Pathophysiological relationship ofmitochondria to neuronal death during brain ischemia
| Project/Area Number |
22790256
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General pharmacology
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| Research Institution | Kagoshima University |
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Principal Investigator |
KANBE Yuki 鹿児島大学, 大学院・医歯学総合研究科, 助教 (60549913)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2010: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 神経細胞死 / 細胞内情報伝達 / ミトコンドリア / 脳神経疾患 / シグナル伝達 / 脳・神経疾患 |
|---|
| Research Abstract |
Pituitary adenylate cyclase-activating polypeptide (PACAP) increases neurite outgrowth in many kind of neuronal cells, but signaling via its receptor PACAP-specific receptor has not been fully characterized. Because mitochondria also play an important role in neurodevelopment including dendritic branching, axonal guidanceand neurite outgrowth, we examined whether mitochondria contribute to PACAP-mediated neurite outgrowth. Present data suggest that mitochondrial activation plays a key role in PACAP-induced neurite outgrowth via a signaling pathway that includes PAC1R, PKA, andPgc1α.
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Report
(4 results)
Research Products
(34 results)
