of tissue damage caused by the high plasma glucose.
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