2003 Fiscal Year Final Research Report Summary
Neuropathological analysis on abnormal expression of glutamine transporters in human cerebral epileptic foci
| Project/Area Number |
13680834
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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 | Tokyo Metropolitan Organization for Medical Research |
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Principal Investigator |
ARAI Nobutaka Tokyo Metropolitan Organization for Medical Research, Tokyo Metropolitan Institute for Neuroscience, Department of Clinical Neuropathology, Director, 東京都神経科学総合研究所, 副参事研究員 (10167984)
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| Co-Investigator(Kenkyū-buntansha) |
UMITSU Reiko Tokyo Metropolitan Organization for Medical Research, Tokyo Metropolitan Institute for Neuroscience, Department of Clinical Neuropathology, Researcher (40312293)
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| Project Period (FY) |
2001 – 2003
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| Keywords | Epilepsy / glutamine transporter / glutamine / functional neurosurgery |
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| Research Abstract |
Multiple subpial transection (MST) has been known as one of the excellent neurosurgical procedures for treatment of intractable epilepsy, of which mechanism is based on neurophisiological phenomenon which blocks spreads of epileptic activity without neurological complication, although a little has been clarified concerning changes of molecular constitution in the epileptic brain after MST.
This project focused on such an environmental immunohistochistochemical alteration after MST in order to know suggestive mechanism which evoke epilepsy, using antibodies against glutamine transporters (EAAT-1,-2,3-) and others, including glutamine receptors, glial fibrillary acidic protein, synaptophysin, SNAP-25. As a result, we semi-quantitatively clarified that abnormal expression of glial type-EAATs around MST lesions unexpectedly spreaded beyond GFAP -expression., strongly suggesting that MST produces not only transection of nerve fibers but also molecular changes in the astrocytes near MST lesions, and, secondly that neuro-glial correlation is fundamentally altered in epileptic foci.
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