Mechanism of ischemic tolerance phenomenon in hippocampal CAI sector of the gerbil

短暂性脑缺血后，海马神经元对随后的缺血耐受被诱导。本研究旨在探讨脑缺血耐受现象与蛋白质合成的关系。首先，用放射自显影技术研究诱导耐受沙土鼠蛋白质合成的恢复。为观察耐受获得的效果，2天后复制大鼠双侧前脑缺血模型，缺血2min，再缺血5min。在本组中，CA1区蛋白质合成的恢复很快。再循环后第1天，蛋白质合成基本恢复正常。另一方面，缺血5min组蛋白质合成受到严重抑制，再也没有恢复到正常水平。本研究揭示了诱导耐受沙土鼠海马神经元蛋白质合成的早期恢复。其次，耐受诱导动物和注射蛋白质合成抑制剂的动物脑蛋白质的电泳谱可能存在差异。这两组人的蛋白质模式没有差异。第三，我们研究了多发性亚致死性脑缺血是否能提高耐受性诱导能力或延长耐受期。在多次暴露于亚致死性2min缺血后1个月，动物未获得对4min致死性缺血的缺血耐受性。为了阐明缺血耐受的机制，还需要进一步的研究。

Following brief cerebral ischemia, tolerance to subsequent ischemia is induced in the hippocampal neurons. The aim of this study was to investigate the relationship between ischemic tolerance phenomenon and protein synthesis. First, recovery of protein synthesis was studied autoradiographically in gerbils with induced tolerance. To observe the effect of tolerance acquisition, double forebrain ischemia, 2-min ischemia followed by 5 min-ischemia, was induced 2 days later. In this group, recovery of protein synthesis in the CAI sector was rapid. At 1 day of recirculation, protein synthesis returned near normal. On the other hand, protein synthesis in the 5-min ischemia group was severely suppressed and never returned to the normal level. The present study revealed an early recovery of protein synthesis in the hippocampal neurons in the gerbil with induced tolerance. Secondly, possible differences in electrophoresis pattern of the brain protein between tolerance-induce animals and animals injected with protein synthesis inhibitor. There was no differences in the pattern of the protein between these two groups. Thirdly, we investigated whether multiple sublethal ishemia can enhance the ability of tolerance induction or prolong the period of tolerance. At 1 month after the multiple exposure to sublethal 2-min ischemia, animals did not acquire ischemic tolerance to 4-min lethal ischemia. To clarify the mechanism of ischemic tolerance, further studies are needed.