Alkon D L, Farley J, Sakakibara M, Hay B
Biophys J. 1984 Nov;46(5):605-14. doi: 10.1016/S0006-3495(84)84059-X.
Two-microelectrode voltage clamp studies were performed on the somata of Hermissenda Type B photoreceptors that had been isolated by axotomy from all synaptic interaction as well as any impulse-generating (i.e., active) membrane. In the presence of 2-10 mM 4-aminopyridine (4-AP) and 100 mM tetraethylammonium ion (TEA), which eliminated two previously described voltage-dependent potassium currents (IA and the delayed rectifier), a voltage-dependent outward current was apparent in the steady state responses to command voltage steps more positive than -40 mV (absolute). This current increased with increasing external Ca++. The magnitude of the outward current decreased and an inward current became apparent following EGTA injection. Substitution of external Ba++ for Ca++ also made the inward current more apparent. This inward current, which was almost eliminated after being exposed for approximately 5 min to a solution in which external Ca++ was replaced with Cd++, was maximally activated at approximately 0 mV. Elevation of external potassium allowed the calcium (ICa++) and calcium-dependent K+ (IC) currents to be substantially separated. Command pulses to 0 mV elicited maximal ICa++ but no IC because no K+ currents flowed at their new reversal potential (0 mV) in 300 mM K+. At a holding potential of -60 mV, which was now more negative than the potassium equilibrium potential, EK+, in 300 mM K+, IC appeared as an inward tail current after positive command steps. The voltage dependence of ICa++ was demonstrated with positive steps in 100 mM Ba++, 4-AP, and TEA. Other data indicated that in 10 mM Ca++, IC underwent pronounced and prolonged inactivation whereas ICa++ did not. When the photoreceptor was stimulated with a light step (with the membrane potential held at -60 mV), there was also a prolonged inactivation of IC. In elevated external Ca++, ICa++ also showed similar inactivation. These data suggest that IC may undergo prolonged inactivation due to a direct effect of elevated intracellular Ca++, as was previously shown for a voltage-dependent potassium current, IA. These results are discussed in relation to the production of training-induced changes of membrane currents on retention days of associative learning.
对经轴突切断术分离出来、与所有突触相互作用以及任何产生冲动（即具有活性）的膜隔绝的海兔B型光感受器的胞体进行了双微电极电压钳研究。在存在2 - 10 mM 4 - 氨基吡啶（4 - AP）和100 mM四乙铵离子（TEA）的情况下，这消除了先前描述的两种电压依赖性钾电流（IA和延迟整流器），在对指令电压阶跃的稳态响应中，当指令电压比 - 40 mV（绝对值）更正时，一种电压依赖性外向电流明显可见。这种电流随着外部Ca++浓度的增加而增加。注入EGTA后，外向电流的幅度减小，内向电流变得明显。用外部Ba++替代Ca++也使内向电流更明显。这种内向电流在暴露于外部Ca++被Cd++替代的溶液中约5分钟后几乎被消除，在约0 mV时被最大程度激活。外部钾离子浓度升高使得钙电流（ICa++）和钙依赖性钾电流（IC）得以显著分离。向0 mV的指令脉冲引发最大的ICa++但没有IC，因为在300 mM K+中，它们的新反转电位（0 mV）处没有钾电流流动。在 - 60 mV的钳制电位下，此时比300 mM K+中的钾平衡电位EK+更负，在正向指令阶跃后，IC表现为内向尾电流。在100 mM Ba++、4 - AP和TEA中，通过正向阶跃证明了ICa++的电压依赖性。其他数据表明，在10 mM Ca++中，IC经历明显且持久的失活，而ICa++则没有。当用光阶跃刺激光感受器（膜电位保持在 - 60 mV）时，IC也会经历持久的失活。在外部Ca++浓度升高时，ICa++也表现出类似的失活。这些数据表明，IC可能由于细胞内Ca++浓度升高的直接作用而经历持久的失活，正如先前对电压依赖性钾电流IA所显示的那样。结合联想学习记忆期训练诱导的膜电流变化的产生对这些结果进行了讨论。
