| Project/Area Number |
25893178
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Biological pharmacy
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| Research Institution | Nagasaki University |
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Principal Investigator |
SASAKI Keita 長崎大学, 医歯薬学総合研究科(薬学系), 研究員 (80711598)
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| Project Period (FY) |
2013-08-30 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | Cerebral ischemia / 一過性中大脳動脈閉塞 / 線条体 / ドパミン / 神経保護 / 運動障害 / 病態モデル動物 / 加齢 / 薬理学 / 神経生理学 / 生物系薬学 / 創薬 / 行動薬理学 |
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| Outline of Final Research Achievements |
Prothymosin alpha (ProTa) is widely expressed in the brain and plays multiple functions including cell survival. But, it has remained to identify the intrinsic neuroprotective roles of ProTa. Here, I attempted to characterize the physiological, pathological, and neuropharmacological features of mice-specific deficiency of ProTa in the striatum (ProTa cKO mice). ProTa cKO mice exhibited age-dependent deficiency in rotarod behavior. I hypothesized that dopamine D1 receptor agonist SKF38393 would reverse the behavioral abnormality caused by aging in cKO mice. Indeed, the rotarod deficiency was reversed by SKF38393 under single administration. Moreover, ProTa cKO mice have been shown to display increased brain injury and decreased survival ratio following transient middle cerebral artery occlusion. These finding suggest that ProTa has a key role in maintaining motor function, and lack of ProTa is more susceptible to ischemic neuronal damage in the striatum.
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