A novel acid-sensitive K+ channel in rat dorsal root ganglia neurons
A novel acid-sensitive K+ channel in rat dorsal root ganglia neurons
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大鼠背根神经节神经元中一种新型酸敏感钾离子通道
DOI：
10.1016/j.neulet.2006.07.039
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发表时间：
2006
影响因子：
2.5
通讯作者：
Jaehee Han
中科院分区：
文献类型：
--
作者：
J. La;D. Kang;Jae;Seong;Jaehee Han
最近的研究表明，酸敏感背景K+通道（例如双孔结构域K+（K2 P）通道家族成员Task-1和Task-3）在背根神经节（DRG）中表达并参与细胞外酸化诱导的反应。神经元。然而，它仍然要解决其他酸敏感的背景K+通道是否在DRG神经元中功能性表达。在这里，我们的特点是生物物理和药理学特性的一种新的酸敏感性背景K+通道的DRG神经元分离的新生大鼠。我们记录了一个80 pS的K+通道与一个弱的内向整流电流-电压关系在细胞贴附补丁在150 mM KCl浴溶液。细胞外低pH（pH6.3）可抑制80 pS的K+通道。有趣的是，该通道在生物物理和药理学性质上与从小鼠和大鼠中克隆的ASK-2相似。然而，细胞外碱性条件激活的任务2通道，未能激活80 pS的K+通道。利多卡因和奎宁对80 pS钾通道的抑制作用大于对ASK-2通道的抑制作用。我们的研究结果表明，酸敏感性80 pS钾通道可以调节静息膜电位，并可能在各种过程中发挥关键作用，如细胞代谢，pH值，并在DRG神经元的疼痛感觉。
Recent studies have suggested that acid-sensitive background K+channels such as TASK-1 and TASK-3, members of two-pore domain K+(K2P) channel family, express and contribute to extracellular acidification-induced responses in dorsal root ganglia (DRG) neurons. However, it has remained to address whether other acid-sensitive background K+channels are functionally expressed in DRG neurons. Here we characterized biophysical and pharmacological properties of a novel acid-sensitive background K+channel in DRG neurons isolated from neonatal rats. We recorded an 80-pS K+channel with a weak inward rectification current–voltage relationship in cell-attached patches in 150mM KCl bath solution. The 80-pS K+channel was inhibited by extracellular low pH (pHo6.3). Interestingly, the channel was similar to TASK-2 cloned from mouse and rat in biophysical and pharmacological properties. However, extracellular alkaline condition which activates TASK-2 channel, failed to activate the 80-pS K+channel. Lidocaine and quinine more inhibited the channel activity of 80-pS K+channel than that of TASK-2 channel. Our results suggest that the acid-sensitive 80-pS K+channels may regulate resting membrane potential and may play a critical role in various processes such as cell metabolism, pH, and pain sensation in DRG neurons.
影响因子：
8.8
作者：
Kindler, CH;Yost, CS;Gray, AT
通讯作者：
Gray, AT