Brehm P, Eckert R
Science. 1978 Dec 15;202(4373):1203-6. doi: 10.1126/science.103199.
Under depolarizing voltage clamp of Paramecium an inward calcium current developed and subsequently relaxed within 10 milliseconds. The relaxation was substantially slowed when most of the extracellular calcium was replaced by either strontium or barium. Evidence is presented that the relaxation is not accounted for by a drop in electromotive force acting on calcium, or by activation of a delayed potassium current. Relaxation of the current must, therefore, result from an inactivation of the calcium channel. This inactivation persisted after a pulse, as manifested by a reduced calcium current during subsequent depolarization. Inactivation was retarded by procedures that reduce net entry of calcium, and was independent of membrane potential. The calcium channel undergoes inactivation as a consequence of calcium entry during depolarization. In this respect, inactivation of the calcium channel departs qualitatively from the behavior described in the Hodgkin-Huxley model of the sodium channel.
在草履虫的去极化电压钳制下,内向钙电流产生并在10毫秒内随后松弛。当大部分细胞外钙被锶或钡取代时,松弛显著减慢。有证据表明,松弛不是由作用于钙的电动势下降或延迟钾电流的激活引起的。因此,电流的松弛必定是由钙通道的失活导致的。这种失活在脉冲后持续存在,表现为随后去极化期间钙电流的减少。减少钙净内流的程序会延迟失活,且失活与膜电位无关。钙通道在去极化期间由于钙内流而发生失活。在这方面,钙通道的失活在性质上不同于霍奇金-赫胥黎钠通道模型中描述的行为。