Neuron-glia interactions at the node of Ranvier.
Rapid, faithful, and efficient action potential propagation in mammalian axons is a consequence of myelin and clustered Na+ channels. Both myelination and node of Ranvier formation require complex intercellular interactions between neurons and glia that result in profound molecular, morphological, and functional changes in each cell type. This review will focus on the molecular and cellular mechanisms that underlie neuron-glia interactions at the node of Ranvier. In particular, the proteins and protein complexes, and how they participate in node of Ranvier formation and maintenance, will be discussed. Traditionally, myelinating glia have been viewed as merely passive players in neuronal function, conferring on the axons they ensheath various electrical properties that facilitate action potential conduction. However, it is now recognized that this view is incomplete. This review will discuss several examples illustrating how myelinating glia actively regulate the excitable properties of axons including the kinds of channels expressed and their subcellular localization.
Rasband
Matthew N
MN
Department of Neuroscience, University of Connecticut Health Center, Farmington 06030-3401, USA. Rasband@uchc.edu
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001369:Axons / Q000378:metabolism; D007473:Ion Channels / Q000502:physiology; D009186:Myelin Sheath / Q000378:metabolism; D009413:Nerve Fibers, Myelinated / Q000502:physiology; D009457:Neuroglia / Q000166:cytology / Q000502:physiology* / Q000648:ultrastructure; D009474:Neurons / Q000166:cytology / Q000502:physiology* / Q000648:ultrastructure; D011901:Ranvier's Nodes / Q000378:metabolism* / Q000648:ultrastructure; D015222:Sodium Channels / Q000378:metabolism
D007473:Ion Channels; D015222:Sodium Channels