The Axon-Myelin Unit in Development and Degenerative Disease

Axons are electrically excitable, cable-like neuronal processes that relay information between neurons within the nervous system and between neurons and peripheral target tissues. In the central and peripheral nervous systems, most axons over a critical diameter are enwrapped by myelin, which reduce...

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Main Authors: Ruth M. Stassart, Wiebke Möbius, Klaus-Armin Nave, Julia M. Edgar
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-07-01
Series:Frontiers in Neuroscience
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fnins.2018.00467/full
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spelling doaj-36cee101f16f499598b7b22a430b063c2020-11-24T20:50:18ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2018-07-011210.3389/fnins.2018.00467368527The Axon-Myelin Unit in Development and Degenerative DiseaseRuth M. Stassart0Ruth M. Stassart1Wiebke Möbius2Klaus-Armin Nave3Julia M. Edgar4Julia M. Edgar5Department of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, GermanyDepartment of Neuropathology, University Medical Center Leipzig, Leipzig, GermanyDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, GermanyDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, GermanyDepartment of Neurogenetics, Max-Planck-Institute of Experimental Medicine, Göttingen, GermanyInstitute of Infection, Immunity and Inflammation, College of Medical Veterinary and Life Sciences, University of Glasgow, Glasgow, United KingdomAxons are electrically excitable, cable-like neuronal processes that relay information between neurons within the nervous system and between neurons and peripheral target tissues. In the central and peripheral nervous systems, most axons over a critical diameter are enwrapped by myelin, which reduces internodal membrane capacitance and facilitates rapid conduction of electrical impulses. The spirally wrapped myelin sheath, which is an evolutionary specialisation of vertebrates, is produced by oligodendrocytes and Schwann cells; in most mammals myelination occurs during postnatal development and after axons have established connection with their targets. Myelin covers the vast majority of the axonal surface, influencing the axon's physical shape, the localisation of molecules on its membrane and the composition of the extracellular fluid (in the periaxonal space) that immerses it. Moreover, myelinating cells play a fundamental role in axonal support, at least in part by providing metabolic substrates to the underlying axon to fuel its energy requirements. The unique architecture of the myelinated axon, which is crucial to its function as a conduit over long distances, renders it particularly susceptible to injury and confers specific survival and maintenance requirements. In this review we will describe the normal morphology, ultrastructure and function of myelinated axons, and discuss how these change following disease, injury or experimental perturbation, with a particular focus on the role the myelinating cell plays in shaping and supporting the axon.https://www.frontiersin.org/article/10.3389/fnins.2018.00467/fulloligodendrocyteSchwann cellcytoskeletonaxonal transportenergyneuroinflammation
collection DOAJ
language English
format Article
sources DOAJ
author Ruth M. Stassart
Ruth M. Stassart
Wiebke Möbius
Klaus-Armin Nave
Julia M. Edgar
Julia M. Edgar
spellingShingle Ruth M. Stassart
Ruth M. Stassart
Wiebke Möbius
Klaus-Armin Nave
Julia M. Edgar
Julia M. Edgar
The Axon-Myelin Unit in Development and Degenerative Disease
Frontiers in Neuroscience
oligodendrocyte
Schwann cell
cytoskeleton
axonal transport
energy
neuroinflammation
author_facet Ruth M. Stassart
Ruth M. Stassart
Wiebke Möbius
Klaus-Armin Nave
Julia M. Edgar
Julia M. Edgar
author_sort Ruth M. Stassart
title The Axon-Myelin Unit in Development and Degenerative Disease
title_short The Axon-Myelin Unit in Development and Degenerative Disease
title_full The Axon-Myelin Unit in Development and Degenerative Disease
title_fullStr The Axon-Myelin Unit in Development and Degenerative Disease
title_full_unstemmed The Axon-Myelin Unit in Development and Degenerative Disease
title_sort axon-myelin unit in development and degenerative disease
publisher Frontiers Media S.A.
series Frontiers in Neuroscience
issn 1662-453X
publishDate 2018-07-01
description Axons are electrically excitable, cable-like neuronal processes that relay information between neurons within the nervous system and between neurons and peripheral target tissues. In the central and peripheral nervous systems, most axons over a critical diameter are enwrapped by myelin, which reduces internodal membrane capacitance and facilitates rapid conduction of electrical impulses. The spirally wrapped myelin sheath, which is an evolutionary specialisation of vertebrates, is produced by oligodendrocytes and Schwann cells; in most mammals myelination occurs during postnatal development and after axons have established connection with their targets. Myelin covers the vast majority of the axonal surface, influencing the axon's physical shape, the localisation of molecules on its membrane and the composition of the extracellular fluid (in the periaxonal space) that immerses it. Moreover, myelinating cells play a fundamental role in axonal support, at least in part by providing metabolic substrates to the underlying axon to fuel its energy requirements. The unique architecture of the myelinated axon, which is crucial to its function as a conduit over long distances, renders it particularly susceptible to injury and confers specific survival and maintenance requirements. In this review we will describe the normal morphology, ultrastructure and function of myelinated axons, and discuss how these change following disease, injury or experimental perturbation, with a particular focus on the role the myelinating cell plays in shaping and supporting the axon.
topic oligodendrocyte
Schwann cell
cytoskeleton
axonal transport
energy
neuroinflammation
url https://www.frontiersin.org/article/10.3389/fnins.2018.00467/full
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