A model for axonal propagation incorporating both radial and axial ionic transport.
We present an axonal model that explicitly includes ionic diffusion in the intracellular, periaxonal, and extracellular spaces and that incorporates a Hodgkin-Huxley membrane, extended with potassium channel inactivation and active ion transport. Although ionic concentration changes may not be significant in the time course of one action potential, they are important when considering the long-term behavior (seconds to minutes) of an axon. We demonstrate this point with simulations of transected axons where ions are moving between the intra- and extracellular spaces through an opening that is sealing with time. The model predicts that sealing must occur within a critical time interval after the initial injury to prevent the entire axon from becoming permanently depolarized. This critical time interval becomes considerably shorter when active ion transport is disabled. Furthermore, the model can be used to study the effects of sodium and potassium channel inactivation; e.g., sodium inactivation must be almost complete (within 0.02%) to obtain simulation results that are realistic.
Department of Physics and Astronomy, Vanderbilt University, Nashville, Tennessee 37235.
J M
JM
van Egeraat
J P
JP
Wikswo
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001369:Axons / Q000502:physiology*; D055592:Biophysical Phenomena; D001703:Biophysics; D049832:Decapodiformes; D004058:Diffusion; D004594:Electrophysiology; D066298:In Vitro Techniques; D017136:Ion Transport / Q000502:physiology; D008280:Magnetics; D008959:Models, Neurological; D015221:Potassium Channels / Q000378:metabolism; D015222:Sodium Channels / Q000378:metabolism
D015221:Potassium Channels; D015222:Sodium Channels