Analysis of ischemic tolerance in view of neurotrophic factors
Project/Area Number |
08671566
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Cerebral neurosurgery
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Research Institution | University of Tokyo |
Principal Investigator |
KAWAHARA Nobutaka University of Tokyo, Department of Neurosurgery, Assistant Professor, 医学部・附属病院, 助手 (60214673)
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Project Period (FY) |
1996 – 1997
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Project Status |
Completed (Fiscal Year 1997)
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Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1996: ¥1,500,000 (Direct Cost: ¥1,500,000)
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Keywords | cerebral ischemia / neurotrophic factors / spreading depression / ischemic tolerance / BDNF / brain trauma / 脳由来神経栄養因子 |
Research Abstract |
Cortical spreading depression(CSD)is known to induce ischemic tolerance in a rat model of cerebral ischemia. CSD reduces volume of cerebral infarction in a focal ischemia model and attenuates hippocampal neuronal injury in a global ischemia model, when elicited 3 days prior to these insults. Recently, brain-derived neurotrophic factor(BDNF)has been shown to protect neurons against various insults in in vivo model. This study, therefore, investigated relationship between CSD-induced ischemic tolerance and expression of BDNF in rats. CSD was induced by applying KCl solution onto the cortex for 1 hour. For control animals, NaCl solution was used.Northern blot and in situ hybridization study showed that mRNA was dramatically upregulated biphasically in the ipsilateral cortex at 4 hours and 3 days in the CSD animals, but not in the controls. In the hippocampus, no detectable changes were not observed. For analysis of protein level, BDNF ELISA assay was performed. This study revealed that BDNF protein was also increased at 12 hours and 3 days post CSD in the ipsilateral cortex, but not in the hippocampus. The increase of BDNF mNA and protein coincided in time with the induction of ischemic tolerance in the cortex, but not in the hippocampus. These results suggested that increase of BDNF may be involved in the mechanism of endogenous mechanism of ischemic tolerance in the cortex.
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Report
(3 results)
Research Products
(7 results)
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[Publications] Kawahara, N., Belayev, L., Orzi, F., C-olangelo, V., Klatzo, I.: "Maturation Phenomenon in Cerebra-l Ischemia II:Neruonal recovery and pla-sticity,Ito U,Kirino T.Kuroiwa T.KlatzoI(eds).Springer-Verlag,Berlin Heidelberg." Transneuronal induction of toler-ance in cerebral ischemia, 105-111 (1997)
Description
「研究成果報告書概要(和文)」より
Related Report
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[Publications] Kawahara N,Belayv L,Orzi F,Colangelo V,Klatzo I: "Transneuronal induction of tolerance in cerebral ischemia" Maturation Phenomenon in Cerebral Ischemia II : Neruonal recovery and plasticity, Ito U,Kirino T,Kuroiwa T,Klatzo I(eds), Springer-Verlag, Berlin Heidelberg. 105-111 (1997)
Description
「研究成果報告書概要(欧文)」より
Related Report
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[Publications] Kawahara N, Belayev L, Orzi F, Colangelo V, Klatzo I: "Maturation Phenomenon in Cerebral Ischemia II:Neruonal recovery and plasticity,Ito U,Kirino T,Kuroiwa T,Klatzo I(eds).Springer-Verlag,Berlin Heidelberg," Transneuronal induction of tolerance in cerebral ischemia, 105-111 (1997)