匹罗卡平诱导的癫痫持续状态和戊四唑诱导的点火后突触肌动蛋白网络的重排

Yan-Feng Zhang, Shu-lei Li, Tianqing Xiong, Yan-Chao Li
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引用次数: 3

摘要

经匹罗卡品处理的C57BL/6小鼠表现出典型的f -肌动蛋白网络改变,包括CA1-CA3区和脑门区f -肌动蛋白的严重减少。相比之下,f -肌动蛋白网络似乎受戊四氮点燃的影响较小,CA1区和脐区几乎没有明显的改变。海马中f -肌动蛋白的总体标记与两种癫痫模型中报道的树突棘病理观察大体一致。由于重组的f -肌动蛋白网络可以导致突触变化的长期稳定和增强的神经元活动的巩固,f -肌动蛋白网络的改变可能与癫痫动物的异常高兴奋性有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The rearrangement of synaptic actin networks after pilocarpine-induced status epilepticus and pentylenetetrazol-induced kindling
Post status epilepticus (SE) and chemical kindling are two widely used animal models for epileptic studies The pilocarpine-treated C57BL/6 mice exhibited stereotypical alterations of F-actin networks, including a severe reduction of F-actin in area CA1-CA3 and in the hilum. By contrast, F-actin networks seemed less affected by pentylenetetrazol kindling, and almost no remarkable alterations were noted in area CA1 or in the hilum. The overall labeling of F-actin in the hippocampus was generally consistent with the pathological observations on dendritic spines reported in both the epileptic models. Because the reorganized F-actin network can lead to long-term stabilization of synaptic changes and to consolidation of the enhanced neuronal activity, the alterations of F-actin networks may be related to the aberrant hyperexcitability in the epileptic animals.
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