ArticleJournal of neuroscience research2022
Endogenous µ-opioid receptor activity in the lateral and capsular subdivisions of the right central nucleus of the amygdala prevents chronic postoperative pain.
Article in Journal of neuroscience research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Central amygdalar PKCδ neurons mediate fentanyl withdrawal.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Distinctive biochemical properties of the μ-opioid receptor-corticotropin- releasing factor CRFPharmacological research · 2025Article
- Sex differences in the transition to chronic pain.The Journal of clinical investigation · 2025Review
- Article
- Tissue damage-induced axon injury-associated responses in sensory neurons: requirements, prevention, and potential role in persistent post-surgical pain.Frontiers in pain research (Lausanne, Switzerland) · 2025Article
- Neuropeptide Y Y2 Receptors in Sensory Neurons Tonically Suppress Nociception and Itch but Facilitate Postsurgical and Neuropathic Pain Hypersensitivity.Anesthesiology · 2024Article
- Single-neuron projectome-guided analysis reveals the neural circuit mechanism underlying endogenous opioid antinociception.National science review · 2024Article
- Widespread latent hyperactivity of nociceptors outlasts enhanced avoidance behavior following incision injury.bioRxiv : the preprint server for biology · 2024Article
- Contribution of µ Opioid Receptor-expressing Dorsal Horn Interneurons to Neuropathic Pain-like Behavior in Mice.Anesthesiology · 2023Article
- Cell-type specific molecular architecture for mu opioid receptor function in pain and addiction circuits.Neuropharmacology · 2023Review
- Brainstem Modulation of Nociception by Periaqueductal Gray Neurons Expressing the μ-Opioid Receptor in Mice.Anesthesiology · 2023Article
- Human OPRM1 and murine Oprm1 promoter driven viral constructs for genetic access to μ-opioidergic cell types.Nature communications · 2023Article
- Neuropeptide Y-expressing dorsal horn inhibitory interneurons gate spinal pain and itch signalling.eLife · 2023Article
- Pain-related cortico-limbic plasticity and opioid signaling.Neuropharmacology · 2023Review
- Olfactory bulbectomy induces nociceptive alterations associated with gliosis in male rats.IBRO neuroscience reports · 2023Article
- Evidence for Endogenous Opioid Dependence Related to Latent Sensitization in a Rat Model of Chronic Inflammatory Pain.International journal of molecular sciences · 2023Article
- The mechanisms and management of persistent postsurgical pain.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Postsurgical Latent Pain Sensitization Is Driven by Descending Serotonergic Facilitation and Masked by µ-Opioid Receptor Constitutive Activity in the Rostral Ventromedial Medulla.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Developmental mechanisms of CPSP: Clinical observations and translational laboratory evaluations.Canadian journal of pain = Revue canadienne de la douleur · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Tissue injury induces a long-lasting latent sensitization (LS) of spinal nociceptive signaling that is kept in remission by an opposing µ-opioid receptor (MOR) constitutive activity. To test the hypothesis that supraspinal sites become engaged, we induced hindpaw inflammation, waited 3 weeks for mechanical hypersensitivity to resolve, and then injected the opioid receptor inhibitors naltrexone, CTOP or β-funaltrexamine subcutaneously, and/or into the cerebral ventricles. Intracerebroventricular injection of each inhibitor reinstated hypersensitivity and produced somatic signs of withdrawal, indicative of LS and endogenous opioid dependence, respectively. In naïve or sham controls, systemic naloxone (3 mg/kg) produced conditioned place aversion, and systemic naltrexone (3 mg/kg) increased Fos expression in the central nucleus of the amygdala (CeA). In LS animals tested 3 weeks after plantar incision, systemic naltrexone reinstated mechanical hypersensitivity and produced an even greater increase in Fos than in sham controls, particularly in the capsular subdivision of the right CeA. One third of Fos+ profiles co-expressed protein kinase C delta (PKCδ), and 35% of PKCδ neurons co-expressed tdTomato+ in Oprm1
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.