| Project/Area Number |
13671147
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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 |
Embryonic/Neonatal medicine
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| Research Institution | National Institute of Neuroscience, National Center of Neurology and Psychiatry |
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Principal Investigator |
ITO Masayuki National Institute of Neuroscience, National Center of Neurology and Psychiatry, Department of Mental Retardation and Birth Defect Research, Division Head, 神経研究所・疾病研究第2部, 室長 (50243407)
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| Co-Investigator(Kenkyū-buntansha) |
MOTONAGA Kozo National Institute of Neuroscience, National Center of Neurology and Psychiatry, Department of Mental Retardation and Birth Defect Research, Researcher, 神経研究所・疾病研究第2部, 流動研究員
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Neonatal Hypoxic-Ischemic Brain Damage / Apoptosis |
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| Research Abstract |
We studied an apoptosis phenomenon and its role on neonatal hypoxic-ischemic brain damage (HIE). From our results, we revealed apoptosis was an important role on forming perinatal HIE.
The subjects were obtained by the below method. Two-weeks old mice were performed sham-operation and 5-minites ligation of common carotid arteries under ether anesthesia. At one to 14 days after operation, the research materials were removed.
The brain tissue were stained with hematoxyline-eosin, nick end-labeling (TUNEL), immunohistochemistry (IHC) and in situ hybrydization (ISH).
The results showed the number of apoptosis, which were detected by TUNEL, increased to 7 days after operation. And on the concerning of the protein and mRNA expression of c-fos and bcl-2 family, the peak was 3 days after operation.
The furthermore studies are needed to clarify the pathomechanism of neonatal HIE.
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