The subthalamic nucleus (STN) holds a strategic position in the basal ganglia circuit, controlling both motor and non-motor functions. Alterations in its neuronal activity have been shown to be involved in the pathophysiology of Parkinson’s disease (PD). In addition to its classical intra-basal ganglia connections, STN neurons also project to several cortical areas. However, the degree of involvement of these subthalamo-cortical projections in motor and non-motor functions, and in the pathophysiology of PD has never been characterized.The aim of this study was to investigate the effects of inhibition of STN glutamatergic neurons and the anatomo-functional role of the subthalamo-cortical pathway involving the M1 cortex, in motor and nociceptive functions in physiological and pathological conditions. We used VGlut2-Cre mice rendered hemiparkinsonian by stereotaxic injection of 6-OHDA into the MFB, and infected at the STN with viral vectors designed for chemogenetics and optogenetics approaches. Behavioral tests were performed to evaluate motor and nociceptive functions and immunohistochemical analysis to assess the lesion and infection of the targets. Our results show that inhibition of STN glutamatergic neurons improved both motor disabilities and mechanical allodynia in hemiparkinsonian mice. Furthermore, specific optogenetic inhibition of the STN-M1 pathway induced the same effects, demonstrating the implication of this pathway in motor and nociceptive disabilities. Electrophysiological data shows that these improvements are associated with changes in the firing activity of STN and M1 neurons. The present study sheds new insight on the PD pathological circuits, highlighting the involvement of the STN-M1 cortical pathway in this disease's pathophysiology.