2001 Fiscal Year Final Research Report Summary
Molecular indentification of the pathway for amino acids relased from swollen cell
| Project/Area Number |
12670051
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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 | Okazaki National Research Institutes,Center for Integrative Bioscience |
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Principal Investigator |
HAZAMA Akihiro Okazaki National Research Institutes, Center for Integrative Bioscience, Associate Professor, 統合バイオサイエンスセンター, 助教授 (60218394)
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| Project Period (FY) |
2000 – 2001
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| Keywords | glutamic acid / cell swelling / hyototonic / ischemia / C6 / glia / channek / chioride |
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| Research Abstract |
Glutamic acid released from glial cells has pathophysiological roles in brain under ischemic conditions. The pathways for the glutamic acid release are still unknown. We investigate the characteristics of the glutamic acid release from the hyposmotically swollen glioma cell line (C6). First we established the efficient method for the measurement of glutamic acid using glutamic acid dehydorgenease and the chromogenic substrate for NAD. With this method, we measured the glutamic acid released from C6 cells in the hypotonic solutions. The extracellular concentration of glutamic acid increased from 〜3uM under the isotonic condition to 〜10 uM under the hypotonic condition. The glutamic acid release was less sensitive to the temperature between 16℃ and 36℃, suggesting that glutamic acid might be released via the channel pathway, not via transporters nor exocytosis. Since volume-sensitive Cl channels are candidates for the pathway for glutamic acid release, we tested several reagents, including phloretin and arachidonic acid, reported to block volume-sensitive Cl channels and found that those failed to inhibit glutamic acid release from C6 cells. Gd, the blocker for ATP release from swollen cells, also failed to block glutamic acid release. Taken together, we conclude that glutamic acid is released from C6 cells under hypotonic condition via the channel pathway, which is distinct from Cl channels or the permeation pathway for ATP.
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Research Products
(2 results)
