Expression of Glutamate and GABA Receptors in Brain Specimens from Intractable Pediatric Epilepsy.
| Project/Area Number |
11670167
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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 |
Human pathology
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| Research Institution | Dokkyo University School of Medicine |
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Principal Investigator |
YAMANOUCHI Hideo Dokkyo University School of Medicine, PEDIATRICS, Lecturer, 医学部, 講師 (10250226)
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| Co-Investigator(Kenkyū-buntansha) |
EGUCHI Mitsuoki Dokkyo University School of Medicine, PEDIATRICS, Professor, 医学部, 教授 (60020799)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | epilepsy / developmental disturbance / cortical dysplasia / glutamate receptors / NMDA receptors / 脳形成異常 / GABA受容体 |
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| Research Abstract |
To explore the role of glutamate receptors in cortical dysplasia, we examined gene expression of NMDAR1 receptor in surgical specimens from fifteen pediatric patients with intractable epilepsy, which were pathologically diagnosed as cortical dysplasia. Histopathologically, thirteen cases were judged as grade 2 and two cases were as grade 3. In situ hybridization with NMDAR1 non-radioactive antisense riboprobe showed increased signal in large dysplastic neurons, less intensely in the nearly-normal sized neurons in dysplastic cortex, but only faint in neurons in normal appearing cortex. These results suggest that the expression of NMDAR1 receptor gene is enhanced in cortical dysplasia, speculating that excitatory condition may be related with abnormal expression of NMDAR1 receptors in cortical dysplasia.
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Report
(4 results)
Research Products
(10 results)
