Robustness of Neural Coding inDrosophilaPhotoreceptors in the Absence of Slow Delayed Rectifier K+Channels

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Abstract
Determining the contribution of a single type of ion channel to information processing within a neuron requires not only knowledge of the properties of the channel but also understanding of its function within a complex system. We studied the contribution of slow delayed rectifier K+channels to neural coding inDrosophilaphotoreceptors by combining genetic and electrophysiological approaches with biophysical modeling. We show that theShabgene encodes the slow delayed rectifier K+channel and identify a novel voltage-gated K+conductance. Analysis of thein vivorecorded voltage responses together with their computer-simulated counterparts demonstrates thatShabchannels inDrosophilaphotoreceptors attenuate the light-induced depolarization and prevent response saturation in bright light. We also show that reduction of theShabconductance in mutant photoreceptors is accompanied by a proportional drop in their input resistance. This reduction in input resistance partially restores the signaling range, sensitivity, and dynamic coding of light intensities ofShabphotoreceptors to those of the wild-type counterparts. However, loss of theShabchannels may affect both the energy efficiency of coding and the processing of natural stimuli. Our results highlight the role of different types of voltage-gated K+channels in the performance of the photoreceptors and provide insight into functional robustness against the perturbation of specific ion channel composition.