The central pattern generator (CPG) for locomotion is a set of pacemaker neurons endowed with inherent bursting driven by the persistent sodium current (I_NaP). How they proceed to regulate the locomotor rhythm remained unknown. Here, in neonatal rodents, we identified a persistent potassium current critical in regulating pacemakers and locomotion speed. This current recapitulates features of the M-current (I_M): a subthreshold noninactivating outward current blocked by 10,10-bis(4-pyridinylmethyl)-9(10H)-anthracenone dihydrochloride (XE991) and enhanced by N-(2-chloro-5-pyrimidinyl)-3,4-difluorobenzamide (ICA73). Immunostaining and mutant mice highlight an important role of Kv7.2-containing channels in mediating I_M. Pharmacological modulation of I_M regulates the emergence and the frequency regime of both pacemaker and CPG activities and controls the speed of locomotion. Computational models captured these results and showed how an interplay between I_M and I_NaP endows the locomotor CPG with rhythmogenic properties. Overall, this study provides fundamental insights into how I_M and I_NaP work in tandem to set the speed of locomotion.

用于运动的中央模式发生器（CPG）是起搏器神经元的集合，这些神经元具有由持续钠电流（I _NaP）驱动的内在爆发。他们如何进行调节运动节律仍然未知。在这里，我们在新生啮齿动物中发现了持续存在的钾电流，这对调节起搏器和运动速度至关重要。该电流概括了M电流（I _M）的特征：被10,10-双（4-吡啶基甲基）-9（10H）-蒽醌二盐酸盐（XE991）阻断并被N-（2-氯-5-嘧啶基）-3,4-二氟苯甲酰胺（ICA73）。免疫染色和突变小鼠突出了介导I的Kv7.2通道的重要作用_中号。I _M的药理调节可调节起搏器和CPG活动的出现和频率，并控制运动的速度。计算模型捕获了这些结果，并显示了I _M和I _NaP之间的相互作用如何使运动型CPG具有节律性。总体而言，这项研究提供了基本的认识到如何我_中号和我_的NaP协同工作来设置运动的速度。