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dc.contributor.authorTalavera, Karel-
dc.contributor.authorGees, Maarten-
dc.contributor.authorKarashima, Yuji-
dc.contributor.authorMeseguer, Víctor M.-
dc.contributor.authorVanoirbeek, Jeroen A. J.-
dc.contributor.authorDamann, Nils-
dc.contributor.authorEveraerts, Wouter-
dc.contributor.authorBenoit, Melissa-
dc.contributor.authorJanssens, Annelies-
dc.contributor.authorVennekens, Rudi-
dc.contributor.authorViana, Félix-
dc.contributor.authorNemery, Benoit-
dc.contributor.authorNilius, Bernd-
dc.contributor.authorVoets, Thomas-
dc.date.accessioned2009-09-14T09:45:17Z-
dc.date.available2009-09-14T09:45:17Z-
dc.date.issued2009-09-13-
dc.identifier.citationNature Neuroscience (2009), doi: 10.1038/nn.2379 (In press)en_US
dc.identifier.issn1097-6256-
dc.identifier.urihttp://hdl.handle.net/10261/16906-
dc.description8 pages, 7 figures.-- Supporting information available at: http://www.nature.com/neuro/journal/vaop/ncurrent/suppinfo/nn.2379_S1.htmlen_US
dc.descriptionArticle in press.-
dc.description.abstractTopical application of nicotine, as used in nicotine replacement therapies, causes irritation of the mucosa and skin. This reaction has been attributed to activation of nicotinic acetylcholine receptors (nAChRs) in chemosensory neurons. In contrast with this view, we found that the chemosensory cation channel transient receptor potential A1 (TRPA1) is crucially involved in nicotine-induced irritation. We found that micromolar concentrations of nicotine activated heterologously expressed mouse and human TRPA1. Nicotine acted in a membrane-delimited manner, stabilizing the open state(s) and destabilizing the closed state(s) of the channel. In the presence of the general nAChR blocker hexamethonium, nociceptive neurons showed nicotine-induced responses that were strongly reduced in TRPA1-deficient mice. Finally, TRPA1 mediated the mouse airway constriction reflex to nasal instillation of nicotine. The identification of TRPA1 as a nicotine target suggests that existing models of nicotine-induced irritation should be revised and may facilitate the development of smoking cessation therapies with less adverse effects.en_US
dc.description.sponsorshipK.T. and J.A.J.V. were supported by a postdoctoral mandate from KU Leuven and are currently postdoctoral fellows of the Research Foundation–Flanders (Fonds voor Wetenschappelijk Onderzoek, FWO). M.G. and W.E. are doctoral FWO fellows. V.M.M was supported by Spanish CONSOLIDER-INGENIO 2010 CSD2007-00023. This work was supported by grants from Inter-university Attraction Poles Programme (Belgian Science Policy, P6/28), FWO (G.0172.03 and G.0565.07), the Research Council of the KU Leuven (GOA 2004/07) and the Flemish Government (Excellentiefinanciering, EF/95/010).en_US
dc.format.extent918459 bytes-
dc.format.mimetypeapplication/pdf-
dc.language.isoengen_US
dc.publisherNature Publishing Groupen_US
dc.rightsclosedAccessen_US
dc.titleNicotine activates the chemosensory cation channel TRPA1en_US
dc.typeartículoen_US
dc.identifier.doi10.1038/nn.2379-
dc.description.peerreviewedPeer revieweden_US
dc.relation.publisherversionhttp://dx.doi.org/10.1038/nn.2379en_US
dc.identifier.e-issn1546-1726-
local.message.claim2023-03-27T20:25:06.504+0200|||rp14886|||submit_approve|||dc_contributor_author|||None*
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairetypeartículo-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.grantfulltextopen-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
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