The acquisition of ischemic tolerance in gerbil hippocampus.

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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.