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Transient acidosis induces delayed neurotoxicity in cultured hippocampal slices.

机译:短暂性酸中毒在培养的海马切片中诱导延迟的神经毒性。

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摘要

It remains unknown if tissue acidosis contributes to neuronal loss during cerebral ischemia. We report that brief intracellular acidification (pH 6.62) results in delayed neuronal loss in cultured hippocampal slices. Cell loss was located primarily in stratum pyramidale and the hilus suggesting that neurons were preferentially damaged. Removal of molecular oxygen greatly attenuated cell loss suggesting that generation of reactive oxygen species may underlie acidosis-induced toxicity. These data suggest that acidosis and incomplete anoxia contributes to the delayed neuronal loss in the ischemic penumbra.
机译:组织酸中毒是否会导致脑缺血期间神经元的丢失仍然未知。我们报告,短暂的细胞内酸化(pH 6.62)导致培养的海马切片中延迟的神经元丢失。细胞丢失主要位于锥体细胞层和希尔斯,提示神经元优先受到损害。分子氧的去除大大降低了细胞的损失,表明活性氧的产生可能是酸中毒诱发的毒性的基础。这些数据表明,酸中毒和不完全的缺氧导致缺血性半影​​的神经元延迟丢失。

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