| Project/Area Number |
09671000
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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 |
Psychiatric science
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| Research Institution | Osaka City University |
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Principal Investigator |
MUI Koji Osaka City University Medical School, Lecturer, 医学部, 講師 (20219835)
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| Co-Investigator(Kenkyū-buntansha) |
KATSUMOTO Eiichi Osaka City University Medical School, Research Associate, 医学部, 助手 (90271189)
KIOKA Tetsuro Osaka City University Medical School, Lecturer, 医学部, 講師 (40254396)
YAMAGAMI Sakae Osaka City University Medical School, Professor, 医学部, 名誉教授 (20047004)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | EL mice / Epilepsy / RAP-PCR / Seizure / Epileptogenesis / Elマウス / SEIZURE / EPIIEPTOGENESIS / mRNA |
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| Research Abstract |
In present study we tried to identify the gene appeared on the process of the epileptogenesis in the EL mouse that is a model for human regional related epilepsy by RNA arbitrarily primed PCR method.
We got twenty PCR products existing in loss-up stimulated and seizure experienced EL mouse (EL [s]) brain but not existing in seizure unexperienced EL mouse (EL[ns]) brain at 100 days of age. After second PCR products were subcloned to the pBSK II vector, we determined partial sequence, followed by researched the homology with already known genes. Six clones were unknown genes and three clones were mitochondrial DNAs and two clones were genomic DNAs. Nine clones were unknown of function or have not cleared relating with epilepsy or seizure, although they were already known genes. We tried to analyze fifteen clones by Northen blotting, but only two clones hybridized with mRNA from both El mice brains without significance. Remaining thirteen clones did not hybridize with mRNA from both mice by Northen blotting or RNA protection assay. Using quantitative RT-PCR, twelve clones were not significant different between EL [s] and EL [ns] mice. Only one clone, that was homologous with pipin protein over 98%, was clearly more abundant in EL [s] mice brain that EL [ns]. Since pinin is a cell junction-associated protein with a little understanding about its distribution in brain and relationship with epilepsy or seizure, we are investigating in histochemistory and comparing with both EL mouse brains.
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