2004 Fiscal Year Final Research Report Summary
To clarify the mechanisms of epileptogenecity in cortical dysgenesis
| Project/Area Number |
14571310
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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 |
Cerebral neurosurgery
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| Research Institution | Kyoto University |
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Principal Investigator |
MIKUNI Nobuhiro KYOTO UNIVERSITY, Faculty of Medicine, Assistant professor, 医学研究科, 助手 (60314217)
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| Co-Investigator(Kenkyū-buntansha) |
AMANO Shigeru KYOTO UNIVERSITY, Faculty of Medicine, Professor, 医学研究科, 教授 (50111886)
IKEDA Akio KYOTO UNIVERSITY, Faculty of Medicine, Lecturer, 医学研究科, 講師 (90212761)
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| Project Period (FY) |
2002 – 2004
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| Keywords | epilepsy / cortical dysgenesis |
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| Research Abstract |
We have studied the mechanisms underlying epileptogenesis in cortical dysplasia by using a rat model and a human specimen. The results have shown that excitatory postsynaptic NMDA receptors played a critical role of epilepsy associated with cortical dysplasia. To clarify the mechanisms of human epilepsy, we examined the total protein levels of both NR1 and calmodulin, as well as their coassembly in the human non- epileptogenic cortical areas compared to those in the epileptogenic cortical areas (ictal EEG seizure onset areas as determined by subdural grid electrode recordings). The coassembly of calmodulin and NMDAR1 was decreased in epileptogenic dysplastic cortex compared with normal appearing non-epileptogenic cortex, while there was no significant difference in the total protein levels of calmodulin or NMDAR1 between the two EEG groups. These results suggest that decreased calmodulin-NMDAR1 coassembly is a cellular mechanism that contributes to hyperexcitability in dysplastic cortical neurons and in focal seizure onsets. Reagarding the brain function, epileptic cortical dysplasia have language or motor function which could be compensated following resection. Furthermore, our results have shown that some of brain tumors were accompanied with epileptic cortical dysplasia.
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