The freezing of gait (FOG) is a debilitating symptom of Parkinson’s disease (PD), which is resistant to dopamine replacement and deep brain stimulation (DBS) therapies, thus it is a clinical and scientific challenge. Modern DBS devices can record brain activity from chronically implanted electrodes, and animal models can be used to investigate motor network impairments at different biological scales. The combination of these tools posits a plethora of opportunities to identify gait-related biomarkers to improve gait therapy using closed-loop DBS in patients. Towards this goal, my PhD project aims to compare the mechanistic effects of spinal cord stimulation and dopaminergic medication for returning abnormal oscillations in the gait network in rat models of PD. In this preliminary work, we show that PD model rats exhibit a sharp beta peak in the hindlimb motor cortex during spontaneous locomotion, and the power of this peak is reduced when the rats are challenged with apomorphine. Apomorphine shifts the motor state of the PD rats from akinesia to gait. On the other hand, electrical stimulation of the cervical spinal cord segments improves gait kinematics, despite not altering motor state distribution of the animals. These observations indicate that motor cortex beta oscillations can be neuromodulation targets for gait therapy. In the next step, we will build on these findings and compare the network modulating effects of spinal cord during locomotion.