| Project/Area Number |
18591582
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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 |
Cerebral neurosurgery
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| Research Institution | University of Yamanashi |
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Principal Investigator |
UCHIDA Mikito University of Yamanashi, Hosipital, Assistant Professor (30313795)
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| Co-Investigator(Kenkyū-buntansha) |
KINOUCHI Hiroyuki University of Yamanashi, Department of Research, Interdisciplinary Graduate School of Medicine and Engineering, Professor (30241623)
YOSHIOKA Hideyuki University of Yamanashi, Hosipital, Medical Official (20402076)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,910,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | brain fatty acid bindine nrotein / neurogenesis / ischemic neuronal injury / 虚血性脳障害 |
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| Research Abstract |
Brain fatty acid binding protein (B-FABP) which participates in the metabolism of free fatty acid, is believed to have an important role during cellular growth and differentiation. In this study, we estimated the expression of B-FABP after transient forebrain ischemia, and studied the role of B-FABP in the ischemic neuronal injury and neurogenesis. [Methods] Transient forebrain ischemia was produced by bilateral carotid artery occlusion for 30 minutes. Ischemic neuronal cell death in the hippocampi was evaluated 3 days after ischemia. Expression of B-FABP in the ischemic brain was evaluated by the immunohistochemical staining. Furthermore, the neurogenesis was observed by uptake of the bromodeoxyuridine (BrdU) (50mg/kg) administered intraperitoneally twice a day for 7 days. Subgranullar zone (SGZ) of the dentate gyro was observed using triple immunofluorescence staining with the antibody against BrdU, B-FABP, and cell markers (Nestin, NeuN, GFAP)). [Results] After ischemia, the expression of B-FABP increased in SGZ and glial cells around the injured region. In SGZ, most of the B-FABP positive cells were colocalized with BrdU and Nestin, and some of them were colocalized with GFAP. The severity of ischemic injury was not significantly different between the wild type and B-FABP knockout mouse. BrdU positive cells were significantly increased in SGZ (584.2 / mm^2) in wild type mouse; however, this increase was suppressed in the knockout mouse. [Discussion] B-FABP was expressed in radial glial cells and immature neurons, and an important role of B-FABP in the neurogenesis after ischemia was suggested.
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