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.
Elliott
J R
JR
Department of Anatomy and Physiology, University of Dundee, UK. j.r.elliott@dundee.ac.uk
D000200:Action Potentials; D000818:Animals; D001369:Axons / Q000502:physiology*; D003198:Computer Simulation; D004553:Electric Conductivity; D007700:Kinetics; D008433:Mathematics; D008959:Models, Neurological; D009475:Neurons, Afferent / Q000502:physiology*; D010146:Pain / Q000503:physiopathology*; D015221:Potassium Channels / Q000502:physiology*; D015222:Sodium Channels / Q000502:physiology*
D015221:Potassium Channels; D015222:Sodium Channels