Axotomy

Axotomy
Intervention
MeSH	D019771
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An axotomy is the cutting or otherwise severing of an axon. Derived from axo- (=axon) and -tomy (=surgery). This type of denervation is often used in experimental studies on neuronal physiology and neuronal death or survival as a method to better understand nervous system diseases.

Axotomy may cause neuronal cell death, especially in embryonic or neonatal animals, as this is the period in which neurons are dependent on their targets for the supply of survival factors. In mature animals, where survival factors are derived locally or via loops, axotomy of peripheral neurons and motoneurons can lead to a robust regenerative response without any neuronal death. In both cases, autophagy is observed to markedly increase. Autophagy could either clear the way for neuronal degeneration or it could be a medium for cell destruction.

Upon injury of a peripheral axon, the entire neuron immediately reacts in order to regenerate the axon. This reaction requires an increased metabolic activity and is initiated by chromatolysis. Chromatolysis is characterized as the dissolution of protein-producing structures in the cell body of a neuron and is a term used to characterize apoptosis of neuronal cells. During chromatolysis, the soma and nucleus round and enlarge, the Nissl bodies and Golgi bodies both disintegrate, and the cytocentrum is cleared. In most cases, the axotomy response in peripheral axons ends in cell healing and regeneration, though it may occasionally end in cell death. Regeneration occurs because of microglial hyperplasia and astroglial hypertrophy, activities that are lacking in the central axotomy response.

In contrast to the peripheral response, the axotomy response in central neurons (neurons in the Central Nervous System) almost always leads to cell death. Central neurons, upon being severed, generally fail to up-regulate the expression of trophic factors, a type of regeneration-associated protein. These trophic factors are responsible for the regulation of neuron vitality and are a critical aspect of neuroprotection. Trophic factors guarantee the survival of neuron synapsing, meaning they essentially maintain the functionality of the neuron. The lack of increased expression of these proteins will ultimately lead to cellular atrophy.

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