Internodal mechanism of pathological afterdischarges in myelinated axons

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).

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.

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.

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.