Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8321977 | The International Journal of Biochemistry & Cell Biology | 2018 | 14 Pages |
Abstract
Irritable bowel syndrome and inflammatory bowel disease are major forms of chronic visceral pain, which affect over 15% of the global population. In order to identify new therapies, it is important to understand the underlying causes of chronic visceral pain. This review provides recent evidence demonstrating that inflammation or infection of the gastrointestinal tract triggers specific changes in the neuronal excitability of sensory pathways responsible for the transmission of nociceptive information from the periphery to the central nervous system. Specific changes in the expression and function of a variety of ion channels and receptors have been documented in inflammatory and chronic visceral pain conditions relevant to irritable bowel syndrome and inflammatory bowel disease. An increase in pro-nociceptive mechanisms enhances peripheral drive from the viscera and provides an underlying basis for enhanced nociceptive signalling during chronic visceral pain states. Recent evidence also highlights increases in anti-nociceptive mechanisms in models of chronic visceral pain, which present novel targets for pharmacological treatment of this condition.
Keywords
5-HTIBS-CCVHCVPIBS-DENSmGluRGuanylate Cyclase-Cchronic visceral hypersensitivityGPCRGC-CK2PCGRPCaMKIIAMPAIBS5-hydroxytryptamineIBDMAPKKCAVDRGα-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acidgamma-aminobutyric acidInflammatory bowel diseaseCNSirritable bowel syndromeenteric nervous systemcentral nervous systemNavcalcium/calmodulin-dependent protein kinase IImitogen-activated protein kinase kinasecalcitonin gene-related peptideGABAdorsal root gangliacannabinoid receptorHistamine receptorMetabotropic glutamate receptorG protein-coupled receptor
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Authors
Mahsa Sadeghi, Andelain Erickson, Joel Castro, Annemie Deiteren, Andrea M. Harrington, Luke Grundy, David J. Adams, Stuart M. Brierley,