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Ocular surface wetness is regulated by TRPM8-dependent cold thermoreceptors of the cornea
Basal tearing is crucial to maintaining ocular surface wetness. Corneal cold thermoreceptors sense small oscillations in ambient temperature and change their discharge accordingly. Deletion of the cold-transducing ion channel Transient receptor potential cation channel subfamily M member 8 (TRPM8) in mice abrogates cold responsiveness and reduces basal tearing without affecting nociceptor-mediated irritative tearing. Warming of the cornea in humans also decreases tearing rate. These findings indicate that TRPM8-dependent impulse activity in corneal cold receptors contributes to regulating basal tear flow. © 2010 Nature America, Inc. All rights reserved.This work was supported by the Spanish MICINN: projects BFU2008-04425 to C.B., BFU2007-61855 to F.V., SAF2008-00529 to J.G., SAF2008-01004 to D.E. and CONSOLIDER-INGENIO 2010 CSD2007-00023, and by the Fundación de Investigación Oftalmológica, Instituto de Oftalmología Fernandez-Vega and Fundación M.C.- Masadeu-Peterson. R.M. thanks the support of FONDECYT-1100983.Peer Reviewe