A low level of spontaneous impulse discharge is generated within dorsal root ganglia (DRGs) in intact animals, and this activity is enhanced following nerve injury. Many physiological stimuli present in vivo are capable of augmenting this ectopic discharge. Whatever their cause, episodes of sharply accelerated DRG firing tend to be followed by ‘after‐suppression’ during which discharge falls below baseline rate. In this study we examined the process of postexcitation suppression of firing rate, and how it shapes spike patterning in primary sensory neurons.

We recorded intracellularly from sensory neurons in excised rat DRGs in vitro. Trains of spikes triggered by intracellular current pulses evoked a prolonged hyperpolarizing shift. This shift appeared to be due to activation of a Ca²⁺‐dependent K⁺ conductance (g_K(Ca)). Spikes evoked by just‐suprathreshold pulses triggered a hyperpolarizing shift and spike cessation. As the shift decayed, spiking was restored. The net result was bursty (on–off) discharge, a previously unexplained peculiarity of ectopic discharge in some DRG neurons in vivo.

Conditioning nerve tetani delivered to axons of neurons which share the DRG with the impaled neuron evoked transient depolarization (‘cross‐depolarization’). However, when stimulus strength was increased so as to include the axon of the impaled neuron, the net result was a hyperpolarizing shift. Nerve stimulation that straddled the threshold of the axon of the impaled neuron drove it intermittently, but it always drove axons of at least some neighbouring neurons. The result was dynamic modulation of the membrane potential of the impaled neuron as cross‐depolarization and spike‐evoked hyperpolarizing shifts played off against one another. Membrane potential shifted in the hyperpolarizing direction whenever the axon was activated, and shifted in the depolarizing direction whenever it was silent. Dynamic modulation of this sort probably also occurs in vivo when stimuli are drawn over the surface of the skin.