title: The axon as a physical structure in health and acute trauma.
abstract: The physical structure of neurons - dendrites converging on the soma, with an axon conveying activity to distant locations - is uniquely tied to their function. To perform their role, axons need to maintain structural precision in the soft, gelatinous environment of the central nervous system and the dynamic, flexible paths of nerves in the periphery. This requires close mechanical coupling between axons and the surrounding tissue, as well as an elastic, robust axoplasm resistant to pinching and flattening, and capable of sustaining transport despite physical distortion. These mechanical properties arise primarily from the properties of the internal cytoskeleton, coupled to the axonal membrane and the extracellular matrix. In particular, the two large constituents of the internal cytoskeleton, microtubules and neurofilaments, are braced against each other and flexibly interlinked by specialised proteins. Recent evidence suggests that the primary function of neurofilament sidearms is to structure the axoplasm into a linearly organised, elastic gel. This provides support and structure to the contents of axons in peripheral nerves subject to bending, protecting the relatively brittle microtubule bundles and maintaining them as transport conduits. Furthermore, a substantial proportion of axons are myelinated, and this thick jacket of membrane wrappings alters the form, function and internal composition of the axons to which it is applied. Together these structures determine the physical properties and integrity of neural tissue, both under conditions of normal movement, and in response to physical trauma. The effects of traumatic injury are directly dependent on the physical properties of neural tissue, especially axons, and because of axons' extreme structural specialisation, post-traumatic effects are usually characterised by particular modes of axonal damage. The physical realities of axons in neural tissue are integral to both normal function and their response to injury, and require specific consideration in evaluating research models of neurotrauma.
authors.affiliation: School of Medicine, University of Tasmania, Australia; Wicking Dementia Research and Education Centre, Faculty of Health, University of Tasmania, Australia. Electronic address: matthew.kirkcaldie@utas.edu.au.
authors.forename: Matthew T K
authors.initials: MT
authors.lastname: Kirkcaldie
authors.affiliation: Wicking Dementia Research and Education Centre, Faculty of Health, University of Tasmania, Australia.
authors.forename: Jessica M
authors.initials: JM
authors.lastname: Collins
mesh_terms: D000818:Animals; D001369:Axons / Q000473:pathology* / Q000502:physiology* / Q000648:ultrastructure; D001930:Brain Injuries / Q000473:pathology*; D003599:Cytoskeleton / Q000473:pathology; D006801:Humans; D008870:Microtubules / Q000473:pathology
keywords: Axon; Cytoskeleton; Diffuse axonal injury; Myelin; Neurofilaments; Neurotrauma; Traumatic axonal injury