| Project/Area Number |
07680852
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | Jichi Medical School |
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Principal Investigator |
SHIMAZAKI Kuniko Jichi Medical School, Assistant Professor, 医学部, 講師 (40142153)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1995: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | ischemia / bcl-2 / gerbil / apoptosis / CA1 / tolerance to ischemia / delayd neuronal death / CA1 / 虚血 / 神経細胞死 / 海馬 / bcl-2 / スナネズミ |
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| Research Abstract |
We previously reported that immunoreactivity of Bcl-2 greatly increased in the gerbil hippocampal CA1 sector in parallel with acquisition of tolerance for delayd neuronal death (Shimazaki et al., Neurosci.Res.1994).
This finding suggests that bcl-2 may be an endogenous neuroprotectant. To confirm this hypothesis, we studied time course and location of bcl-2 protein and mRNA using gerbil model of sublethal brief ischemia. We have examined bcl-2 mRNA expression in the gerbil hippocampus by in situ hybridization and ribinuclease protection assay.
The level of bcl-2 mRNA was markedly increased above 2 min of ischemicinsult. The bcl-2 mRNA was increased in CA1 and CA3 regions and the dentate gyrus (DG). Ribinuclease protection assay analysis supported the result showing marked increase in bcl-2 mRNA after both 2 min of ischemia and 5 min of ischemia. On the other hand no increase in the level of bcl-2 mRNA was found in the gerbil treated with 1 min ischemia. The results suggest close correlation between acquisition of tolerance for delayd neuronal death and expression of Bcl-2, which is known to support survival of the neuronal death. While bcl-2 mRNA was expressed in the hippocampal neurons after more than 2 min of ischemia. Bcl-2 protein was stlongly expressed in CA1 neurons that are rescured from cell death.
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