...Your eyes get drier but they still water. Another of the perennial counterintuitive parts of what is more appropriately, though not quite so handily, called dysfunctional tear syndrome. Hand me my Wileys, will you?

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.
Nat Med. 2010 Dec;16(12):1396-9. Epub 2010 Nov 14.
Parra A, Madrid R, Echevarria D, del Olmo S, Morenilla-Palao C, Acosta MC, Gallar J, Dhaka A, Viana F, Belmonte C.
Instituto de Neurociencias de Alicante, Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas, San Juan de Alicante, Spain.