2005 Fiscal Year Final Research Report Summary
The functional role of glutamate transporter associated protein (GTRAP3-18) in the epileptogenesis
| Project/Area Number |
16591146
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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 | University of Miyazaki |
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Principal Investigator |
UEDA Yuto University of Miyazaki, Dept of Psychiatry, Associate Professor, 医学部, 助教授 (70244192)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAJIMA Akira University of Miyazaki, Dept of Chemistry, Associate Professor, 医学部, 助教授 (10041857)
DOI Taku University of Miyazaki, Dept of Psychiatry, Research associate, 医学部, 助手 (70274793)
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| Project Period (FY) |
2004 – 2005
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| Keywords | Epilepsy / Glutamate / GABA / Transporter / Knock down |
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| Research Abstract |
As well known the knockdown EAAC-1 by anti-sense induces epileptic convulsion in rats, EAAC-1 is important protein to connect glutamate re-uptake with GABA synthesis, It is important study to elucidate the role of glutamate transporter associated protein 3-18 (GTRAP3-18), because GTRAP3-18 inhibitory regulates the glutamate re-uptake through EAAC-1 into GABAergic neurons. In this study, suppression of GTRAP3-18 protein expression was long-lasted after PTZ kindling, and GTRAP3-18 knockdown by anti-sense method decreases seizure threshold and accelerates the kindling phenomena. Hippocampal glutamate and GABA basal release in GTRAP3-18 knockdown group higher rather than those of sense-injected group suggested knockdown of GTRAP3-18 promotes GABA synthesis.
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