Pain is one of the non-motor symptoms affecting quality of life in Parkinsonian patients. More than 80% of patients suffer from pathological nociceptive hypersensitivity, which may be due to changes in the processing of somatosensory information in basal ganglia, including the subthalamic nucleus (STN). However, the underlying mechanisms are not yet defined.The aim of this study was i) to characterize the responses of STN neurons to peripheral nociceptive stimulation under normal and pathological conditions and ii) to investigate the effects of deep brain stimulation (DBS) of the STN on nociception abnormalities and on the electrical activity of dorsal horn of spinal cord (DHSC) neurons. We used the 6-OHDA rat model of Parkinson's disease (PD).In vivo electrophysiological results have shown that STN neurons are able to detect nociceptive stimuli, encode their intensity and generate windup-like plasticity. However, these phenomena are impaired in dopamine-depleted animals. Indeed, the intensity response is altered in both subthalamic and wide dynamic range spinal neurons. Moreover, STN deep brain stimulation in 6-OHDA rats showed an improvement in mechanical and thermal allodynia compared to sham animals. This effect is mediated by descending brainstem projections leading to normalization of nociceptive integration in DHSC neurons.Our study highlights the centrality of the STN in nociceptive circuits, its interaction with the DHSC and its key involvement in pain sensation in Parkinson's disease. Furthermore, our results provide for the first-time evidence that subthalamic DBS produces analgesia by normalizing the responses of spinal WDR neurons via descending brainstem pathways.