Hayashi J H, Stuart A E
Department of Physiology, University of North Carolina, Chapel Hill 27599-7545.
Vis Neurosci. 1993 Mar-Apr;10(2):261-70. doi: 10.1017/s0952523800003667.
We have described the currents flowing across the presynaptic membranes of the four median photoreceptors of the giant barnacle, Balanus nubilus, using a quasi-voltage clamp arrangement. Membrane potential, measured in the terminal region of one photoreceptor, was controlled in all four terminals by feedback current supplied through the nerve containing the photoreceptors' axons. The [Ca2+]o in the saline was reduced to decrease the Ca2+ current, enabling better voltage control, and tetraethylammonium ion (TEA, 20 mM) was added to block a fast voltage-dependent K+ conductance. Depolarizing voltage steps from the resting potential in the dark (-60 mV) evoked slow, inward Ca(2+)-dependent currents which could be blocked by Co2+, Mg2+, or Cd2+. The Ca2+ currents were followed by large outward currents that persisted for many seconds after the offset of moderate or large pulses. These tail currents increased in magnitude and duration with pulse duration and reversed at about -80 mV, consistent with previous evidence for a Ca(2+)-activated K+ conductance in this membrane. When the Ca(2+)-activated outward current was reduced to zero by increasing the [K+]o so as to set EK at -20 mV, and then stepping the voltage to this value, the step evoked a steady inward Ca2+ current. Thus, the Ca2+ current did not show voltage- or Ca(2+)-dependent inactivation. When Ba2+ was substituted for Ca2+, 500-ms depolarizing steps evoked steady inward currents but no outward currents. In any given experiment, the activation voltage of the Ca2+ or Ba2+ current did not depend on holding potential. At the barnacle photoreceptor's synapse, the postsynaptic cell adapts to maintained presynaptic voltage by a mechanism that is not understood. We conclude that neither Ca2+ current inactivation nor a shift in activation voltage with holding potential can account for this adaptation.
我们使用一种准电压钳装置，描述了巨型藤壶（Balanus nubilus）四个中位光感受器突触前膜上流动的电流。在一个光感受器的终末区域测量的膜电位，通过包含光感受器轴突的神经所提供的反馈电流，在所有四个终末中得到控制。降低盐溶液中的[Ca2+]o以减少Ca2+电流，从而实现更好的电压控制，并添加四乙铵离子（TEA，20 mM）来阻断快速电压依赖性K+电导。从黑暗中的静息电位（-60 mV）进行去极化电压阶跃，会诱发缓慢的内向Ca(2+)依赖性电流，该电流可被Co2+、Mg2+或Cd2+阻断。Ca2+电流之后是大的外向电流，在中等或大脉冲结束后会持续许多秒。这些尾电流的幅度和持续时间随脉冲持续时间增加，并在约-80 mV时反转，这与该膜中存在Ca(2+)激活的K+电导的先前证据一致。当通过增加[K+]o将Ca(2+)激活的外向电流降低到零时，使EK设置为-20 mV，然后将电压阶跃到该值，该阶跃会诱发稳定的内向Ca2+电流。因此，Ca2+电流未表现出电压或Ca(2+)依赖性失活。当用Ba2+替代Ca2+时，500毫秒的去极化阶跃会诱发稳定的内向电流，但没有外向电流。在任何给定的实验中，Ca2+或Ba2+电流的激活电压不依赖于钳制电位。在藤壶光感受器的突触处，突触后细胞通过一种尚不清楚的机制适应持续的突触前电压。我们得出结论，Ca2+电流失活或激活电压随钳制电位的变化都不能解释这种适应现象。
