Endogenous μ-opioid-Neuropeptide Y Y1 receptor synergy silences chronic postoperative pain in mice.
G-protein-coupled receptor
chronic postsurgical pain
endogenous analgesia
latent sensitization
neuropeptide Y Y1 receptor
spinal cord dorsal horn
synergy
μ-opioid receptor
Journal
PNAS nexus
ISSN: 2752-6542
Titre abrégé: PNAS Nexus
Pays: England
ID NLM: 9918367777906676
Informations de publication
Date de publication:
Aug 2023
Aug 2023
Historique:
received:
20
07
2022
revised:
09
03
2023
accepted:
31
07
2023
medline:
31
8
2023
pubmed:
31
8
2023
entrez:
31
8
2023
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 37649580
doi: 10.1093/pnasnexus/pgad261
pii: pgad261
pmc: PMC10465188
doi:
Types de publication
Journal Article
Langues
eng
Pagination
pgad261Subventions
Organisme : NIDA NIH HHS
ID : R01 DA037621
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS045954
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS062306
Pays : United States
Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of National Academy of Sciences.
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