| Project/Area Number |
10680749
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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 |
Neuroscience in general
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| Research Institution | Jichi Medical School |
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Principal Investigator |
SHIMAZAKI Kuniko Jichi Medical School, Dept of Physiol, Assistant Professor, 医学部, 講師 (40142153)
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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 |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Bcl-2 / apoptosis / gerbil / hippocampus / brain ischermia / adeno-associated virus vecoor / delayed neuronal death / 遅発性神経細胞死 / GLT-1 |
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| Research Abstract |
In the gerbil hippocampus, a short (2mim) sublethal ischemic episode preceding lethal (5mim) ischemia is known to increase tolerance against death in CA1 pyramydal neurons. Intracellular calcium elevation level after exposing to the anoxic-aglycemic medium (95%NィイD22ィエD2/5%C0ィイD22ィエD2, glucose-free) in the rhod-2-loaded hippocampal slices was compared between ischemia-tolerant and non-tolerant gerbils. In non-tolerant gerbils, after switching the normal ringer to anoxic-aglycemic medium an abrupt increase in fluorescence in the Ca1area was seen. Thereafter, a steady increase in intracellular calcium took place with the peak fluorescence intensity at nearly 3 times of the base line. In ischemia-tolerant gerbils, however, the fluorescence increase stayed at significantly lower level than non-tolerant gerbils. Tolerance for ischema was known to be acquired from 1 to 7 days after 2 min ischemia but after 14 days no protective effect was observed. Pretreatment with 1 min ischemia was found to be too brief to induce tolerance. In agreement with these data, magnitude of fluorescence elevation in gerbils at 14 days after 2 min ischemia and at 2 days after 1 min ischemia were almost the same as in the non-tolerant gerbils. Our results suggest that conditioning sublethal ischemia induced to tolerance for ischemic neuronal death which is deeply related to acute increase in intracellular calcium.
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