ArticlePain2005
Role of NK-1 neurotransmission in opioid-induced hyperalgesia.
Article in Pain, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01839461 (Personalizing Perioperative Morphine Analgesia for Adolescents Undergoing Major Spine Surgeries), which is not on this map. Cited by 60 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Personalizing Perioperative Morphine Analgesia for Adolescents Undergoing Major Spine Surgeries
Who cites it
60 citing papers in PubMed, 164 citations in OpenAlex.
- PET-scan shows peripherally increased neurokinin 1 receptor availability in chronic tennis elbow: visualizing neurogenic inflammation?PloS one · 2013Trial
- Lack of effect of chronic dextromethorphan on experimental pain tolerance in methadone-maintained patients.Addiction biology · 2008Trial
- Repeated Morphine Administration IncreasesBiomolecules & therapeutics · 2022Article
- Review
- Neuron Type-Dependent Synaptic Activity in the Spinal Dorsal Horn of Opioid-Induced Hyperalgesia Mouse Model.Frontiers in synaptic neuroscience · 2021Article
- In Vivo, In Vitro and In Silico Studies of the Hybrid Compound AA3266, an Opioid Agonist/NK1R Antagonist with Selective Cytotoxicity.International journal of molecular sciences · 2020Article
- Rescue of HSP70 in Spinal Neurons Alleviates Opioids-Induced Hyperalgesia via the Suppression of Endoplasmic Reticulum Stress in Rodents.Frontiers in cell and developmental biology · 2020Article
- Article
- Substance P and pain chronicity.Cell and tissue research · 2019Review
- Novel Molecular Strategies and Targets for Opioid Drug Discovery for the Treatment of Chronic Pain.The Yale journal of biology and medicine · 2017Review
- Article
- Neurokinin 1 and opioid receptors: relationships and interactions in nervous system.Translational perioperative and pain medicine · 2016Article
- Dual Alleviation of Acute and Neuropathic Pain by Fused Opioid Agonist-Neurokinin 1 Antagonist Peptidomimetics.ACS medicinal chemistry letters · 2015Article
- Discovery of tripeptide-derived multifunctional ligands possessing delta/mu opioid receptor agonist and neurokinin 1 receptor antagonist activities.Bioorganic & medicinal chemistry letters · 2015Article
- Targeting Opioid-Induced Hyperalgesia in Clinical Treatment: Neurobiological Considerations.CNS drugs · 2015Review
- Synthesis and biological evaluation of compact, conformationally constrained bifunctional opioid agonist - neurokinin-1 antagonist peptidomimetics.European journal of medicinal chemistry · 2015Article
- The mechanism of μ-opioid receptor (MOR)-TRPV1 crosstalk in TRPV1 activation involves morphine anti-nociception, tolerance and dependence.Channels (Austin, Tex.) · 2015Review
- Effects of opium addiction on level of sensory block in spinal anesthesia with bupivacaine for lower abdomen and limb surgery: a case-control study.Anesthesiology and pain medicine · 2014Article
- Building a better analgesic: multifunctional compounds that address injury-induced pathology to enhance analgesic efficacy while eliminating unwanted side effects.The Journal of pharmacology and experimental therapeutics · 2013Article
- Opioid administration following spinal cord injury: implications for pain and locomotor recovery.Experimental neurology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Opiates are among the most important drugs for treatment of moderate to severe pain and prolonged opiate administration is often required to treat chronic pain states. We investigated the neurobiological actions of sustained opiate administration revealing paradoxical pronociceptive adaptations associated with NK-1 receptor function. Sustained morphine delivered over 6 days elicited hyperalgesia in rats and mice during the period of opiate delivery. Sustained morphine administration increased substance P (SP) and NK-1 receptor expression in the spinal dorsal horn. Sustained morphine treatment also enhanced capsaicin-evoked SP release in vitro, and increased internalization of NK-1 receptors in response to noxious stimulation. While NK-1 receptor internalization was observed primarily in the superficial laminae of placebo-treated rats, NK-1 receptor internalization was seen in both superficial and deep lamina of the dorsal horn in morphine-treated animals. Morphine-induced hyperalgesia was reversed by spinal administration of an NK-1 receptor antagonist in rats and mice, and was observed in wildtype (NK-1(+/+)), but not NK-1 receptor knockout (NK-1(-/-)), mice. These data support a critical role for the NK-1 receptor in the expression of sustained morphine-induced hyperalgesia. Additionally, these data indicate that sustained opiate administration induces changes reminiscent of those associated with inflammatory pain. These opiate-induced changes might produce unintended deleterious actions in the course of pain treatment in patients. Understanding of sustained morphine-induced neurochemical changes will help identify approaches that limit the deleterious actions of opiates.
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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.