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Role of A-type K+ channels in spike broadening observed in soma and axon of Hermissenda type-B photoreceptors: A simulation study

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Abstract

In Hermissenda type-B photoreceptors, the spike is generated in the axon and back-propagated to the soma, resulting in smaller somatic spikes. Experimentally, blocking the A-type K+ current (I K,A) results in broadening of somatic spikes. Similarly, in a compartmental model of the photoreceptor, reducing the maximum A-type K+ conductance (g K,A max) results in broadening of somatic spikes. However, simulations predict that little or no broadening of axonal spikes occurs when g K,A max is reduced. The results can be explained by the voltage-dependent properties of I K,A and the different potential ranges that the somatic and axonal spike traverse. Because of the steeper I-V curve and faster activation of the K+ channels at higher potentials, the recruitment of additional K+ channels in the axon is able to compensate for the decrease in K+ conductance, yielding less spike broadening. These results also support the idea that spike duration in the axon may not be reliably inferred based upon recordings collected from the soma.

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Correspondence to Yidao Cai.

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Action Editor: Jonathan D. Victor

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Cai, Y., Flynn, M., Baxter, D.A. et al. Role of A-type K+ channels in spike broadening observed in soma and axon of Hermissenda type-B photoreceptors: A simulation study. J Comput Neurosci 21, 89–99 (2006). https://doi.org/10.1007/s10827-006-7426-1

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  • DOI: https://doi.org/10.1007/s10827-006-7426-1

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