Complex rectification of Muller cell kir currents
Complex rectification of Muller cell kir currents
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DOI：
10.1002/glia.20652
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发表时间：
2008-05-01
期刊：
影响因子：
6.2
通讯作者：
Skatchkov, Sergue N.
中科院分区：
文献类型：
--
作者：
Kucheryavykh, Yuriy V.;Shuba, Yaroslav M.;Skatchkov, Sergue N.
尽管Kir4.1通道是神经胶质细胞中主要的内向整流通道，被广泛认为支持神经系统中K+和谷氨酸的摄取，但Kir4.1通道在K+和多胺重要变化过程中的特性仍然知之甚少。因此，本研究在Miller神经胶质细胞和表达重组Kir4.1通道的tsA201细胞中检测了不同的生理和病理生理外[K+]和管内精胺([SP])浓度对K+电导的电压依赖性。两种不同类型的[SP]阻滞剂被描述为：“快”和“慢”。FAST BLOCK具有强烈的电压依赖性，对精胺的敏感性较低，对胞外钾浓度[K+](O)的依赖性较强。慢阻断具有较强的电压敏感性，开始时更接近静止膜电位，基本上不依赖于[K+](O)，但具有较高的精胺和[K‘](I)敏感性。利用改进的Woodhull模型和对全细胞记录的I/V曲线拟合，我们计算出Muller神经胶质细胞的游离[SP](In)为0.81+/-0.24 mm。这比之前在神经元中估计的要高得多。双相块性质是[K+]和[SP]精馏程度显著不同的基础。虽然证实了胶质细胞Kir和重组Kir4.1的相似特性，但结果也提示了神经胶质细胞中K‘缓冲的机制：当[K+](O)迅速增加时，就像神经元兴奋时一样，“快速阻断”将被解除，促进钾离子内流到神经胶质细胞。[K+](In)的增加将导致“慢阻”的缓解，进一步促进K+-内流。(C)2008年Wiley-Liss，Inc.
Although Kir4.1 channels are the major inwardly rectifying channels in glial cells and are widely accepted to support K+ and glutamate-uptake in the nervous system, the properties of Kir4.1 channels during vital changes of K+ and polyamines remain poorly understood. Therefore, the present study examined the voltage-dependence of K+ conductance with varying physiological and pathophysiological external [K+] and intrapipette spermine ([SP]) concentrations in Miller glial cells and in tsA201 cells expressing recombinant Kir4.1 channels. Two different types of [SP] block were characterized: "fast" and "slow." Fast block was steeply voltage-dependent, with only a low sensitivity to spermine and strong dependence on extracellular potassium concentration, [K+](o). Slow block had a strong voltage sensitivity that begins closer to resting membrane potential and was essentially [K+](o)-independent, but with a higher spermine- and [K'](i)-sensitivity. Using a modified Woodhull model and fitting i/V curves from whole cell recordings, we have calculated free [SP](in) in Muller glial cells as 0.81 +/- 0.24 mM. This is much higher than has been estimated previously in neurons. Biphasic block properties underlie a significantly varying extent of rectification with [K+] and [SP]. While confirming similar properties of glial Kir and recombinant Kir4.1, the results also suggest mechanisms underlying K' buffering in glial cells: When [K+](o) is rapidly increased, as would occur during neuronal excitation, "fast block" would be relieved, promoting potassium influx to glial cells. Increase in [K+](in) would then lead to relief of "slow block," further promoting K+-influx. (c) 2008 Wiley-Liss, Inc.