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Parabrachial Npy1r-Expressing Neurons Drive Pain in a Mouse Model of Parkinson's Disease
Tyler S Nelson1, Heather N Allen1, Dan Wang1
1Department of Pharmacology and Therapeutics, McKnight Brain Institute, and Center for Advanced Pain Therapeutics and Research (CAPToR), College of Medicine, University of Florida, Gainesville, Florida, USA.
Background:
Pain is a common and debilitating non-motor symptom of Parkinson's disease (PD), yet its underlying neural mechanisms remain poorly defined.
Objectives:
The aim was to test whether neuropeptide Y Y1 receptor (Npy1r)-expressing parabrachial neuronsdrive PD-associated pain.
Methods:
In a unilateral 6 hydroxydopamine (6-OHDA) mouse model, pain-related behaviors, neuronal activation, and intrinsic excitability of parabrachial nucleus (PBN) neurons were assessed using behavioral assays, fluorescence in situ hybridization, and ex vivo whole-cell patch-clamp electrophysiology. Cell type-specific chemogenetic inhibition.
Results:
Following 6-OHDA injection, mice developed robust multimodal hypersensitivity accompanied by increased recruitment of Npy1r-expressing PBN neurons. Chemogenetic silencing of Npy1r-expressing PBN neurons abolished PD-associated hypersensitivity, whereas activation induced pain-like behaviors in naïve mice.
Conclusions:
Npy1r-expressing PBNs are a discrete supraspinal population that drives pain in a preclinical model of PD. © 2026 International Parkinson and Movement Disorder Society.
