| Project/Area Number |
17590479
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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 |
Applied pharmacology
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| Research Institution | Fukuoka University |
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Principal Investigator |
MISHIMA Kenichi Fukuoka University, Pharmaceutical Science, Assistant Professor, 薬学部, 助手 (00320309)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIWARA Michihiro Fukuoka University, Pharmaceutical Science, Professor, 薬学部, 教授 (10091331)
IWASAKI Katsunori Fukuoka University, Pharmaceutical Science, Professor, 薬学部, 教授 (10183196)
IKEDA Tomoaki National Cardiovascular Center, Perinatology, Director, 周産期科, 部長 (80202894)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2005: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | neonate / astrocyte / hypoxia-ischemia / corticosterone / learning and memory / 回転行動 / GDNF |
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| Research Abstract |
The present study was designed to determine potential associations between the brain damage induced by hypoxic-ischemic (HI) insult and spatial learning impairment in 8-arm radial maze task. The brain damage was progressed from 2 weeks of recovery and up to 17 weeks of recovery. The magnetic resonance imaging (MRI) changes were similar with the histological changes, and the brain damages were exacerbated in contralateral hemisphere after 57 weeks of recovery following the HI. The spatial learning impairments of 8-arm radial maze starting at 16 weeks of recovery were more severe than those at 7 weeks of recovery, indicating that the spatial learning impairments were progressive and depended on the degree of brain damage. Therefore we called this phenomenon, slowly progressive brain damage (SPBD, Nuerosci Lett, 376,194-199,2005). We examined this mechanism of the SPBD.
1) The time course of astrocyte in thalamus and hypothalamus The GFAP-positive cell progressively increased in the thalamus from 2 weeks and in the hypothalamus from 9 weeks after the HI. The S-100 protein-positive cells were observed in both thalamus and hypothalamus 17 weeks after the HI.
2) The time course of glutamate, NOx and corticosterone in the CSF The glutamate decreased from 2 weeks to 17 weeks after the HI, and the NOx increased from 9 weeks after the HI. The corticosterone tended to decrease in the female rats.
3) Effect of the CSF at 17 weeks after the HI on the CRT task in intact rats.
The CSF was corrected at 17 weeks after the HI and was injected i.c.v. in intact rats. The CSF (20-40 uL) did not affect the CRT task.
These results suggest that the SPBD was related to the activating of astrocyte in the hypothalamus, a decrease in the glutamate and an increase in the NOx.
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