Abstract
Transient receptor potential (TRP) channels transduce signals of chemical irritation and temperature change from the ocular surface to the brain. Dry eye disease (DED) is a multifactorial disorder wherein the eyes react to trivial stimuli with abnormal sensations, such as dryness, blurring, presence of foreign body, discomfort, irritation, and pain. There is increasing evidence of TRP channel dysfunction (i.e., TRPV1 and TRPM8) in DED pathophysiology. Here, we review some of this literature and discuss one strategy on how to manage DED using a TRPM8 agonist.
Highlights
Transient receptor potential (TRP) channels transduce signals of chemical irritation and temperature change from the ocular surface to the brain
Polymodal nociceptors in the eye that preferentially contain neuropeptides are expressed through a TRPV1 channel, and those without neuropeptides are expressed through a TRPA1 channel [8,20,27,28]
For confirmation of the benefits of cooling, it must be accurately stated how a TRPM8 agonist applied to the ocular surface will affect sensation or discomfort in patients with Dry eye disease (DED)
Summary
Dry eye disease (DED) is a multifactorial disorder of the ocular surface, and especially of the sensory and motor nerves that regulate the physiology of this surface [1]. Considering the pathophysiology of DED, the treatment strategy has shifted from just hydrating and lubricating the ocular surface to modifying the underlying disease process. Aqueous tear deficiency is considered one of the major symptoms of DED, which is caused by a deficit of lacrimal and conjunctival tear secretion [3]. Increased attention has focused on the neuronal regulation of glandular tear secretion [3,4,5]. Studies show that thermal changes at the ocular surface activate cool neurons and may affect surface wetness [6,7,8]
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