Potassium Channels in Chara corallina: CONTROL AND INTERACTION WITH THE ELECTROGENIC H PUMP.
Potassium Channels in Chara corallina: CONTROL AND INTERACTION WITH THE ELECTROGENIC H PUMP.
复制标题
珊瑚轮藻中的钾通道：与电动 H 泵的控制和相互作用。
DOI：
10.1104/pp.69.4.781
复制
发表时间：
1982
期刊：
影响因子：
7.4
通讯作者：
W. J. Lucas
中科院分区：
文献类型：
--
作者：
D. W. Keifer;W. J. Lucas
利用质膜电特性研究了珊瑚轮藻 (Chara Corallina Klein ex Willd., em R.D.W.) 节间细胞中 K(+) 的转运及其控制。电池暴露于含有 10 mm KCl 的溶液中会导致电位（通常为 -250 毫伏（平均值））分两步去极化。第一步是 21 毫伏的去极化，持续 1 到 40 分钟。第二步从动作电位开始，将膜电位保持在 -91 毫伏，电阻降低了 10 倍。我们认为第二步是由膜中 K(+) 通道的开放引起的。这降低了电阻并提供了使电动泵部分短路的电流路径。虽然大部分短路，但发电泵仍在运行，如下所示： (a) -91 毫伏的去极化电位比 Ek 更负（= 10 mm K(+) 中的 -42 毫伏）； (b) 当细胞去极化时，发生大量 K(+) 净吸收； (c) 生电泵抑制剂己烯雌酚和巯基试剂 N-乙基马来酰亚胺（增加被动膜通透性）进一步使 10 mm KCl 中的电位去极化。将 K(+) 浓度从 10 mm 降低至 0.2 mm 时，发生两相恢复至正常细胞电位。第一阶段是对外部 K(+) 浓度变化的明显能斯特电位响应。第二阶段是突然的超极化，伴随着膜电阻的大幅增加。我们将第二阶段归因于 K(+) 通道的关闭和对电动泵的相关短路效应的消除，从而允许膜超极化。进一步的实验表明，K(+)通道需要Ca(2+)才能正常关闭，但其他离子可以替代，包括：Na(+)、四乙铵和2,4,6-三氨基嘧啶。显然，K(+) 通道电导是由 Ca(2+) 和 K(+) 之间对控制（门控？）结合位点的竞争决定的。
Plasmalemma electrical properties were used to investigate K(+) transport and its control in internodal cells of Chara corallina Klein ex Willd., em R.D.W. Cell exposure to solutions containing 10 mm KCl caused the potential, normally -250 millivolts (average), to depolarize in two steps. The first step was a 21 millivolt depolarization that lasted from 1 to 40 minutes. The second step started with an action potential and left the membrane potential at -91 millivolts, with a 10-fold reduction in resistance. We suggest that the second step was caused by the opening of K(+) -channels in the membrane. This lowered the resistance and provided a current pathway that partially short-circuited the electrogenic pump. Although largely short-circuited, the electrogenic pump was still operating as indicated by: (a) the depolarized potential of -91 millivolts was more negative than Ek (=-42 millivolts in 10 mm K(+)); (b) a large net K(+) uptake occurred while the cell was depolarized; (c) both the electrogenic pump inhibitor, diethylstilbestrol, and the sulfhydryl-reagent N-ethylmaleimide (which increased the passive membrane permeability) further depolarized the potential in 10 mm KCl.A two-phase recovery back to normal cell potentials occurred upon lowering the K(+) concentration from 10 to 0.2 mm. The first phase was an apparent Nernst potential response to the change in external K(+) concentration. The second phase was a sudden hyperpolarization accompanied by a large increase in membrane resistance. We attribute the second phase to the closing of K(+) -channels and the removal of the associated short-circuiting effect on the electrogenic pump, thereby allowing the membrane to hyperpolarize. Further experiments indicated that the K(+) -channel required Ca(2+) for normal closure, but other ions could substitute, including: Na(+), tetraethylammonium, and 2,4,6-triaminopyrimidine. Apparently, K(+) -channel conductance is determined by competition between Ca(2+) and K(+) for a control (gating?) binding site.