Gukovskaya A S, Zinchenko V P
Biochim Biophys Acta. 1985 May 28;815(3):433-40. doi: 10.1016/0005-2736(85)90371-2.
Effects of the Ca2+-ionophore A23187 and concanavalin A on the membrane potential of human lymphocytes and rat thymocytes have been studied using the fluorescent potential probe diS-C3-(5). At concentrations of 10(-8) to 10(-6) M A23187 changes the membrane potential, inducing both hyper- and depolarization. Depending on concentrations of A23187 and the external Ca2+, and on the type of lymphocytes, one of these effects predominates. The hyperpolarization induced by A23187 is caused by activation of Ca2+-dependent K+ channels. It is blocked by quinine and high concentrations of extracellular K+. The dependence of Ca2+-activated K+ transport on extracellular Ca2+ and its sensitivity to calmodulin antagonists is different for human lymphocytes and for thymocytes. As distinct from lymphocytes, in thymocytes calmodulin is not involved in activation of Ca2+-dependent K+ transport. The depolarization induced in lymphocytes by A23187 is caused by an increase in Na+ permeability of the lymphocyte plasma membrane: it is eliminated in a low-Na+ medium. At mitogenic concentrations concanavalin A does not change the membrane potential of the lymphocytes. The results obtained permit elucidation of the relationship between two early events in lymphocyte activation, namely the increase in intracellular Ca2+ concentration and the increase in lymphocyte plasma membrane permeabilities to monovalent cations.
利用荧光电位探针diS-C3-(5)研究了钙离子载体A23187和伴刀豆球蛋白A对人淋巴细胞和大鼠胸腺细胞膜电位的影响。浓度为10(-8)至10(-6)M时，A23187可改变膜电位，引起超极化和去极化。根据A23187的浓度、细胞外钙离子浓度以及淋巴细胞的类型，其中一种效应占主导。A23187诱导的超极化是由钙离子依赖性钾通道的激活引起的。它被奎宁和高浓度的细胞外钾所阻断。人淋巴细胞和胸腺细胞中钙离子激活的钾转运对细胞外钙离子的依赖性及其对钙调蛋白拮抗剂的敏感性不同。与淋巴细胞不同，在胸腺细胞中钙调蛋白不参与钙离子依赖性钾转运的激活。A23187在淋巴细胞中诱导的去极化是由淋巴细胞质膜对钠离子通透性的增加引起的：在低钠培养基中这种去极化被消除。在促有丝分裂浓度下，伴刀豆球蛋白A不会改变淋巴细胞的膜电位。所获得的结果有助于阐明淋巴细胞激活过程中两个早期事件之间的关系，即细胞内钙离子浓度的增加和淋巴细胞质膜对单价阳离子通透性的增加。
