Abstract
Neural-dependent functions are lost when traumatic injury to peripheral nerves severs their axons. Functions recover successfully when axons regenerate rapidly so that prompt reinnervation and restoration of function can follow. Repair fails when regeneration and reinnervation are delayed. The timing of regeneration and reinnervation is affected by the type of injury, the distance of the lesion site from the target tissues, and the nature of cellular and molecular events of Wallerian degeneration that injury induces in the nerve segment situated distal to the lesion site and through which the severed axons regenerate back to their target tissues. Wallerian degeneration is essential to repair because it renders the peripheral nerve tissue permissive to and supportive of axonal regeneration. In this context, innate immunity is central to Wallerian degeneration and repair because innate-immune cells, molecules, and functions control Wallerian degeneration.
Original language | English |
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Title of host publication | Nerves and Nerve Injuries |
Subtitle of host publication | Pain, Treatment, Injury, Disease and Future Directions: Vol 2 |
Publisher | Elsevier |
Pages | 611-628 |
Number of pages | 18 |
Volume | 2 |
ISBN (Electronic) | 9780128026533 |
ISBN (Print) | 9780128026953 |
DOIs | |
State | Published - 1 Jan 2015 |
Bibliographical note
Publisher Copyright:© 2015 Elsevier Ltd. All rights reserved.
Keywords
- Axonal regeneration
- Cytokine
- Inflammation
- Innate-immunity cells
- Macrophage
- Myelin
- Phagocytosis
- Schwann cell
- Wallerian degeneration