| Project/Area Number |
26861028
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Radiation science
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| Research Institution | National Institute of Radiological Sciences |
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Principal Investigator |
Takuwa Hiroyuki 国立研究開発法人放射線医学総合研究所, 分子イメージング研究センター, 研究員 (40508347)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 慢性低灌流 / 脳卒中 / モデル動物 / 二光子励起レーザー顕微鏡 / 小動物PET / PET / 二光子顕微鏡 / 病態モデルマウス / 脳血流 / 神経機能障害 / 神経細胞脱落 / 脳循環代謝障害 / 11C］flumazenil-PET |
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| Outline of Final Research Achievements |
In this study, we investigated the effects of chronic cerebral hypoperfusion on brain induced by a unilateral common carotid artery occlusion (UCCAO). As the first step of this study, we developed a misery perfusion mouse model using UCCAO and measured autoregulatory vasodilation with two-photon microscopy. The diameter of arterioles and capillaries during the resting state were increased 7 days after UCCAO. After UCCAO, autoregulatory vasodilation of arterioles during normocapnia was negatively correlated with a vasodilation during hypercapnia. The second step of this study was to investigate the chronic effects of cerebral hypoperfusion on neuronal density and functional hyperemia. Neuronal density evaluated 28 days after UCCAO using [11C]flumazenil-PET and histology indicated no neurologic deficit in brain. Functional hyperemia induced by sensory stimulation was assessed using laser-Doppler flowmetry and became worse 28 days after UCCAO.
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