Şeniz DEMİRYÜREK?,º, A. Tuncay DEMİRYÜREK??, Aydan BABÜL?

*Gazi University, Faculty of Pharmacy, Departmant of Physiology, 06330 Etiler, Ankara, TURKEY.
**Gazi University, Faculty of Medicine, Department of Pharmacology, 06330 Etiler, Ankara, TURKEY.
oCorresponding Author

Summary:
Axon degeneration occurs as a consequence of various nerve injuries including mechanical, metabolic, toxic, inflammatory, and heritable as well as ischaemic/hypoxic insults. Axonal endbulbs, structures that form at the proximal end of the transacted axons, release peptides and other molecules into the injury milieu where they may exert local actions, including those on microcirculation. Nerve injury leads to changes of the distal nerve segment known as Wallerian degeneration. Macrophages, recruited to the distal segment, remove the vast majority of myelin debris. Molecular changes in the distal segment include the release of neurotrophins, neural cells adhesion molecules, cytokines and other soluble factors and the up-regulation of their receptors. It is known that axon degeneration is associated with influx of Na+ and Ca+2 and efflux of K+. Free radicals may have beneficial effects on neuronal survival provided that their intraneuronal concentrations are maintained at low levels. Antioxidants may protect neurons subjected to an oxidative stress following axotomy or trophic factor-deprivation. The rate of axon degeneration is slower at cooler temperatures and with aging. Axonal injury not only induces muscle weakness and loss of sensation but also leads to adaptive changes and neuropathic pain. A better definition of the underlying mechanisms of peripheral nerve degeneration will be effective for the development and successful treatment methods of peripheral nerve injury.