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首页> 美国卫生研究院文献>SAGE Choice >Spreading depolarizations in the rat endothelin-1 model of focal cerebellar ischemia
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Spreading depolarizations in the rat endothelin-1 model of focal cerebellar ischemia

机译：大鼠局灶性小脑缺血内皮素-1模型中的去极化

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Focal brain ischemia is best studied in neocortex and striatum. Both show highly vulnerable neurons and high susceptibility to spreading depolarization (SD). Therefore, it has been hypothesized that these two variables generally correlate. However, this hypothesis is contradicted by findings in cerebellar cortex, which contains highly vulnerable neurons to ischemia, the Purkinje cells, but is said to be less susceptible to SD. Here, we found in the rat cerebellar cortex that elevated K induced a long-lasting depolarizing event superimposed with SDs. Cerebellar SDs resembled those in neocortex, but negative direct current (DC) shifts and regional blood flow responses were usually smaller. The K threshold for SD was higher in cerebellum than in previous studies in neocortex. We then topically applied endothelin-1 (ET-1) to the cerebellum, which is assumed to cause SD via vasoconstriction-induced focal ischemia. Although the blood flow decrease was similar to that in previous studies in neocortex, the ET-1 threshold for SD was higher. Quantitative cell counting found that the proportion of necrotic Purkinje cells was significantly higher in ET-1-treated rats than sham controls even if ET-1 had not caused SDs. Our results suggest that ischemic death of Purkinje cells does not require the occurrence of SD.
机译：最好在新皮层和纹状体中研究局灶性脑缺血。两者都显示高度脆弱的神经元和高度敏感的扩散去极化（SD）。因此，已经假设这两个变量通常相关。但是，这一假设与小脑皮层的发现相矛盾，小脑皮层中含有对缺血非常敏感的神经元浦肯野细胞，但据说对SD的敏感性较低。在这里，我们在大鼠小脑皮质中发现，升高的K诱导了与SD叠加的长效去极化事件。小脑SD与新皮质的SD类似，但负直流（DC）移位和局部血流响应通常较小。小脑SD的K阈值高于新皮质以前的研究。然后，我们将内皮素-1（ET-1）局部应用到小脑，假设它通过血管收缩引起的局灶性缺血导致SD。尽管新皮层的血流量减少与先前的研究相似，但SD的ET-1阈值较高。定量细胞计数发现，即使ET-1并未引起SD，在ET-1处理的大鼠中坏死的Purkinje细胞的比例也明显高于假对照组。我们的结果表明浦肯野细胞的缺血性死亡不需要SD的发生。

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