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眼部表面湿润度由角膜中 TRPM8 依赖性冷热敏感受器调节。

Ocular surface wetness is regulated by TRPM8-dependent cold thermoreceptors of the cornea.

机构信息

Instituto de Neurociencias de Alicante, Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas, San Juan de Alicante, Spain.

出版信息

Nat Med. 2010 Dec;16(12):1396-9. doi: 10.1038/nm.2264. Epub 2010 Nov 14.

DOI:10.1038/nm.2264
PMID:21076394
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.

摘要

基础泪液分泌对于维持眼表面湿润至关重要。角膜冷感受器感知环境温度的微小波动,并相应改变其放电。在小鼠中删除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)会消除冷反应性,并减少基础流泪而不影响伤害感受器介导的刺激性流泪。人类角膜加温也会降低流泪率。这些发现表明,角膜冷感受器中依赖于 TRPM8 的冲动活动有助于调节基础泪液流量。

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本文引用的文献

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Variable threshold of trigeminal cold-thermosensitive neurons is determined by a balance between TRPM8 and Kv1 potassium channels.三叉神经冷热敏神经元的可变阈值由TRPM8和Kv1钾通道之间的平衡决定。
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Dietary targeting of TRPM8 rewires macrophage immunometabolism reducing colitis severity.通过饮食靶向TRPM8可重塑巨噬细胞免疫代谢,减轻结肠炎严重程度。
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An adamantane-based ligand as a novel chemical tool for thermosensory TRPM8 channel therapeutic modulation.一种基于金刚烷的配体,作为用于热敏TRPM8通道治疗性调节的新型化学工具。
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A functional unbalance of TRPM8 and Kv1 channels underlies orofacial cold allodynia induced by peripheral nerve damage.TRPM8通道与Kv1通道的功能失衡是周围神经损伤所致口面部冷痛觉过敏的基础。
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