Molecular and histochemical approaches to investigate changes of NOS expression in ischemic hippocampus
| Project/Area Number |
06671382
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | HAMAMATSU UNIVERSITY SCHOOL OF MEDICINE |
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Principal Investigator |
ENDOH Mitsutoshi HAMAMATSU UNIVERSITY SCHOOL OF MEDICINE MEDICINE PESEARCH ASSORCIATE, 医学部, 助手 (70213600)
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| Co-Investigator(Kenkyū-buntansha) |
UEMURA Kenichi HAMAMATSU UNIVERSITY SCHOOL OF MEDICINE MEDICINE PROFESSOR, 医学部, 教授 (60009561)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1994: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | NOS (Nitric Oxide Synthase) / NADPH diaphorase / cerebral ischemia / gene / cerebral ischemic tolerance / hippocampus / neuron / bFGF (basic Fibroblast Growth Factor) / bFGF(basic Fibroblan Growth Facter) / 遺伝子発現 / 神経細胞死 / NADPrl diaphorase / 一酸化窒素合成酵素 |
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| Research Abstract |
We investigated changes in the expression of NOS (nitric oxide synthase) in the CA 1 pyramidal cells after rat transient forebrain ischemia to elucidate roles of NO (nitric oxide) in delayd neuronal death. By 24 hours after ischemia, NADPH diaphorase activity, reflecting NOS activity, increased, but the expression of neuronal NOS mRNA decreased. By 3 days after ischemia, when delayd neuronal death occurred, NADPH diaphorase activity decreased and the expression of neuronal NOS mRNA disappeared completely. These results suggest that neurons suppress the transcription of neuronal NOS to avoid overproduction of neurotoxic NO.It reminds of the changes of bFGF (basic Fibroblast Growth Factor) ecpression, which is induced in the CA 1 pyramidal cells after ischemia, suggesting that neurons protect themselves by producing bFGF,beneficial neurotrophic factor. More interestingly, bFGF inhibits the neurotoxicity of NO.Then we studied expression of bFGF in the CA 1 pyramidal cells in the ischemic tolerance phenomenon. After 2 minutes of transient forebrain ischemia, which induces ischemic tolerance, bFGF mRNA was induced but not bFGF protein. However, when 10 minutes of transient forebrain was introduced into ischemic brain, both mRNA and protein of bFGF were induced, suggesting that bFGF plays an important role in the neuroprotective effect of ischemic tolerance via inhibiting NO neurotoxicity.
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Report
(3 results)
Research Products
(3 results)
