| Project/Area Number |
16591146
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Psychiatric science
|
|---|
| Research Institution | University of Miyazaki |
|---|
Principal Investigator |
UEDA Yuto University of Miyazaki, Dept of Psychiatry, Associate Professor, 医学部, 助教授 (70244192)
|
|---|
| 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)
|
|---|
| Project Period (FY) |
2004 – 2005
|
| Project Status |
Completed (Fiscal Year 2005)
|
| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2004: ¥1,700,000 (Direct Cost: ¥1,700,000)
|
|---|
| Keywords | Epilepsy / Glutamate / GABA / Transporter / Knock down / 蛋白発現 / 受容体 |
|---|
| 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.
|
