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首页> 外文期刊>Neuron >Ion permeation through a voltage- sensitive gating pore in brain sodium channels having voltage sensor mutations.
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Ion permeation through a voltage- sensitive gating pore in brain sodium channels having voltage sensor mutations.

机译：离子通过具有电压传感器突变的脑钠通道中的电压敏感门控孔渗透。

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Voltage-gated sodium channels activate in response to depolarization, but it is unknown whether the voltage-sensing arginines in their S4 segments pivot across the lipid bilayer as voltage sensor paddles or move through the protein in a gating pore. Here we report that mutation of pairs of arginine gating charges to glutamine induces cation permeation through a gating pore in domain II of the Na(V)1.2a channel. Mutation of R850 and R853 induces a K(+)-selective inward cationic current in the resting state that is blocked by activation. Remarkably, mutation of R853 and R856 causes an outward cationic current with the opposite gating polarity. These results support a model in which the IIS4 gating charges move through a narrow constriction in a gating pore in the sodium channel protein during gating. Paired substitutions of glutamine allow cation movement through the constriction when appropriately positioned by the gating movements of the S4 segment.
机译：电压门控的钠通道响应去极化而激活，但是尚不清楚它们的S4段中的电压感应精氨酸是否随着电压传感器的搅动而横穿脂质双层或在门控孔中穿过蛋白质。在这里，我们报告的精氨酸门控电荷对谷氨酰胺突变诱使阳离子通过Na（V）1.2a通道域II中的门控孔渗透。 R850和R853的突变在静止状态下诱导K（+）选择性向内阳离子电流，该电流被激活阻止。值得注意的是，R853和R856的突变会导致门极极性相反的向外的阳离子电流。这些结果支持了一个模型，其中IIS4门控电荷在门控期间穿过钠通道蛋白的门控孔中狭窄的收缩。当通过S4段的门控运动适当定位时，谷氨酰胺的成对取代可使阳离子通过缩颈移动。

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