A NEUROMECHANICAL MODEL REVEALS THAT DI3-TO-Γ PATHWAYS PROVIDE SPINDLE FEEDBACK CONTROL OF GAIT KINEMATICS AND PHASE TRANSITIONS

dI3 neurons are glutamatergic premotor neurons located in the deep dorsal horn that integrate sensory information and contribute to locomotor control. In mice, dI3 neuron silencing alters limb kinematics and delays the stance-to-swing phase transition. dI3 neurons exhibit substantial synaptic connections to γ-motoneurons, which control Ia and II spindle sensitivity, positioning dI3s to modulate movement via phase-dependent γ drive. We therefore hypothesize that the effects of dI3 silencing on kinematics and phase transitions arise from γ-mediated control of spindle sensitivity. Because this pathway may also contribute to recovery after spinal cord injury, defining dI3 function has clear translational relevance. To test this hypothesis, we incorporated γ-motoneurons with partial dI3 control to our 2D neuromechanical hindlimb mouse model that couples a spinal locomotor circuitry model to a musculoskeletal model (seven muscles per limb; hip, knee, and ankle joints) via motoneuron output and Ia, Ib, II and cutaneous afferent feedback. γ-motoneurons were modeled to follow α-motoneuron activity. The model was optimized for functional locomotion and closely reproduced kinematics of intact animals. Removing phase-dependent γ activation of ankle extensors resulted in increased dorsiflexion yield after ground acceptance, while reducing hip flexor II spindle sensitivity delayed the stance-to-swing transition and caused hip hyperextension at the end of stance. When combined, these changes mirrored locomotor deficits observed after dI3 silencing. Thus, our modeling results suggest that dI3-to-γ-motoneuron pathways shape spindle feedback, and their disruption can account for kinematic and timing deficits seen after dI3 silencing, underscoring their critical role in adaptive locomotor transitions.