Owen W G, Torre V
Biophys J. 1983 Mar;41(3):325-39. doi: 10.1016/S0006-3495(83)84444-0.
The high-pass filtering of small signals by the rod photoreceptor network was studied by intracellular recording in the isolated, perfused retina of the toad, Bufo marinus. Data were analyzed and interpreted in terms of the network analysis described in the preceding paper. External concentrations of Cs+ as high as 10 mM, which blocked the relaxation from peak to plateau of the rod's response to bright light, did not affect the filtering of small signals. The effects of reducing [Na+]o were not consistent with a direct action upon the mechanism underlying this filtering property. By contrast, raising external [K+] from 2.6 to 10 mM, which caused a fourfold reduction in EK, abolished the high-pass filtering of small signals. Analysis of the effects of external [K+] changes indicates that the underlying mechanism involves a K+ conductance that decreases with a delay when the rod is hyperpolarized. This conductance is not blocked by externally applied tetraethylammonium. Other experiments did not rule out the possibility that it might be activated by Ca++.
通过在海蟾蜍（Bufo marinus）分离的灌注视网膜中进行细胞内记录，研究了视杆光感受器网络对小信号的高通滤波作用。根据前文所述的网络分析方法对数据进行了分析和解释。高达10 mM的外部Cs +浓度可阻断视杆对强光反应从峰值到平台期的弛豫，但不影响小信号的滤波。降低[Na + ] o的影响与对该滤波特性潜在机制的直接作用不一致。相比之下，将外部[K + ]从2.6 mM提高到10 mM，使E K降低了四倍，消除了小信号的高通滤波。对外部[K + ]变化影响的分析表明，潜在机制涉及一种K +电导，当视杆超极化时，该电导会延迟降低。这种电导不会被外部施加的四乙铵阻断。其他实验并未排除它可能被Ca ++激活的可能性。
