| Project/Area Number |
10671406
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Niigata University |
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Principal Investigator |
FUJIWARA Naoshi Niigata University School of Medicine Assistant professor, 医学部, 助教授 (70181419)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Eiichiro Kurume University School of Medicine Lecturer, 医学部, 講師 (80188284)
WATANABE Ippei Niigata University Medical Hospital Assistant, 医学部・附属病院, 助手 (00251819)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | brain slices / potential sensitive dye / membrane potential / propagation of neuronal excitation / transient brain ischemia / ischemic neuronal damages / 大脳皮質 / 海馬 / 膜電位感受性色素 / 神経細胞興奮 / 脳虚血 / スプレディングデプレション |
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| Research Abstract |
1) The propagation of neuronal excitation was optically recorded in gerbil hippocampal and cortical slices which were dyed with a potential sensitive fluorescence dye, RH 414. When the Schaffer collaterals of hippocampal CA1 region were electrically stimulated, the propagation of membrane depolarization extended to both stratum radiatum and stratum oriens. In cortical slices, neuronal excitation evoked by a stimulation onto the layer IV axially propagated to the layer II, and then extended over the same layer.
2) The extent of neuronal depolarization was also observed in gerbil brain slices which were prepared 18-20 hr after 4 min of transient forebrain ischemia. When the Schaffer collaterals were stimulated, the extent of neuronal depolarization spread only within the stratum radiatum and the propagation of neuronal excitation to the stratum pyramidale and stratum oriens was inhibited. Thus, neuronal dysfunction might already occur 18-20 hr after the transient ischemia, although degeneration of pyramidal neurons was not found.
3) The cortical spreading depression which was evoked by high-KィイD1+ィエD1 stimulation did not significantly affect to the extent of neuronal depolarization evoked by electrical stimulation in cortical slices.
4) Gerbils pre-treated with or without 2 min of forebrain ischemia (pre-conditioning) were insulted to 5 min of forebrain ischemia. The propagation of neuronal excitation was improved in hippocampal slices from pre-conditioned gerbils in comparison with those from gerbils without pre-conditioning. Hence, the pre-conditioning may induce the tolerance against functional ischemic neuronal damages.
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