Ocular surface wetness is regulated by TRPM8-dependent cold thermoreceptors of the cornea
Ocular surface wetness is regulated by TRPM8-dependent cold thermoreceptors of the cornea
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DOI：
10.1038/nm.2264
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发表时间：
2010-12-01
期刊：
影响因子：
82.9
通讯作者：
Belmonte, Carlos
中科院分区：
文献类型：
--
作者：
Parra, Andres;Madrid, Rodolfo;Belmonte, Carlos
基底撕裂是维持眼表湿润的关键。角膜冷热感受器感知环境温度的微小波动，并相应地改变其放电。小鼠冷转导离子通道瞬时受体电位阳离子通道亚家族M成员8 （TRPM8）的缺失可消除冷反应性并减少基底撕裂，而不影响伤害感受器介导的刺激性撕裂。人类角膜温度升高也会降低撕裂率。这些发现表明，角膜冷受体中trpm8依赖的冲动活动有助于调节基础泪液流。(C) 2010自然美国公司版权所有。
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. (C) 2010 Nature America, Inc. All rights reserved.