Department of Neurobiology, University of Chicago, Chicago, IL, USA.
Department of Biochemistry and Molecular Biology, University of Chicago, Chicago, IL, USA.
J Gen Physiol. 2025 Jan 6;157(1). doi: 10.1085/jgp.202413667. Epub 2024 Nov 27.
Fast inactivation is a key feature of voltage-gated sodium channels and is pivotal for countless physiological functions. Despite the prevalence of the canonical ball-and-chain model, more recent structural results suggest that fast inactivation requires multiple conformational changes beyond the binding of the inactivation particle, the IFM motif. Combining ionic current, gating current, and fluorescent measurements, here we showed that a double mutant at the bottom of the pore domain (CW) removes fast inactivation by interrupting the communication of the IFM motif and the pore. Instead of triggering fast inactivation, the IFM motif binding in CW allows the channel to enter an alternative open state. This alternative open state severely influenced the voltage sensor movements and was not accessible to wild type or other fast inactivation-deficient channels. Our results highlight the multistep nature of the fast inactivation process in mammalian voltage-gated sodium channels and demonstrate that CW modifies the channel behaviors more profoundly than simple removal of fast inactivation.
快速失活是电压门控钠离子通道的一个关键特征,对无数生理功能至关重要。尽管经典的球链模型已经很普遍,但最近的结构研究结果表明,快速失活需要除了失活粒子(IFM 基序)结合之外的多个构象变化。通过结合离子流、门控电流和荧光测量,我们在这里表明,位于孔域底部的双突变体(CW)通过中断 IFM 基序和孔之间的通讯来去除快速失活。IFM 基序结合 CW 并没有引发快速失活,而是允许通道进入替代的开放状态。这种替代的开放状态严重影响了电压传感器的运动,而野生型或其他快速失活缺陷通道则无法进入这种状态。我们的结果强调了哺乳动物电压门控钠离子通道中快速失活过程的多步骤性质,并表明 CW 对通道行为的改变比简单地去除快速失活更为深刻。