Attenuated cold sensitivity in TRPM8 null mice
Attenuated cold sensitivity in TRPM8 null mice
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DOI：
10.1016/j.neuron.2007.04.017
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发表时间：
2007-05-03
期刊：
影响因子：
16.2
通讯作者：
Qin, Ning
中科院分区：
文献类型：
--
作者：
Colburn, Raymond W.;Lubin, Mary Lou;Qin, Ning
热感觉是一种重要的感觉功能，由多种传感器分子提供，包括瞬态受体电位（TRP）离子通道超家族的分子。其成员之一TRPM8 （CMR1）是一种配体门控的非选择性阳离子通道，在体外可被冷刺激和化学刺激激活。然而，其在体内冷、热感觉和疼痛中的作用尚未完全阐明。在这里，我们发现来自TRPM8缺失小鼠的感觉神经元缺乏可检测水平的TRPM8 mRNA和蛋白质，并且这些神经元对寒冷（18℃）和薄荷醇（100 μ M）的反应数量大大减少。此外，与WT小鼠相比，TRPM8缺失小鼠在某些行为上表现出缺陷，包括青霉素诱导的跳跃和冷感觉，以及损伤诱导的对丙酮冷却的反应性显著降低。这些结果表明，TRPM8可能在人类某些类型的冷致疼痛中发挥重要作用。
Thermosensation is an essential sensory function that is subserved by a variety of transducer molecules, including those from the Transient Receptor Potential (TRP) ion channel superfamily. One of its members, TRPM8 (CMR1), a ligand-gated, nonselective cation channel, is activated by both cold and chemical stimuli in vitro. However, its roles in cold thermosensation and pain in vivo have not been fully elucidated. Here, we show that sensory neurons derived from TRPM8 null mice lack detectable levels of TRPM8 mRNA and protein and that the number of these neurons responding to cold (18 degrees C) and menthol (100 mu M) is greatly decreased. Furthermore, compared with WT mice, TRPM8 null mice display deficiencies in certain behaviors, including icilin-induced jumping and cold sensation, as well as a significant reduction in injury-induced responsiveness to acetone cooling. These results suggest that TRPM8 may play an important role in certain types of cold-induced pain in humans.