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Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/16906
Título

Nicotine activates the chemosensory cation channel TRPA1

AutorTalavera, Karel; Gees, Maarten; Karashima, Yuji; Meseguer, Víctor M.; Vanoirbeek, Jeroen A. J.; Damann, Nils; Everaerts, Wouter; Benoit, Melissa; Janssens, Annelies; Vennekens, Rudi; Viana, Félix; Nemery, Benoit; Nilius, Bernd; Voets, Thomas
Fecha de publicación13-sep-2009
EditorNature Publishing Group
CitaciónNature Neuroscience (2009), doi: 10.1038/nn.2379 (In press)
ResumenTopical 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.
Descripción8 pages, 7 figures.-- Supporting information available at: http://www.nature.com/neuro/journal/vaop/ncurrent/suppinfo/nn.2379_S1.html
Article in press.
Versión del editorhttp://dx.doi.org/10.1038/nn.2379
URIhttp://hdl.handle.net/10261/16906
DOI10.1038/nn.2379
ISSN1097-6256 (Print)
1546-1726 (Online)
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