The Role of Myelin in Malfunctions of Neuron Transmittance

•Wave-type model of saltatory conduction is formulated in terms of synchronized plasmon-polariton oscillations.•The speed of plasmon-polariton signal in myelinated axons agrees with observed velocity of saltatory conduction.•The plasmon-polariton kinetics reveals a control role of the myelin thickness in agreement with observations.•Variation in the thickness of myelin disrupts neuronal signaling in a different way than previously thought.•The plasmon-polariton model is supported by micro-saltatory conduction in ultra-thin C-fibers of pain sensation. Because of different mechanism of electro-signaling in myelinated axons than in dendrites or unmyelinated axons, the role of the myelin needs to be reconsidered upon new premises in distinction to conventional cable model. It occurs that the latter model is inapplicable for so-called saltatory conduction in myelinated axons and the former imagination on the role of the myelin based on the cable model is confusing. We show how the myelin sheath of axons controls the electro-signaling in myelinated neurons upon a wave-type ionic oscillation model of electro-signaling, ion plasmon-polariton model, in close agreement with observations of the saltatory conduction not reachable within traditional cable model approach. This is of particular importance for better understanding of malfunctions of neuron communication due to demyelination diseases and for the strategy of future therapy methods at paralysis and at demyelination syndromes. The new mechanism of signaling in myelinated neurons is also supported by recent advances in recognition of so-called micro-saltatory conduction in C-fibers of pain sensation, also exceeding the range of applicability of the conventional cable model.