Abstract

Tissue injury creates a delicate balance between latent pain sensitization (LS) and compensatory endogenous analgesia. Inhibitory G-protein-coupled receptor (GPCR) interactions that oppose LS, including μ-opioid receptor (MOR) or neuropeptide Y Y1 receptor (Y1R) activity, persist in the spinal cord dorsal horn (DH) for months, even after the resolution of normal pain thresholds. Here, we demonstrate that following recovery from surgical incision, a potent endogenous analgesic synergy between MOR and Y1R activity persists within DH interneurons to reduce the intensity and duration of latent postoperative hypersensitivity and ongoing pain. Failure of such endogenous GPCR signaling to maintain LS in remission may underlie the transition from acute to chronic pain states.

Details

Title
Endogenous μ-opioid—Neuropeptide Y Y1 receptor synergy silences chronic postoperative pain in mice
Author
Nelson, Tyler S 1   VIAFID ORCID Logo  ; Santos, Diogo F S 1   VIAFID ORCID Logo  ; Prasoon, Pranav 1   VIAFID ORCID Logo  ; Gralinski, Margaret 1 ; Allen, Heather N 1 ; Taylor, Bradley K 1 

1  Department of Anesthesiology and Perioperative Medicine, Center for Neuroscience, Pittsburgh Center for Pain Research, Pittsburgh Project to end Opioid Misuse, University of Pittsburgh School of Medicine , 200 Lothrop Street, Pittsburgh, PA 15213 , USA 
Publication year
2023
Publication date
Aug 2023
Publisher
Oxford University Press
e-ISSN
27526542
Source type
Scholarly Journal
Language of publication
English
DOI
https://doi.org/10.1093/pnasnexus/pgad261
ProQuest document ID
3191892659
Copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of National Academy of Sciences. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.