ArticleMolecular pain2016
Transcriptomic and behavioural characterisation of a mouse model of burn pain identify the cholecystokinin 2 receptor as an analgesic target.
Article in Molecular pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Administration of meloxicam to improve the welfare of mice in research: a systematic review (2000 - 2020).Veterinary research communications · 2022Pooled it
- Discovery and development of an oral analgesic targeting the α2B adrenoceptor.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The Orphan Receptor GPR151: Discovery, Expression, and Emerging Biological Significance.ACS chemical neuroscience · 2025Review
- Unlocking New Therapeutic Options for Vincristine-Induced Neuropathic Pain: The Impact of Preclinical Research.Life (Basel, Switzerland) · 2024Review
- The role of orphan G protein-coupled receptors in pain.Heliyon · 2024Review
- Netazepide, an Antagonist of Cholecystokinin Type 2 Receptor, Prevents Vincristine-Induced Sensory Neuropathy in Mice.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Non-severe thermal burn injuries induce long-lasting downregulation of gene expression in cortical excitatory neurons and microglia.Frontiers in molecular neuroscience · 2024Article
- An Overview of Recent Developments in the Management of Burn Injuries.International journal of molecular sciences · 2023Review
- Blockade of Cholecystokinin Type 2 Receptors Prevents the Onset of Vincristine-Induced Neuropathy in Mice.Pharmaceutics · 2022Article
- Recent advances in neuropeptide-related omics and gene editing: Spotlight on NPY and somatostatin and their roles in growth and food intake of fish.Frontiers in endocrinology · 2022Review
- ZNF382 controls mouse neuropathic pain via silencer-based epigenetic inhibition of Cxcl13 in DRG neurons.The Journal of experimental medicine · 2021Article
- The Cholecystokinin Type 2 Receptor, a Pharmacological Target for Pain Management.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Inhibition of inflammatory pain and cough by a novel charged sodium channel blocker.British journal of pharmacology · 2021Article
- Recent Advances in Experimental Burn Models.Biology · 2021Review
- Methods for Evaluating Sensory, Affective and Cognitive Disorders in Neuropathic Rodents.Current neuropharmacology · 2021Review
- Perioperative Multimodal Analgesia Reduces Opioid Use Following Skin Grafting in Nonintubated Burn Patients.Journal of burn care & research : official publication of the American Burn Association · 2020Article
- Deletion of the Gene Encoding the NMDA Receptor GluN1 Subunit in Schwann Cells Causes Ultrastructural Changes in Remak Bundles and Hypersensitivity in Pain Processing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Characterization of Synthetic Tf2 as a NaBiomedicines · 2020Article
- Activation of a nerve injury transcriptional signature in airway-innervating sensory neurons after lipopolysaccharide-induced lung inflammation.American journal of physiology. Lung cellular and molecular physiology · 2020Article
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
Burn injury is a cause of significant mortality and morbidity worldwide and is frequently associated with severe and long-lasting pain that remains difficult to manage throughout recovery. We characterised a mouse model of burn-induced pain using pharmacological and transcriptomic approaches. Mechanical allodynia elicited by burn injury was partially reversed by meloxicam (5 mg/kg), gabapentin (100 mg/kg) and oxycodone (3 and 10 mg/kg), while thermal allodynia and gait abnormalities were only significantly improved by amitriptyline (3 mg/kg) and oxycodone (10 mg/kg). The need for relatively high opioid doses to elicit analgesia suggested a degree of opioid resistance, similar to that shown clinically in burn patients. We thus assessed the gene expression changes in dorsal root ganglion neurons and pathophysiological mechanisms underpinning burn injury-induced pain using a transcriptomic approach. Burn injury was associated with significantly increased expression of genes associated with axon guidance, neuropeptide signalling, behavioural defence response and extracellular signalling, confirming a mixed neuropathic and inflammatory aetiology. Notably, among the pain-related genes that were upregulated post-injury was the cholecystokinin 2 receptor (Cckbr), a G protein-coupled receptor known as a pain target involved in reducing opioid effectiveness. Indeed, the clinically used cholecystokinin receptor antagonist proglumide (30 mg/kg) was effective at reversing mechanical allodynia, with additional analgesia evident in combination with low-dose oxycodone (1 mg/kg), including significant reversal of thermal allodynia. These findings highlight the complex pathophysiological mechanisms underpinning burn injury-induced pain and suggest that cholecystokinin-2 receptor antagonists may be useful clinically as adjuvants to decrease opioid requirements and improve analgesic management.
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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.