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Cytoskeletal transition at the paranodes: the Achilles' heel of myelinated axons

Published online by Cambridge University Press:  15 March 2007

Aurea D. Sousa
Affiliation:
Current address: Section on Structural Cell Biology, NIDCD/NIH, 50 South Drive, Bldg 50 Rm.4249, Bethesda, MD 20892-8027, USA
Manzoor A. Bhat*
Affiliation:
Department of Cell and Molecular Physiology, Curriculum in Neurobiology, Neurodevelopmental Disorders Research Center and, UNC-Neuroscience Center, University of North Carolina School of Medicine, Chapel Hill, NC, USA
*
Correspondence should be addressed to Manzoor Bhat PhD., Neuroscience Research Building #5109F, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7545, USA phone: +1 919 966 1018 fax: +1 919 843 2777 email: Manzoor_Bhat@med.unc.edu

Abstract

Myelination organizes axons into distinct domains that allow nerve impulses to propagate in a saltatory manner. The edges of the myelin sheath are sealed at the paranodes by axon–glial junctions that have a crucial role in organizing the axonal cytoskeleton. Here we propose a model in which the myelinated axons depend on the axon–glial junctions to stabilize the cytoskeletal transition at the paranodes. Thus paranodal regions are likely to be particularly susceptible to damage induced by demyelinating diseases such as multiple sclerosis.

Type
Review Article
Copyright
Copyright © Cambridge University Press 2007

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