Jones S W, Marks T N
Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106.
J Gen Physiol. 1989 Jul;94(1):169-82. doi: 10.1085/jgp.94.1.169.
Calcium currents in bullfrog sympathetic neurons inactivate slowly and partially during depolarizations lasting 0.5-1 s. There is also a slower (minutes) inactivation process with a broad voltage dependence. An irreversible loss of current (rundown) is prominent with low concentrations of intracellular Ca2+ buffers, with either Ca2+ or Ba2+ as the charge carrier. The extent and rate of the more rapid inactivation process are maximal near the voltage at which the peak inward current is generated, suggesting that inactivation might be Ca2+ dependent. However, inactivation occurs with either Ca2+ or Ba2+ as the charge carrier, is not prevented by strong buffering of intracellular Ca2+ with 10 mM BAPTA, and varies little as the peak current is changed 10-fold by changing the divalent ion concentration. That is, rapid inactivation is not explained by simple versions of voltage, Ca2+- or current-dependent inactivation models. A model in which ion binding within the channel allows a slower, rate-limiting inactivation process fits some but not all of the observed features of inactivation. A purely voltage-dependent three-state cyclic model fits the data if microscopic inactivation is favored by hyperpolarization.
牛蛙交感神经元中的钙电流在持续0.5 - 1秒的去极化过程中缓慢且部分失活。还存在一个较慢(数分钟)的失活过程,其电压依赖性较宽。在低浓度细胞内Ca²⁺缓冲剂存在的情况下,以Ca²⁺或Ba²⁺作为电荷载体时,电流的不可逆损失(衰减)很明显。更快的失活过程的程度和速率在产生内向电流峰值的电压附近最大,这表明失活可能依赖于Ca²⁺。然而,以Ca²⁺或Ba²⁺作为电荷载体时都会发生失活,用10 mM BAPTA对细胞内Ca²⁺进行强缓冲并不能阻止失活,并且当通过改变二价离子浓度使峰值电流变化10倍时,失活变化很小。也就是说,简单的电压、Ca²⁺或电流依赖性失活模型无法解释快速失活现象。一种通道内离子结合允许较慢的限速失活过程的模型符合部分但并非所有观察到的失活特征。如果超极化有利于微观失活,那么一个纯电压依赖性的三态循环模型符合这些数据。