Internodal sodium channels ensure active processes under myelin manifesting in depolarizing afterpotentials

A possible link of oxaliplatin‐induced neuropathy with potassium channel deficit

“…In any case, after the passing of a saltatory action potential (sAP), and of the internodal action potentials induced by it, 26 transition zones were formed at the boundaries of the internodal region devoid of potassium channels. 27 In turn, these zones became sources of internodal action potentials that back-propagated to the closest nodes.…”

“…To simulate processes in an MA we used a multicable Hodgkin-Huxley-type model 26 consisting of 21 nodes and 20 internodes. Figure 1 is a schematic drawing of a half of the node-to-node portion of an MA, the terms used, and lengths of the different axon regions.…”

“…[28][29][30][31][32] Ionic accumulation in periaxonal and intracellular spaces was taken into account. 26,27 The simulations were initiated by intracellular stimulation of the first node of Ranvier by a single rectangular current pulse with an intensity of 14 nA and duration 50 ls applied at time zero. Channel gating (G) for sodium (na) as well as for fast (kf) and slow (ks) potassium ions is summarized as follows 33 :…”

“…Adelsberger et al 21 found no effect of oxaliplatin on potassium channels, which is in contrast to studies reporting an effect of oxaliplatin on potassium channels in frog 23 and adult rat 25 peripheral myelinated axons (MA). Dimitrov 26 proposed a model predicting that the very thin periaxonal space (about a few nanometers) made the low density of internodal sodium channels sufficient for generation of active internodal processes. Based on this model, a mechanism of MA hyperactivity, 27 induced by blockage of internodal potassium channels, was proposed.…”

Differences in Membrane Properties in Simulated Cases of Demyelinating Neuropathies: Internodal Focal Demyelinations with Conduction Block

“…electrotonic potentials) as well as the excitability properties in the case of adaptation to be investigated. The papers with complicated geometry of paranodal region [30,31] cannot simulate and do not investigate the processes of accommodation and adaptation which are the basis of our investigations. Nevertheless these limitations, our double cable model still remains the only one in literature describing the membrane properties of normal and abnormal human myelinated nerve fibres.…”