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

Brain Res. 1997 Apr 18;754(1-2):221-6. doi: 10.1016/s0006-8993(97)00072-3.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Action Potentials
  • Animals
  • Axons / physiology*
  • Computer Simulation
  • Electric Conductivity
  • Kinetics
  • Mathematics
  • Models, Neurological*
  • Neurons, Afferent / physiology*
  • Pain / physiopathology*
  • Potassium Channels / physiology*
  • Sodium Channels / physiology*

Substances

  • Potassium Channels
  • Sodium Channels