The Node of Ranvier as an Interface for Axo-Glial Interactions: Perturbation of Axo-Glial Interactions in Various Neurological Disorders

The action potential conduction along the axon is highly dependent on the healthy interactions between the axon and myelin-producing glial cells. Myelin, which facilitates action potential, is the protective insulation around the axon formed by Schwann cells and oligodendrocytes in the peripheral (PNS) and central nervous system (CNS), respectively. Myelin is a continuous structure with intermittent gaps called nodes of Ranvier, which are the sites enriched with ion channels, transmembrane, scaffolding, and cytoskeletal proteins. Decades-long extensive research has identified a comprehensive proteome with strictly regularized localization at the node of Ranvier. Concurrently, axon-glia interactions at the node of Ranvier have gathered significant attention as the pathophysiological targets for various neurodegenerative disorders. Numerous studies have shown the alterations in the axon-glia interactions culminating in neurological diseases. In this review, we have provided an update on the molecular composition of the node of Ranvier. Further, we have discussed in detail the consequences of disruption of axon-glia interactions during the pathogenesis of various CNS and PNS disorders.

Automated summary

The conduction of action potential along the axon relies heavily on the interaction between the axon and myelin-producing glial cells. Myelin, formed by Schwann cells in the peripheral nervous system and oligodendrocytes in the central nervous system, serves as insulation and facilitates action potential. The nodes of Ranvier, intermittent gaps along the myelin sheath, play a crucial role in this process. Research has identified a comprehensive proteome at the nodes of Ranvier and highlighted the importance of axon-glia interactions in various neurological disorders. This review provides an update on the molecular composition of the nodes of Ranvier and discusses the consequences of disrupted axon-glia interactions in CNS and PNS disorders.