The basal ganglia are essential for executing motor actions. How the basal ganglia engage spinal motor networks has remained elusive. Medullary Chx10 gigantocellular (Gi) neurons are required for turning gait programs, suggesting that turning gaits organized by the basal ganglia are executed via this descending pathway. Performing deep brainstem recordings of Chx10 Gi Ca²⁺ activity in adult mice, we show that striatal projection neurons initiate turning gaits via a dominant crossed pathway to Chx10 Gi neurons on the contralateral side. Using intersectional viral tracing and cell-type-specific modulation, we uncover the principal basal ganglia–spinal cord pathway for locomotor asymmetries in mice: basal ganglia → pontine reticular nucleus, oral part (PnO) → Chx10 Gi → spinal cord. Modulating the restricted PnO → Chx10 Gi pathway restores turning competence upon striatal damage, suggesting that dysfunction of this pathway may contribute to debilitating turning deficits observed in Parkinson’s disease. Our results reveal the stratified circuit architecture underlying a critical motor program.

基底神经节对于执行运动动作至关重要。基底神经节如何参与脊髓运动网络仍然难以捉摸。髓质Chx10巨细胞 (Gi) 神经元是转动步态程序所必需的，这表明基底神经节组织的转动步态是通过这条下行通路执行的。对成年小鼠的Chx10 Gi Ca ²⁺活动进行深部脑干记录，我们发现纹状体投射神经元通过与对侧Chx10 Gi 神经元的主导交叉路径启动转动步态。利用交叉病毒示踪和细胞类型特异性调节，我们揭示了小鼠运动不对称的主要基底神经节-脊髓通路：基底神经节→桥脑网状核，口腔部分（PnO）→  Chx10 Gi→脊髓。调节受限的 PnO→  Chx10 Gi 通路可恢复纹状体损伤时的转动能力，表明该通路的功能障碍可能导致帕金森病中观察到的使转动缺陷衰弱。我们的结果揭示了关键运动程序背后的分层电路架构。