Slow Na+ channel inactivation and bursting discharge in a simple model axon: implications for neuropathic pain.

Neuropathic pain may result from sustained firing of sensory neurones. The questions are what initiates and what stops that firing? Spontaneous firing of a modified Hodgkin-Huxley model axon is induced here by: (1) a depolarizing shift in the K+ channel activation parameter; and (2) a positive change in the K+ equilibrium potential. The duration and pattern of spontaneous discharge is seen to be critically dependent on the level and kinetics of Na+ channel slow inactivation. Slow inactivation of voltage-gated ion channels could be major factors in the induction and treatment of neuropathic pain.