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

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,Amax) results in broadening of somatic spikes. However, simulations predict that little or no broadening of axonal spikes occurs when g_K,Amax 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. Action Editor: Jonathan D. Victor