Alkon D L, Sakakibara M
Biophys J. 1985 Dec;48(6):983-95. doi: 10.1016/S0006-3495(85)83861-3.
Light-induced currents were measured with a two-microelectrode voltage clamp of type B photoreceptor somata, which had been isolated by axotomy from all synaptic interactions as well as from all membranes capable of generating impulse activity. In artificial seawater (ASW), light elicited a transient early inward current, INa+, which depended on Na+o and had a linear current-voltage relation and an extrapolated reversal potential of 30-40 mV (absolute). In 0-Na+ ASW, light elicited a transient short-latency outward current that dependent on K+o, increased exponentially with more positive voltages (greater than or equal to -40 mV), and reversed at -70 to -75 mV. This outward current was not blocked by Ca++ channel blockers (e.g., Cd++, Co++) or substitution of Ba++o, for Ca++o, but was reduced by iontophoretic injection of EGTA. In both ASW and 0-Na+ ASW, light also elicited a delayed, apparently inward current, which was associated with a decreased conductance, depended on K+o, increased exponentially with more positive voltages (greater than or equal to -40 mV), reversed at the equilibrium potential for K+ flux in elevated K+o was eliminated by substitution of Ba++o for Ca++o, and was greatly reduced by Cd++o or Co++o. Thus, light elicited an early Ca++-dependent K+ current, IC, and a prolonged decrease of IC. Iontophoretic injection of Ca++ through a third microelectrode caused prolonged reduction of both IC and the light-induced decrease of IC, but did not alter ICa++ or the current-voltage relation of IC. Ruthenium red (1 microM) in the external medium caused a prolongation of the light-induced decrease of IC. Iontophoretic injection of EGTA often eliminated the light-induced IC decrease while decreasing peak IC (during depolarizing steps to -5 or 0 mV) by less than one-half. EGTA injection, on the average, did not affect steady state IC but reduced the light-induced decrease of steady state IC to approximately one-third of its original magnitude. The prolonged IC decrease, elicited by dim light in the absence of light-induced IC or INa+, was more completely eliminated by EGTA injection. It was concluded that light, in addition to inducing a transient inward Na+ current, causes both a transient increase and a prolonged decrease of IC via elevation of Ca++i.
采用双微电极电压钳测量B型光感受器胞体的光诱导电流，这些胞体已通过轴突切断术与所有突触相互作用以及所有能够产生冲动活动的膜隔离开来。在人工海水（ASW）中，光引发一个短暂的早期内向电流，即INa +，它依赖于细胞外Na +（Na+o），具有线性电流 - 电压关系，外推反转电位为30 - 40 mV（绝对值）。在无Na +的ASW中，光引发一个短暂的短潜伏期外向电流，该电流依赖于细胞外K +（K+o），在更正的电压（大于或等于 - 40 mV）下呈指数增加，并在 - 70至 - 75 mV处反转。这种外向电流不被Ca++通道阻滞剂（如Cd++、Co++）阻断，也不会因用Ba++o替代Ca++o而受到影响，但通过离子电泳注入乙二醇双乙醚二胺四乙酸（EGTA）会使其减小。在ASW和无Na +的ASW中，光还引发一个延迟的、明显的内向电流，该电流与电导降低有关，依赖于K+o，在更正的电压（大于或等于 - 40 mV）下呈指数增加，在高K+o中K+通量的平衡电位处反转，用Ba++o替代Ca++o可消除该电流，而Cd++o或Co++o可使其大幅降低。因此，光引发一个早期的Ca++依赖性K +电流，即IC，以及IC的持续降低。通过第三个微电极离子电泳注入Ca++会导致IC和光诱导的IC降低均持续减少，但不会改变ICa++或IC的电流 - 电压关系。外部介质中的钌红（1 microM）会导致光诱导的IC降低持续时间延长。离子电泳注入EGTA通常会消除光诱导的IC降低，同时使峰值IC（在去极化至 - 5或0 mV期间）降低不到一半。平均而言，EGTA注入不影响稳态IC，但将光诱导的稳态IC降低幅度减小至其原始幅度的约三分之一。在没有光诱导的IC或INa +的情况下，由暗光引发的IC持续降低被EGTA注入更完全地消除。得出的结论是，光除了诱导短暂的内向Na +电流外，还通过升高细胞内Ca++（Ca++i）导致IC的短暂增加和持续降低。
