Elvira Carina C, Jenkins Paul M
Cellular and Molecular Biology Program, University of Michigan Medical School, Ann Arbor, MI, USA.
Department of Pharmacology, University of Michigan Medical School, Ann Arbor, MI, USA; Department of Psychiatry, University of Michigan Medical School, Ann Arbor, MI, USA.
Curr Opin Cell Biol. 2025 Jul 16;96:102570. doi: 10.1016/j.ceb.2025.102570.
The initiation and propagation of action potentials (APs) depend on the precise localization of voltage-gated sodium (Na) and potassium (K) channels in neurons. In neocortical pyramidal neurons, Na1.2 and Na1.6 are key at the axon initial segment (AIS) and nodes of Ranvier (noR), driving AP initiation and propagation. Na1.2 also supports AP backpropagation in the soma and dendrites. Ankyrin-G anchors these channels at the AIS and noR, while new findings reveal that ankyrin-B scaffolds Na1.2 in dendrites. This review highlights how ankyrins stabilize Na and K channels across neuronal domains, ensuring proper function crucial for excitability, synaptic plasticity, and signaling. Recent findings explore how ankyrins differentially localize Na1.2 and Na1.6, with implications for understanding neurological disorders linked to disrupted channel localization.
动作电位（AP）的起始和传播取决于神经元中电压门控钠（Na）通道和钾（K）通道的精确定位。在新皮质锥体神经元中，Na1.2和Na1.6在轴突起始段（AIS）和郎飞结（noR）发挥关键作用，驱动动作电位的起始和传播。Na1.2还支持动作电位向胞体和树突的逆向传播。锚蛋白-G将这些通道锚定在轴突起始段和郎飞结，而新的研究结果表明，锚蛋白-B在树突中构成Na1.2的支架。这篇综述强调了锚蛋白如何在整个神经元区域稳定钠通道和钾通道，确保对兴奋性、突触可塑性和信号传导至关重要的正常功能。最近的研究结果探讨了锚蛋白如何使Na1.2和Na1.6定位不同，这对于理解与通道定位紊乱相关的神经系统疾病具有重要意义。
