An array of rapidly inactivating voltage-gated K~+ channels is distributed throughout the nervous systems of vertebrates and invertebrates. Although these channels are thought to regulate the excitability of neurons by attenuating voltage signals, their specific functions are often poorly understood. We studied the role of the prototypical inactivating K~+ conductance, Shaker, in Drosophila photoreceptors by recording intracellularly from wild-type and Shaker mutant photoreceptors. Here we show that loss of the Shaker K~+ conductance produces a marked reduction in the signal-to-noise ratio of photoreceptors, generating a 50% decrease in the information capacity of these cells in fully light-adapted conditions. By combining experiments with modelling, we show that the inactivation of Shaker K~+ channels amplifies voltage signals and enables photoreceptors to use their voltage range more effectively. Loss of the Shaker conductance attenuated the voltage signal and induced a compensatory decrease in impedance. Our results demonstrate the importance of the Shaker K~+ conductance for neural coding precision and as a mechanism for selectively amplifying graded signals in neurons, and highlight the effect of compensatory mechanisms on neur-onal information processing.
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机译：一系列快速失活的电压门控钾离子通道分布在脊椎动物和无脊椎动物的神经系统中。尽管人们认为这些通道通过衰减电压信号来调节神经元的兴奋性，但人们对其功能的了解却很少。我们通过从野生型和Shaker突变型光感受器的细胞内记录，研究了果蝇光感受器中典型的K + +电导灭活剂Shaker的作用。在这里，我们表明，摇床K +电导率的损失会显着降低感光器的信噪比，从而在完全光适应的条件下使这些细胞的信息容量降低50％。通过将实验与建模相结合，我们表明，振荡器K〜+通道的失活会放大电压信号，并使感光器更有效地利用其电压范围。摇床电导的损失会衰减电压信号，并导致阻抗的补偿性下降。我们的结果证明了Shaker K +电导对神经编码精度的重要性以及作为选择性放大神经元中分级信号的机制的重要性，并突出了补偿机制对神经信息处理的影响。
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