Role of the neuronal glutamate transporter in neurological disorders
| Project/Area Number | 13680824 |
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | Kyushu University |
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Principal Investigator |
FURUTA Akiko Kyushu University, Graduate School of Medical Sciences, Neuropathology, Instructor, 大学院・医学研究院, 助手 (50229118)
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| Co-Investigator(Kenkyū-buntansha) |
IWAKI Toru Kyushu University, Graduate School of Medical Sciences, Neuropathology, Professor, 大学院・医学研究院, 教授 (40221098)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed(Fiscal Year 2002)
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| Budget Amount *help |
¥3,000,000 (Direct Cost : ¥3,000,000)
Fiscal Year 2002 : ¥800,000 (Direct Cost : ¥800,000)
Fiscal Year 2001 : ¥2,200,000 (Direct Cost : ¥2,200,000)
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| Keywords | glutamate transporter / epilepsy / brain ischemia / EAAC1 / EAAT3 / Golgi complex / neuronal cell death |
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| Research Abstract |
Glutamate transporters are thought to have a role for preventing the excitotoxicity in the various neurological disorders including epilepsy, hypoxia-ischemia and neurodegenerative diseases. We have demonstrated that neuronal glutamate transporter subtype EAAC1 (EAAT3) exhibited dynamic changes in the hypoxia-ischemia and epilepsy. In the rat neonatal hypoxia-ischemia, expression of EAAC1 increased in the border area (penumbra). Therefore, EAAC1 in neurons may be induced by hypoxic-ischemic insult. In the kainate-induced rat epilepsy, we found that EAAC1 was transiently translocated from the plasma membrane to the Golgi complex in the large pyramidal neurons during the post-ictal state. This phenomenon was also observed dysplastic neurons in focal cortical dysplasia, which is often epileptogenic. The changes of subcellular localization of EAAC1 may be important for neuronal protection because it could prevent excessive uptake of glutamate. Further studies for EAAC1 function are conducted in vitro with GFP-tagged EAAC1 to elucidate the mechanism of internalization.
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Report
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Research Products
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