Abstract

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.

Highlights

  • Neurons are highly polarized cells, with a long axon and shorter dendrites

  • The myelinic channel, which we suggest plays an important role in glial-mediated axonal maintenance, is best understood if the myelin sheath is “virtually unwrapped” (Figure 3B)

  • Taking advantage of the X-linked nature of the Plp1 gene and female heterozygotes harbouring a mosaic of wild type and PLP-deficient myelin, we demonstrated that secondary axonal changes, such as organelle-filled focal swellings, are localised to the internodes formed by the PLP-deficient myelin (Edgar et al, 2004)

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Summary

INTRODUCTION

Axons, which are the focus of this review, are unique among cellular processes, being capable of transmitting electrical impulses (spiking) and occupying, in many cases, an inordinately disproportionate amount of the neuron’s volume. Extrapolation to humans, of serially reconstructed EM data from the highly branched basal cholinergic neurons of the forebrain in mice, suggests that single neurons can have a total axon length of 100 m (Wu et al, 2014). This extraordinary cellular asymmetry is initiated during early development when neuronal polarisation is established (Schelski and Bradke, 2017). All subsequent growth and maintenance of the axon is enabled by bidirectional axonal transport comprising molecular motors and microtubule tracks that convey materials between the cell body and the axon

Paranode Septate junction Spheroid
The Ultrastructure of the Myelinated Axon
Constitute CNS White Matter and PNS
Axonal Dimensions
Axon Initial Segment
Signalling Regulate Axon and Myelin
Axonal Transport
Energy Use and Supply
GENERAL PATHOLOGY AND MECHANISMS OF AXONAL INJURY
Axonal Dysfunction
Caused by Oligodendroglial Defects
Caused by Schwann Cell Defects
Findings
HUMAN DISEASES
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