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首页> 外文期刊>The European Journal of Neuroscience >Myosin II activity is required for structural plasticity at the axon initial segment
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Myosin II activity is required for structural plasticity at the axon initial segment

机译：轴突初始段的结构可塑性需要肌球蛋白II活性

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摘要

In neurons, axons possess a molecularly defined and highly organised proximal region - the axon initial segment (AIS) - that is a key regulator of both electrical excitability and cellular polarity. Despite existing as a large, dense structure with specialised cytoskeletal architecture, the AIS is surprisingly plastic, with sustained alterations in neuronal activity bringing about significant alterations to its position, length or molecular composition. However, although the upstream activity-dependent signalling pathways that lead to such plasticity have begun to be elucidated, the downstream mechanisms that produce structural changes at the AIS are completely unknown. Here, we use dissociated cultures of rat hippocampus to show that two forms of AIS plasticity in dentate granule cells-long-term relocation, and more rapid shortening - are completely blocked by treatment with blebbistatin, a potent and selective myosin II ATPase inhibitor. These data establish a link between myosin II and AIS function, and suggest that myosin II's primary role at the structure may be to effect activity-dependent morphological alterations.
机译：在神经元中，轴突具有分子定义和高度有组织的近端区域 - 轴突初始区段（AIS） - 这是电兴奋性和细胞极性的关键调节器。尽管存在具有专门的细胞骨架架构的大，密集的结构，但AIS令人惊讶的是塑料，并且神经元活动的持续改变具有其位置，长度或分子组合物的显着改变。然而，尽管已经阐明了导致这种可塑性的上游活性依赖的信号传导途径，但是在AIS处产生结构变化的下游机制是完全未知的。在这里，我们使用大鼠海马的解离培养，以表明牙齿颗粒细胞长期迁移中的两种形式的AIS可塑性，并且通过用Blebbistatin，一种有效和选择性肌蛋白II ATPase抑制剂进行完全阻止缩短和更快速的缩短。这些数据建立了肌蛋白II和AIS功能之间的联系，并表明肌素II在结构上的主要作用可能是影响活动依赖性形态改变。

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