Ion channels at the nodes of Ranvier (NRs) are believed to play essential roles in intrinsic electrophysiological properties and saltatory conduction of action potentials (AP) at the NRs of myelinated nerves. While we have recently shown that two-pore domain potassium (K2P) channels play a key role at the NRs of Aβ-afferent nerves, K⁺ channels and their functions at the NRs of mammalian motor nerves remain elusive. Here we addressed this issue by using ex vivo preparations of lumbar spinal ventral nerves from both male and female rats and the pressure-patch-clamp recordings at their NRs. We found that depolarizing voltages evoked large noninactivating outward currents at NRs. The outward currents could be partially inhibited by voltage-gated K⁺ channel blockers, largely inhibited by K2P blockers and cooling temperatures. Inhibition of the outward currents by voltage-gated K⁺ channel blockers, K2P blockers, or cooling temperatures significantly altered electrophysiological properties measured at the NRs, including resting membrane potential, input resistance, AP width, AP amplitude, AP threshold, and AP rheobase. Furthermore, K2P blockers and cooling temperatures significantly reduced saltatory conduction velocity and success rates of APs in response to high-frequency stimulation. Voltage-gated K⁺ channel blockers reduced AP success rates at high-frequency stimulation without significantly affecting saltatory conduction velocity. Collectively, both K2P and voltage-gated K⁺ channels play significant roles in intrinsic electrophysiological properties and saltatory conduction at NRs of motor nerve fibers of rats. The effects of cooling temperatures on saltatory conduction are at least partially mediated by K2P channels at the NRs.

SIGNIFICANCE STATEMENT Ion channels localized at the NRs are believed to be key determinants of saltatory conduction on myelinated nerves. However, ion channels and their functions at the NRs have not been fully studied in different types of mammalian myelinated nerves. Here we use the pressure-patch-clamp recordings to show that both K2P and voltage-gated K⁺ channels play significant roles in intrinsic electrophysiological properties and saltatory conduction at NRs of lumbar spinal ventral nerves of rats. Furthermore, cooling temperatures exert effects on saltatory conduction via inhibition of ion channels at the NRs. Our results provide new insights into saltatory conduction on myelinated nerves and may have physiological as well as pathologic implications.

Ranvier (NRs) 节点处的离子通道被认为在有髓神经的 NRs 的内在电生理特性和动作电位 (AP) 的跃动传导中起重要作用。虽然我们最近表明双孔结构域钾 (K2P) 通道在 Aβ 传入神经的 NR 中起着关键作用，但 K ⁺通道及其在哺乳动物运动神经 NR 中的功能仍然难以捉摸。在这里，我们通过使用来自雄性和雌性大鼠的腰椎腹侧神经的离体制剂和它们的 NR 处的压力膜片钳记录来解决这个问题。我们发现去极化电压在 NR 处引起大的非失活外向电流。^{电压门控 K +}可以部分抑制外向电流通道阻滞剂，主要受 K2P 阻滞剂和冷却温度的抑制。^{电压门控 K +}通道阻滞剂、K2P 阻滞剂或冷却温度对外向电流的抑制显着改变了在 NR 处测量的电生理特性，包括静息膜电位、输入电阻、AP 宽度、AP 振幅、AP 阈值和 AP 流变基。此外，K2P 阻滞剂和冷却温度显着降低了跳跃式传导速度和 AP 响应高频刺激的成功率。电压门控 K ⁺通道阻滞剂降低了高频刺激下的 AP 成功率，而不会显着影响跳跃式传导速度。总的来说，K2P 和电压门控 K ⁺通道在大鼠运动神经纤维 NRs 的内在电生理特性和跳跃式传导中起重要作用。冷却温度对跳跃式传导的影响至少部分由 NR 处的 K2P 通道介导。

意义声明位于 NRs 的离子通道被认为是有髓神经跳跃式传导的关键决定因素。然而，在不同类型的哺乳动物有髓神经中，离子通道及其在 NR 的功能尚未得到充分研究。在这里，我们使用压力膜片钳记录显示 K2P 和电压门控 K ⁺通道在大鼠腰脊髓腹神经 NRs 的内在电生理特性和跳跃式传导中起着重要作用。此外，冷却温度通过抑制 NR 处的离子通道对跳跃式传导产生影响。我们的结果为有髓神经的跳跃式传导提供了新的见解，并且可能具有生理学和病理学意义。