This study was supported by the Bulgarian Science Fund (DMU 03/72).
Internodal mechanism of pathological afterdischarges in myelinated axons
Article first published online: 11 SEP 2013
Copyright © 2013 Wiley Periodicals, Inc.
Muscle & Nerve
Volume 49, Issue 1, pages 47–55, January 2014
How to Cite
Dimitrov, A. G. and Dimitrova, N. A. (2014), Internodal mechanism of pathological afterdischarges in myelinated axons. Muscle Nerve, 49: 47–55. doi: 10.1002/mus.23874
- Issue published online: 16 DEC 2013
- Article first published online: 11 SEP 2013
- Accepted manuscript online: 12 APR 2013 04:10AM EST
- Manuscript Accepted: 5 APR 2013
- Bulgarian Science Fund. Grant Number: DMU 03/72
- potassium channel;
Introduction: Recent optical recordings of transmembrane potentials in the axons of pyramidal neurons have shown that the internodal action potentials (APs) predicted in our previous studies do exist. These novel processes are not well understood. In this study we aim to clarify electrical phenomena in peripheral myelinated axons (MAs). Methods: We used a multi-cable Hodgkin–Huxley-type model to simulate MAs with potassium channels that were either normal or inhibited along a short region of the internodal membrane. A brief stimulus was applied to the first node. Results: We demonstrated peculiarities in the internodal APs induced by a saltatory AP: They existed across internodal membranes, were detectable in periaxonal space but not in intracellular space, propagated continuously, collided near the mid-internodes, and produced internodal sources of afterdischarges. Conclusions: These results highlight the importance of the MA internodal regions as new therapeutic targets for avoiding afterdischarges provoked by reduced axonal fast potassium channel expression. Muscle Nerve 49: 47–55, 2014