Janssen L J, Sims S M
Department of Physiology, University of Western Ontario, London, Canada.
Pflugers Arch. 1994 Jul;427(5-6):473-80. doi: 10.1007/BF00374263.
Spontaneous transient inward currents (STICs) were recorded in canine and guinea-pig tracheal myocytes held at negative membrane potentials. STICs were Cl- selective since their reversal potential was dependent on the Cl- gradient and they were blocked by the Cl- channel blocker niflumic acid. STICs were insensitive to Cs+, charybdotoxin, and nifedipine. Ca(2+)-activated K+ currents often preceded STICs, suggesting that the STICs are Ca2+ dependent. In support of this suggestion, we found the Cl- currents were: (1) abolished by depleting intracellular Ca2+ stores using caffeine, acetylcholine, histamine, or substance P; (2) enhanced by increasing external concentrations of Ca2+; (3) evoked by voltage-dependent Ca2+ influx. The channels responsible for this Cl- current are of small unitary conductance (< 20 pS). Decay of the STICs was described by a single exponential with a time constant of 94 +/- 9 ms at -70 mV; the time constant increased considerably at more positive potentials. Using Ca(2+)-dependent Cl- currents and contractions as indices of internal levels of Ca2+, we found that isolated tracheal cells are capable of exhibiting rhythmic behaviour: bursts of currents and contractions with a periodicity of less than 0.1 Hz and which continued for more than 20 min. These rhythmic events were recorded at negative membrane potentials, suggesting that cyclical release of internally sequestered Ca2+ is responsible. We conclude that spontaneous release of Ca2+ from intracellular stores in tracheal muscle cells leads to transient currents in some cases accompanied by rhythmic contractions. Our studies provide evidence for a cellular mechanism that could underly myogenic oscillations of membrane potential in smooth muscle.
在保持负膜电位的犬和豚鼠气管肌细胞中记录到自发瞬态内向电流（STICs）。STICs具有Cl-选择性，因为其反转电位取决于Cl-梯度，并且它们被Cl-通道阻滞剂氟尼酸阻断。STICs对Cs+、大蝎毒素和硝苯地平不敏感。Ca(2+)激活的K+电流常常先于STICs出现，这表明STICs依赖于Ca2+。为支持这一观点，我们发现Cl-电流：(1) 使用咖啡因、乙酰胆碱、组胺或P物质耗尽细胞内Ca2+储存后被消除；(2) 通过增加细胞外Ca2+浓度而增强；(3) 由电压依赖性Ca2+内流诱发。负责这种Cl-电流的通道具有小的单通道电导（<20 pS）。在-70 mV时，STICs的衰减由单指数描述，时间常数为94±9 ms；在更正的电位下，时间常数显著增加。使用Ca(2+)依赖性Cl-电流和收缩作为细胞内Ca2+水平的指标，我们发现分离的气管细胞能够表现出节律性行为：电流和收缩的爆发，周期小于0.1 Hz且持续超过20分钟。这些节律性事件在负膜电位下记录到，表明细胞内储存的Ca2+的周期性释放是其原因。我们得出结论，气管肌细胞中细胞内储存的Ca2+的自发释放导致在某些情况下伴有节律性收缩的瞬态电流。我们的研究为一种可能是平滑肌膜电位肌源性振荡基础的细胞机制提供了证据。
