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 (IK,A) results in broadening of somatic spikes. Similarly, in a compartmental model of the photoreceptor, reducing the maximum A-type K+ conductance (gK,Amax) results in broadening of somatic spikes. However, simulations predict that little or no broadening of axonal spikes occurs when gK,Amax is reduced. The results can be explained by the voltage-dependent properties of IK,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.