Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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4-Aminopyridine / metabolism
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Animals
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Cold Temperature
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Cornea / metabolism*
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Dry Eye Syndromes / etiology*
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Dry Eye Syndromes / metabolism
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Menthol / pharmacology
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Mice
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Mice, Transgenic
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Ocular Physiological Phenomena*
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Pyrazines / pharmacology
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Pyridines / pharmacology
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Shaker Superfamily of Potassium Channels / metabolism
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TRPA1 Cation Channel
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TRPM Cation Channels / metabolism*
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Tears / physiology*
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Thermoreceptors / metabolism*
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Transient Receptor Potential Channels / genetics
Substances
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N-(4-tert-butylphenyl)-4-(3-chloropyridin-2-yl)tetrahydropyrazine-1(2H)-carboxamide
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Pyrazines
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Pyridines
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Shaker Superfamily of Potassium Channels
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TRPA1 Cation Channel
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TRPM Cation Channels
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TRPM8 protein, mouse
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Transient Receptor Potential Channels
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Trpa1 protein, mouse
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Menthol
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4-Aminopyridine