Summary
We investigated electrophysiological aspects of ischemic tolerance phenomenon in gerbil hippocampus using extracellular recordings from hippocampal slice preparations. Firstly, the capacity for long-term potentiation triggered by tetanic stimulation, which is a putative synaptic background of memory, was examined in hippocampal slices from gerbils subjected to double ischemia. Capacity for long-term potentiation was transiently inhibited 2 days following double ischemia but then recovered 7 days following double ischemia, suggesting that preconditioning ischemia functionally protected CA1 neurons. Secondly, the latency of anoxic depolarization and postanoxic potentiation of N-methyl-d-aspartate (NMDA) receptor-mediated transmission was examined by subjecting hippocampal slices to in vitro anoxia. Latency of anoxic depolarization was not significantly different between slices from gerbils 2 days after sham operations and those from gerbils 2 days after preconditioning ischemia. Postanoxic potentiation of NMDA receptor-mediated transmission was not observed in slices from gerbils 2 days following preconditioning ischemia, while it was observed in slices from gerbils 2 days following sham operations or 9 days following preconditioning ischemia, suggesting that inhibition of anoxic potentiation of NMDA receptor-mediated transmission may be one of the mechanisms by which induced tolerance protects CA1 neurons.
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© 1997 Springer-Verlag Berlin Heidelberg
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Kawai, K., Nakagomi, T., Kirino, T., Tamura, A., Kawai, N. (1997). Electrophysiological Evaluation of Ischemic Tolerance Phenomenon. In: Ito, U., Kirino, T., Kuroiwa, T., Klatzo, I. (eds) Maturation Phenomenon in Cerebral Ischemia II. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60546-8_11
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DOI: https://doi.org/10.1007/978-3-642-60546-8_11
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