In the Aplysia mechanoafferent B21, afferent transmission is in part regulated via the control of active spike propagation. When B21 is peripherally activated at its resting membrane potential, spikes fail to propagate to an output process, and afferent transmission does not occur. In this report we show that the propagation failure is in part a result of the fact that the somatic region of B21 is relatively inexcitable. We isolate this region and demonstrate that net currents evoked by depolarizing pulses are outward. Furthermore, we show that all or none spikes are not triggered when current is injected. Previous reports have, however shown that spiking is triggered when current is somatically injected, and cells are intact. We demonstrate that spikes evoked under these circumstances do not originate in the soma. Instead they originate in an adjacent part of the neuron that is excitable (the medial process). In summary we show that the mechanoafferent B21 consists of excitable input and output processes separated by a relatively inexcitable somatic region. A potential advantage of this arrangement is that somatic depolarization can be used to modify spike propagation from the input to the output processes without altering the encoding of peripherally generated activity.