Antidromic propagation of action potentials in branched axons: implications for the mechanisms of action of deep brain stimulation.

Journal Article (Journal Article)

Electrical stimulation of the central nervous system creates both orthodromically propagating action potentials, by stimulation of local cells and passing axons, and antidromically propagating action potentials, by stimulation of presynaptic axons and terminals. Our aim was to understand how antidromic action potentials navigate through complex arborizations, such as those of thalamic and basal ganglia afferents-sites of electrical activation during deep brain stimulation. We developed computational models to study the propagation of antidromic action potentials past the bifurcation in branched axons. In both unmyelinated and myelinated branched axons, when the diameters of each axon branch remained under a specific threshold (set by the antidromic geometric ratio), antidromic propagation occurred robustly; action potentials traveled both antidromically into the primary segment as well as "re-orthodromically" into the terminal secondary segment. Propagation occurred across a broad range of stimulation frequencies, axon segment geometries, and concentrations of extracellular potassium, but was strongly dependent on the geometry of the node of Ranvier at the axonal bifurcation. Thus, antidromic activation of axon terminals can, through axon collaterals, lead to widespread activation or inhibition of targets remote from the site of stimulation. These effects should be included when interpreting the results of functional imaging or evoked potential studies on the mechanisms of action of DBS.

Full Text

Duke Authors

Cited Authors

  • Grill, WM; Cantrell, MB; Robertson, MS

Published Date

  • February 2008

Published In

Volume / Issue

  • 24 / 1

Start / End Page

  • 81 - 93

PubMed ID

  • 17562157

Electronic International Standard Serial Number (EISSN)

  • 1573-6873

International Standard Serial Number (ISSN)

  • 0929-5313

Digital Object Identifier (DOI)

  • 10.1007/s10827-007-0043-9


  • eng