Recoveryfrom neuronal injury tends to be more commonly feasible in the central nervoussystem (CNS) than peripheral nervous system (PNS). In PNS, axon regenerationtakes place with ease whereas in CNS, the process of regeneration is very slowand inefficient. There are differenttypes of neural injuries that can occur. Chromatolysis is one form, in which the Nissl bodies of a neuron disintegrate and althoughthis disintegration happens in both PNS and CNS, it is much more common in theCNS.
When a nerve is cut or damaged, Wallerian degeneration occurs. This iswhen the site furthest away from the soma (cell body) starts to disintegratefirst, followed by myelin clearance. The part closest to the source of injury –proximal segment- initially sends out growth cones as a response signal to theinjury.
These growth cones in early development would allow axons to regrow butin adulthood, CNS axons cannot regrow. This is different to PNS axons which canretain their ability to regenerate over long distances even through adulthood.(Bear, Connors and Paradiso, 2006).Thereare three key difference between axon regeneration in the two nervous systems;the respective environments, speed at which debris are cleared and whetherremyelination is supported or inhibited. Starting off with the PNS, response toinjury in this nervous system is very rapid and efficient. If an axon is cut ordamaged, Schwann cells (PNS glia) produce growth factors that induce regenerationof the damaged axon (Giger et al, 2010). Cellular debris such as lipids, MAG,NoGo and OMgp are cleared quickly enough so that an inflammatory response isn’telicited (Heubner et al,2009). A starkcontrast to this is the CNS response to injury.
Here, clearance of debris ismuch slower, allowing enough time to pass so that an aggressive and cytotoxic immuneresponse takes place. Growth factors produced by the oligodendrocytes (CNSglia) do not promote remyelination, unlike the growth factors excreted bySchwann cells, so this makes regeneration that much more difficult.Remyelination of axons is also quite poor compared to PNS because these oligodendrocytesdie after axonal injury, making them totally redundant as myelin generators,unlike Schwann cells. The presence of proteoglycans and uncleared debris leadsto an inadequate expression of supporting growth factors, which once againrestricts CNS axon regeneration capacity (Gaudet et al, 2011).