DEG/ENaC ion channels involved in sensory transduction are modulated by cold temperature
DEG/ENaC ion channels involved in sensory transduction are modulated by cold temperature
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DOI：
10.1073/pnas.111155398
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发表时间：
2001-05-22
影响因子：
11.1
通讯作者：
Snyder, PM
中科院分区：
文献类型：
--
作者：
Askwith, CC;Benson, CJ;Snyder, PM
一些DEG/ENaC阳离子通道亚基在舌头和皮肤感觉神经元中表达，它们被认为是盐味和酸味以及触摸的感受器。由于这些组织暴露在巨大的温度变化中，我们研究了温度如何影响DEG/ENaC通道功能。我们发现，冷温度显著增加由上皮钠离子通道(ENaC)产生的结构性激活的Na+电流，在25℃时出现半峰值刺激。低温对DEG/ENaC家族的其他成员(BNC1、ASIC和DRASIC)没有诱导电流，然而，当这些通道被酸激活时，低温通过减缓脱敏速度而增强了电流。增强作用被一个改变通道门控的“Deg”突变所消除。生理范围内的温度变化对异源表达酸性门控DEG/ENaC通道的细胞以及背根节感觉神经元的电流有显著影响。低温调节DEG/ENaC通道功能的发现可能为广泛认识的温度改变味觉和机械感觉的能力提供了分子解释。
Several DEG/ENaC cation channel subunits are expressed in the tongue and in cutaneous sensory neurons, where they are postulated to function as receptors for salt and sour taste and for touch. Because these tissues are exposed to large temperature variations, we examined how temperature affects DEG/ENaC channel function. We found that cold temperature markedly increased the constitutively active Na+ currents generated by epithelial Na+ channels (ENaC), Half-maximal stimulation occurred at 25 degreesC. Cold temperature did not induce current from other DEG/ENaC family members (BNC1, ASIC, and DRASIC), However, when these channels were activated by acid, cold temperature potentiated the currents by slowing the rate of desensitization. Potentiation was abolished by a "Deg" mutation that alters channel gating. Temperature changes in the physiologic range had prominent effects on current in cells heterologously expressing acid-gated DEG/ENaC channels, as well as in dorsal root ganglion sensory neurons. The finding that cold temperature modulates DEG/ENaC channel function may provide a molecular explanation for the widely recognized ability of temperature to modify taste sensation and mechanosensation.