Somata of primary sensory neurons are thought to contribute to the ectopic neural discharge that is implicated as a cause of some forms of neuropathic pain. Spiking is triggered by subthreshold membrane potential oscillations that reach threshold. Oscillations, in turn, appear to result from reciprocation of a fast TTX-S Na⁺ current (INa⁺) and a passive outward IK+. We previously simulated oscillatory behavior using a transient Hodgkin-Huxley type voltage-dependent INa+ and ohmic leak. This model, however, diverged from oscillatory parameters seen in live cells and failed to produce characteristic ectopic discharge patterns. Here we show that use of a more complete set of Na⁺ conductances that includes several delayed components enables simulation of the entire repertoire of oscillation-triggered electrogenic phenomena seen in live DRG neurons. This includes a physiological window of induction and natural patterns of spike discharge. An INa⁺ component at 2-20 msec was particularly important even though it represented only a tiny fraction of overall INa⁺ amplitude. With the addition of a delayed rectifier IK⁺ the singlet firing seen in some DRG neurons can also be simulated. The model reveals the key conductances that underlie afferent ectopia, conductances that are potentially attractive targets in the search for more effective treatments of neuropathic pain.