A study published in Nature (DOI: 10.1038/s41593-024-01569-8) reveals the neural circuitry underlying locomotor asymmetries in mice, specifically the basal ganglia–spinal cord pathway that controls turning gait. The research identifies a key pathway involving the pontine reticular nucleus, oral part (PnO) → Chx10 Gi → spinal cord. This pathway is essential for executing turning movements, and its dysfunction may contribute to turning deficits observed in Parkinson's disease. The study shows that striatal projection neurons initiate turning gaits via a dominant crossed pathway to Chx10 Gi neurons on the contralateral side. Using a combination of calcium imaging, viral tracing, and optogenetic experiments, the researchers demonstrate that the PnO → Chx10 Gi → spinal cord pathway is critical for turning. Modulating this pathway can restore turning competence in mice with striatal damage, suggesting its importance in motor control. The study also highlights the role of Chx10 Gi neurons in encoding turning gait asymmetries. These neurons respond to unilateral activation of dopamine receptor 1 (D1) or dopamine receptor 2 (D2) striatal projection neurons, leading to contraversive or ipsiversive turning. The findings suggest that the PnO-Vglut2 contra neurons act as a critical link between the basal ganglia and Chx10 Gi neurons, enabling the execution of turning movements. The research further demonstrates that the PnO → Chx10 Gi pathway is essential for limb-based turning, while the SNr → SC pathway is more involved in head orientation. The study also shows that unilateral striatal dopamine depletion leads to turning deficits, which can be reversed by stimulating the PnO → Chx10 Gi pathway. These findings provide a detailed understanding of the neural mechanisms underlying turning gait asymmetries and suggest potential therapeutic targets for Parkinson's disease.A study published in Nature (DOI: 10.1038/s41593-024-01569-8) reveals the neural circuitry underlying locomotor asymmetries in mice, specifically the basal ganglia–spinal cord pathway that controls turning gait. The research identifies a key pathway involving the pontine reticular nucleus, oral part (PnO) → Chx10 Gi → spinal cord. This pathway is essential for executing turning movements, and its dysfunction may contribute to turning deficits observed in Parkinson's disease. The study shows that striatal projection neurons initiate turning gaits via a dominant crossed pathway to Chx10 Gi neurons on the contralateral side. Using a combination of calcium imaging, viral tracing, and optogenetic experiments, the researchers demonstrate that the PnO → Chx10 Gi → spinal cord pathway is critical for turning. Modulating this pathway can restore turning competence in mice with striatal damage, suggesting its importance in motor control. The study also highlights the role of Chx10 Gi neurons in encoding turning gait asymmetries. These neurons respond to unilateral activation of dopamine receptor 1 (D1) or dopamine receptor 2 (D2) striatal projection neurons, leading to contraversive or ipsiversive turning. The findings suggest that the PnO-Vglut2 contra neurons act as a critical link between the basal ganglia and Chx10 Gi neurons, enabling the execution of turning movements. The research further demonstrates that the PnO → Chx10 Gi pathway is essential for limb-based turning, while the SNr → SC pathway is more involved in head orientation. The study also shows that unilateral striatal dopamine depletion leads to turning deficits, which can be reversed by stimulating the PnO → Chx10 Gi pathway. These findings provide a detailed understanding of the neural mechanisms underlying turning gait asymmetries and suggest potential therapeutic targets for Parkinson's disease.