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dc.contributor.authorXing, Hong
dc.contributor.authorLing, Jennifer X
dc.contributor.authorChen, Meng
dc.contributor.authorJohnson, Richard D
dc.contributor.authorTominaga, Makoto
dc.contributor.authorWang, Cong-Yi
dc.contributor.authorGu, Jianguo
dc.date.accessioned2010-09-24T20:59:19Z
dc.date.available2010-09-24T20:59:19Z
dc.date.issued2008-06-18en_US
dc.identifier.citationMol Pain. 2008 Jun 5; 4:22en_US
dc.identifier.issn1744-8069en_US
dc.identifier.pmid18534015en_US
dc.identifier.doi10.1186/1744-8069-4-22en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/13
dc.description.abstractBreathing cold air without proper temperature exchange can induce strong respiratory autonomic responses including cough, airway constriction and mucosal secretion, and can exacerbate existing asthma conditions and even directly trigger an asthma attack. Vagal afferent fiber is thought to be involved in the cold-induced respiratory responses through autonomic nerve reflex. However, molecular mechanisms by which vagal afferent fibers are excited by cold remain unknown. Using retrograde labeling, immunostaining, calcium imaging, and electrophysiological recordings, here we show that a subpopulation of airway vagal afferent nerves express TRPM8 receptors and that activation of TRPM8 receptors by cold excites these airway autonomic nerves. Thus activation of TRPM8 receptors may provoke autonomic nerve reflex to increase airway resistance. This putative autonomic response may be associated with cold-induced exacerbation of asthma and other pulmonary disorders, making TRPM8 receptors a possible target for prevention of cold-associated respiratory disorders.
dc.rightsThe PMC Open Access Subset is a relatively small part of the total collection of articles in PMC. Articles in the PMC Open Access Subset are still protected by copyright, but are made available under a Creative Commons or similar license that generally allows more liberal redistribution and reuse than a traditional copyrighted work. Please refer to the license statement in each article for specific terms of use. The license terms are not identical for all articles in this subset.en_US
dc.subject.meshAfferent Pathways / physiologyen_US
dc.subject.meshAirway Resistance / physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAutonomic Pathways / physiologyen_US
dc.subject.meshCold Temperatureen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshRespiratory System / innervationen_US
dc.subject.meshTRPM Cation Channels / physiologyen_US
dc.subject.meshVagus Nerve / physiologyen_US
dc.titleTRPM8 mechanism of autonomic nerve response to cold in respiratory airway.en_US
dc.typeJournal Articleen_US
dc.typeResearch Support, Non-U.S. Gov'ten_US
dc.identifier.pmcidPMC2430548en_US
dc.contributor.corporatenameCenter for Biotechnology and Genomic Medicineen_US
refterms.dateFOA2019-04-09T16:25:31Z
html.description.abstractBreathing cold air without proper temperature exchange can induce strong respiratory autonomic responses including cough, airway constriction and mucosal secretion, and can exacerbate existing asthma conditions and even directly trigger an asthma attack. Vagal afferent fiber is thought to be involved in the cold-induced respiratory responses through autonomic nerve reflex. However, molecular mechanisms by which vagal afferent fibers are excited by cold remain unknown. Using retrograde labeling, immunostaining, calcium imaging, and electrophysiological recordings, here we show that a subpopulation of airway vagal afferent nerves express TRPM8 receptors and that activation of TRPM8 receptors by cold excites these airway autonomic nerves. Thus activation of TRPM8 receptors may provoke autonomic nerve reflex to increase airway resistance. This putative autonomic response may be associated with cold-induced exacerbation of asthma and other pulmonary disorders, making TRPM8 receptors a possible target for prevention of cold-associated respiratory disorders.


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