ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Distinct mechanisms underlying pronociceptive effects of opioids.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Pooled it
- Trial
- Reviewing the Impact of Maternal Opioid Use Disorder on Fetal Development and Long-Term Pediatric Health Outcomes.Cureus · 2024Review
- Pharmacological Interventions for Opioid-Induced Hyperalgesia: A Scoping Review of Preclinical Trials.Journal of clinical medicine · 2022Article
- Endogenous opioid systems alterations in pain and opioid use disorder.Frontiers in systems neuroscience · 2022Review
- Pharmacotherapeutic management of co-morbid alcohol and opioid use.Expert opinion on pharmacotherapy · 2020Review
- Mu and delta opioid receptors play opposite nociceptive and behavioural roles on nerve-injured mice.British journal of pharmacology · 2020Article
- Withdrawal from spinal application of remifentanil induces long-term potentiation of c-fiber-evoked field potentials by activation of Src family kinases in spinal microglia.Neurochemical research · 2018Article
- Altered Signaling in the Descending Pain-modulatory System after Short-Term Infusion of the μ-Opioid Agonist Remifentanil.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Increased Hyperalgesia and Proinflammatory Cytokines in the Spinal Cord and Dorsal Root Ganglion After Surgery and/or Fentanyl Administration in Rats.Anesthesia and analgesia · 2018Article
- Involvement of Spinal PKMζ Expression and Phosphorylation in Remifentanil-Induced Long-Term Hyperalgesia in Rats.Cellular and molecular neurobiology · 2017Article
- Targeting human Mas-related G protein-coupled receptor X1 to inhibit persistent pain.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Loss of μ opioid receptor signaling in nociceptors, but not microglia, abrogates morphine tolerance without disrupting analgesia.Nature medicine · 2017Article
- Pronociceptive and Antinociceptive Effects of Buprenorphine in the Spinal Cord Dorsal Horn Cover a Dose Range of Four Orders of Magnitude.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Effect of acute fentanyl treatment on synaptic plasticity in the hippocampal CA1 region in rats.Frontiers in pharmacology · 2015Article
- Influence of intramuscular heat stimulation on modulation of nociception: complex role of central opioid receptors in descending facilitation and inhibition.The Journal of physiology · 2014Article
- Imaging opioid analgesia in the human brain and its potential relevance for understanding opioid use in chronic pain.Neuropharmacology · 2014Review
- Article
- BDNF released during neuropathic pain potentiates NMDA receptors in primary afferent terminals.The European journal of neuroscience · 2014Article
- Carbamazepine potentiates the effectiveness of morphine in a rodent model of neuropathic pain.PloS one · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to analgesia, opioids may also produce paradoxical pain amplification [opioid-induced hyperalgesia (OIH)] either on abrupt withdrawal or during continuous long-term application. Here, we assessed antinociceptive and pronociceptive effects of three clinically used opioids at C-fiber synapses in the rat spinal dorsal horn in vivo. During 60 min of intravenous infusions of remifentanil (450 μg·kg⁻¹·h⁻¹), fentanyl (48 μg·kg⁻¹·h⁻¹), or morphine (14 mg·kg⁻¹·h⁻¹), C-fiber-evoked field potentials were depressed and paired-pulse ratios (PPR) were increased, indicating a presynaptic inhibition by all three opioids. After withdrawal, postsynaptic responses were enhanced substantially for the remaining of the recording periods of at least 3 h. Withdrawal from remifentanil led to long-term potentiation (LTP) of synaptic strength in C-fibers via activation of spinal μ-opioid receptors (MORs) and spinal NMDA receptors (NMDARs). Fentanyl and morphine caused an enhancement of synaptic transmission at C-fibers, which involved two distinct mechanisms: (1) an opioid withdrawal LTP that also required activation of spinal MORs and NMDARs and that was associated with a decrease in PPR suggestive of a presynaptic mechanism of its expression, and (2) an immediate-onset, descending facilitation of C-fiber-evoked field potentials during and after intravenous infusion of fentanyl and morphine. Immediate-onset, descending facilitation was mediated by the activation of extraspinal MORs, descending serotonergic pathways, and spinal 5-hydroxytryptamine-3 receptors (5-HT₃Rs). Our study identified fundamentally different pronociceptive effects of clinically used opioids and suggests that OIH can be prevented by the combined use of NMDAR and 5-HT₃R antagonists.
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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.