| Project/Area Number |
09671201
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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 | Fukuoka University |
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Principal Investigator |
KANEOKA Tsuyoshi Fukuoka Univ., Sch.of Medicine, Prof., 医学部, 教授 (50078755)
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| Co-Investigator(Kenkyū-buntansha) |
YUKITAKE Koh Fukuoka Univ., Sch.of Med., Assist.Prof., 医学部, 講師 (70191476)
IWAKI Toru Kyushu Univ., Fac.of Medicine, Prof., 医学部, 教授 (40221098)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | hypoxia-ischemia / neonatal rat brain / neuronal death / glutamate transporter / nitric oxide synthase / mRNA / fos B / 熟ショック蛋白 |
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| Research Abstract |
Seven-day-old rats were exposed to left carotid artery ligation followed by 2 hours of hypoxia (8% oxygen/92% nitrogen). Immunohistochemical studies of glial glutamate transporter(GLT1) and nitric oxide synthase (nNOS) were performed as compared with MAP2 (as a neuronal marker) and GFAP (as a glial marker). At early stage (3 hours) after ischemic injury, GLT1 expression in ischemic core was preserved in a similar to degree of the contralateral side. At 72 hours after ischemic injury, GLT1 immunoreactivity in both hippocampus and thalamus was increased in reactive astrocytes. On the contrary, nNOS immunoreactivity in ishemic side was markedly decreased following neuronal loss. Thus the glial glutamate transporter may play a role as a neuronal protector against hypoxic-ischemia in immature neonatal rat brains.
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