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Electroconvulsive shock increases the phosphorylation of amphiphysin II in the rat cerebellum.

机译:电痉挛性休克可增加大鼠小脑中的两性纤维蛋白II的磷酸化。

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摘要

Amphiphysin II (Amph2) is known to undergo rapid dephosphorylation and phosphorylation at nerve terminals. After in vivo electroconvulsive shock (ECS) in the rat cerebellum, we found an electrophoretic mobility retardation of Amph2, which suggested an increased degree of phosphorylation above the non-stimulated level. This shifted signal was observed from 1 min, reached the maximum level at 5 min and extended beyond 2 h after ECS. The shifted band was markedly decreased by the phosphatase treatment. Pretreatment with cyclosporin A augmented the mobility retardation of Amph2 after ECS. Our results indicate that ECS induces the phosphorylation of Amph2 in the rat cerebellum.
机译:已知Amphiphysin II(Amph2)在神经末梢发生快速的去磷酸化和磷酸化。在大鼠小脑中进行体内电惊厥性休克(ECS)后,我们发现Amph2的电泳迁移率降低,这表明磷酸化程度增加到非刺激水平以上。从1分钟开始观察到这种偏移的信号,在5分钟后达到最大水平,并在ECS之后延长了2小时以上。磷酸酶处理使转移的带明显减少。 ECS后用环孢菌素A预处理可增加Amph2的运动迟缓。我们的结果表明,ECS诱导大鼠小脑中Amph2的磷酸化。

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