{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T05:52:13Z","timestamp":1790401933422,"version":"4.1.0"},"reference-count":60,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Mol Pain"],"published-print":{"date-parts":[[2016,1]]},"abstract":"<jats:p>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\u2009mg\/kg), gabapentin (100\u2009mg\/kg) and oxycodone (3 and 10\u2009mg\/kg), while thermal allodynia and gait abnormalities were only significantly improved by amitriptyline (3\u2009mg\/kg) and oxycodone (10\u2009mg\/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\u2009mg\/kg) was effective at reversing mechanical allodynia, with additional analgesia evident in combination with low-dose oxycodone (1\u2009mg\/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.<\/jats:p>","DOI":"10.1177\/1744806916665366","type":"journal-article","created":{"date-parts":[[2016,8,29]],"date-time":"2016-08-29T20:32:25Z","timestamp":1472502745000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":61,"title":["Transcriptomic and behavioural characterisation of a mouse model of burn pain identify the cholecystokinin 2 receptor as an analgesic target"],"prefix":"10.1177","volume":"12","author":[{"given":"Kathleen","family":"Yin","sequence":"first","affiliation":[{"name":"Centre for Pain Research, Institute for Molecular Bioscience, University of Queensland, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer R","family":"Deuis","sequence":"additional","affiliation":[{"name":"Centre for Pain Research, Institute for Molecular Bioscience, University of Queensland, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard J","family":"Lewis","sequence":"additional","affiliation":[{"name":"Centre for Pain Research, Institute for Molecular Bioscience, University of Queensland, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irina","family":"Vetter","sequence":"additional","affiliation":[{"name":"Centre for Pain Research, Institute for Molecular Bioscience, University of Queensland, Queensland, Australia"},{"name":"Pharmacy Australia Centre of Excellence, University of Queensland, Queensland, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2016,8,28]]},"reference":[{"key":"bibr1-1744806916665366","volume-title":"A WHO plan for burn prevention and care","author":"Mock C","year":"2008"},{"key":"bibr2-1744806916665366","doi-asserted-by":"publisher","DOI":"10.1016\/j.burns.2011.06.005"},{"key":"bibr3-1744806916665366","doi-asserted-by":"publisher","DOI":"10.1016\/j.jpain.2007.02.426"},{"key":"bibr4-1744806916665366","doi-asserted-by":"publisher","DOI":"10.1097\/00004630-200301000-00003"},{"key":"bibr5-1744806916665366","doi-asserted-by":"publisher","DOI":"10.1097\/00005373-198911000-00013"},{"key":"bibr6-1744806916665366","doi-asserted-by":"publisher","DOI":"10.1682\/JRRD.2011.04.0071"},{"key":"bibr7-1744806916665366","doi-asserted-by":"publisher","DOI":"10.1097\/00001503-200210000-00015"},{"key":"bibr8-1744806916665366","doi-asserted-by":"publisher","DOI":"10.1097\/BCR.0000000000000073"},{"key":"bibr9-1744806916665366","doi-asserted-by":"publisher","DOI":"10.1111\/j.1526-4637.2006.00149.x"},{"key":"bibr10-1744806916665366","doi-asserted-by":"publisher","DOI":"10.1097\/BCR.0b013e31828a4828"},{"key":"bibr11-1744806916665366","doi-asserted-by":"crossref","unstructured":"Deuis JR and Vetter I. 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