Beam K G, Knudson C M
Department of Physiology and Biophysics, University of Iowa School of Medicine, Iowa City 52242.
J Gen Physiol. 1988 Jun;91(6):781-98. doi: 10.1085/jgp.91.6.781.
The whole-cell patch-clamp technique was used to study the properties of inward ionic currents found in primary cultures of rat and mouse skeletal myotubes and in freshly dissociated fibers of the flexor digitorum brevis muscle of rats. In each of these cell types, test depolarizations from the holding potential (-80 or -90 mV) elicited three distinct inward currents: a sodium current (INa) and two calcium currents. INa was the dominant inward current: under physiological conditions, the maximum inward INa was estimated to be at least 30-fold larger than either of the calcium currents. The two calcium currents have been termed Ifast and Islow, corresponding to their relative rates of activation. Ifast was activated by test depolarizations to around -40 mV and above, peaked in 10-20 ms, and decayed to baseline in 50-100 ms. Islow was activated by depolarizations to approximately 0 mV and above, peaked in 50-150 ms, and decayed little during a 200-ms test pulse. Ifast was inactivated by brief, moderate depolarizations; for a 1-s change in holding potential, half-inactivation occurred at -55 to -45 mV and complete inactivation occurred at -40 to -30 mV. Similar changes in holding potential had no effect on Islow. Islow was, however, inactivated by brief, strong depolarizations (e.g., 0 mV for 2 s) or maintained, moderate depolarizations (e.g., -40 mV for 60 s). Substitution of barium for calcium had little effect on the magnitude or time course of either Ifast or Islow. The same substitution shifted the activation curve for Islow approximately 10 mV in the hyperpolarizing direction without affecting the activation of Ifast. At low concentrations (50 microM), cadmium preferentially blocked Islow compared with Ifast, while at high concentrations (1 mM), it blocked both Ifast and Islow completely. The dihydropyridine calcium channel antagonist (+)-PN 200-110 (1 microM) caused a nearly complete block of Islow without affecting Ifast. At a holding potential of -80 mV, the half-maximal blocking concentration (K0.5) for the block of Islow by (+)-PN 200-110 was 182 nM. At depolarized holding potentials that inactivated Islow by 35-65%, K0.5 decreased to 5.5 nM.
采用全细胞膜片钳技术研究了大鼠和小鼠骨骼肌肌管原代培养物以及大鼠趾短屈肌新鲜解离纤维中内向离子电流的特性。在每种细胞类型中,从钳制电位(-80或-90 mV)进行的测试去极化引发了三种不同的内向电流:一种钠电流(INa)和两种钙电流。INa是主要的内向电流:在生理条件下,最大内向INa估计比任何一种钙电流至少大30倍。这两种钙电流分别被称为Ifast和Islow,对应于它们相对的激活速率。Ifast在测试去极化至约-40 mV及以上时被激活,在10-20 ms内达到峰值,并在50-100 ms内衰减至基线。Islow在去极化至约0 mV及以上时被激活,在50-150 ms内达到峰值,并在200 ms的测试脉冲期间几乎没有衰减。Ifast通过短暂、适度的去极化而失活;对于钳制电位1 s的变化,半失活发生在-55至-45 mV,完全失活发生在-40至-30 mV。类似的钳制电位变化对Islow没有影响。然而,Islow会被短暂、强烈的去极化(例如,0 mV持续2 s)或持续、适度的去极化(例如,-40 mV持续60 s)失活。用钡替代钙对Ifast或Islow的幅度或时间进程几乎没有影响。相同的替代使Islow的激活曲线在超极化方向上大约移动10 mV,而不影响Ifast的激活。在低浓度(50 microM)时,镉与Ifast相比优先阻断Islow,而在高浓度(1 mM)时,它完全阻断Ifast和Islow。二氢吡啶钙通道拮抗剂(+)-PN 200-110(1 microM)几乎完全阻断Islow,而不影响Ifast。在钳制电位为-80 mV时,(+)-PN 200-110阻断Islow的半数最大阻断浓度(K0.5)为182 nM。在使Islow失活35-65%的去极化钳制电位下,K0.5降至5.5 nM。