ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Shared mechanisms for opioid tolerance and a transition to chronic pain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 91 citations in OpenAlex.
- Review
- Narrative review of the scientific and methodological explanations for 101 mechanisms of opioid tolerance.Pain reports · 2025Article
- Hyperalgesic Priming in the Transition From Acute to Chronic Pain: Focus on Different Models and the Molecular Mechanisms Involved.Journal of pain research · 2025Review
- FLT3 signaling inhibition abrogates opioid tolerance and hyperalgesia while preserving analgesia.Nature communications · 2024Article
- Tiam1-mediated maladaptive plasticity underlying morphine tolerance and hyperalgesia.Brain : a journal of neurology · 2024Article
- Cannabinoid Analgesia in Postoperative Pain Management: From Molecular Mechanisms to Clinical Reality.International journal of molecular sciences · 2024Review
- Females Are More Likely Than Males to Fill an Opioid Prescription in the Year After Anterior Cruciate Ligament Reconstruction.Arthroscopy, sports medicine, and rehabilitation · 2023Article
- Opioid-Induced Pronociceptive Signaling in the Gastrointestinal Tract Is Mediated by Delta-Opioid Receptor Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Contribution of G-Protein α-Subunits to Analgesia, Hyperalgesia, and Hyperalgesic Priming Induced by Subanalgesic and Analgesic Doses of Fentanyl and Morphine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Reduced activity of adenylyl cyclase 1 attenuates morphine induced hyperalgesia and inflammatory pain in mice.Frontiers in pharmacology · 2022Article
- Mu-opioid receptor and receptor tyrosine kinase crosstalk: Implications in mechanisms of opioid tolerance, reduced analgesia to neuropathic pain, dependence, and reward.Frontiers in systems neuroscience · 2022Review
- Spinal AJournal of neuroscience research · 2022Article
- Opioid Analgesics and Persistent Pain After an Acute Pain Emergency Department Visit: Evidence from a Cohort of Suspected Urolithiasis Patients.The Journal of emergency medicine · 2021Article
- Activation of PKCε-ALDH2 Axis Prevents 4-HNE-Induced Pain in Mice.Biomolecules · 2021Article
- Opioid-Induced Hyperalgesic Priming in Single Nociceptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Dopamine D3 receptor-based medication development for the treatment of opioid use disorder: Rationale, progress, and challenges.Neuroscience and biobehavioral reviews · 2020Review
- Antinociceptive effect of selective G protein-gated inwardly rectifying K+ channel agonist ML297 in the rat spinal cord.PloS one · 2020Article
- Systemic Morphine Produces Dose-dependent Nociceptor-mediated Biphasic Changes in Nociceptive Threshold and Neuroplasticity.Neuroscience · 2019Article
- Activating transcription factor 3 modulates protein kinase C epsilon activation in diabetic peripheral neuropathy.Journal of pain research · 2019Article
- Endogenous and Exogenous Opioids in Pain.Annual review of neuroscience · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Clinical pain conditions may remain responsive to opiate analgesics for extended periods, but such persistent acute pain can undergo a transition to an opiate-resistant chronic pain state that becomes a much more serious clinical problem. To test the hypothesis that cellular mechanisms of chronic pain in the primary afferent also contribute to the development of opiate resistance, we used a recently developed model of the transition of from acute to chronic pain, hyperalgesic priming. Repeated intradermal administration of the potent and highly selective mu-opioid agonist, [d-Ala(2),N-MePhe(4),gly-ol]-enkephalin (DAMGO), to produce tolerance for its inhibition of prostaglandin E(2) hyperalgesia, simultaneously produced hyperalgesic priming. Conversely, injection of an inflammogen, carrageenan, used to produce priming produced DAMGO tolerance. Both effects were prevented by inhibition of protein kinase Cepsilon (PKCepsilon). Carrageenan also induced opioid dependence, manifest as mu-opioid receptor antagonist (d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr-NH(2))-induced hyperalgesia that, like priming, was PKCepsilon and G(i) dependent. These findings suggest that the transition from acute to chronic pain, and development of mu-opioid receptor tolerance and dependence may be linked by common cellular mechanisms in the primary afferent.
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What OpenQuestion holds
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.