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Significance Treatments for pain symptoms in patients with Parkinson’s disease (PD) show inconsistent efficacy across clinical trials, largely owing to our limited understanding of the mechanisms underlying PD pain. Here, we demonstrate that overactivation of subthalamic nucleus (STN) neurons and their projections is adequate to produce a pain hypersensitivity phenotype, and that such overactivation is essential for the hypersensitivity in pain processing pathways and the maintenance of pain hypersensitivity observed in parkinsonian mice. These results suggest that inhibition of STN neurons may be a potential therapeutic strategy for pain relief in PD. Our finding that individual STN projections differentially regulate mechanical and thermal pain thresholds raises the possibility that individual STN projections may be optimal therapeutic targets for different pain phenotypes.

Reversal of hyperactive subthalamic circuits differentially mitigates pain hypersensitivity phenotypes in parkinsonian mice