from neuronal injury tends to be more commonly feasible in the central nervous
system (CNS) than peripheral nervous system (PNS). In PNS, axon regeneration
takes place with ease whereas in CNS, the process of regeneration is very slow
and inefficient. There are different
types of neural injuries that can occur. Chromatolysis is one form, in which the Nissl bodies of a neuron disintegrate and although
this disintegration happens in both PNS and CNS, it is much more common in the
CNS. When a nerve is cut or damaged, Wallerian degeneration occurs. This is
when the site furthest away from the soma (cell body) starts to disintegrate
first, followed by myelin clearance. The part closest to the source of injury –
proximal segment- initially sends out growth cones as a response signal to the
injury. These growth cones in early development would allow axons to regrow but
in adulthood, CNS axons cannot regrow. This is different to PNS axons which can
retain their ability to regenerate over long distances even through adulthood.
(Bear, Connors and Paradiso, 2006).
are three key difference between axon regeneration in the two nervous systems;
the respective environments, speed at which debris are cleared and whether
remyelination is supported or inhibited. Starting off with the PNS, response to
injury in this nervous system is very rapid and efficient. If an axon is cut or
damaged, Schwann cells (PNS glia) produce growth factors that induce regeneration
of 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’t
elicited (Heubner et al,2009).
contrast to this is the CNS response to injury. Here, clearance of debris is
much slower, allowing enough time to pass so that an aggressive and cytotoxic immune
response takes place. Growth factors produced by the oligodendrocytes (CNS
glia) do not promote remyelination, unlike the growth factors excreted by
Schwann cells, so this makes regeneration that much more difficult.
Remyelination of axons is also quite poor compared to PNS because these oligodendrocytes
die after axonal injury, making them totally redundant as myelin generators,
unlike Schwann cells. The presence of proteoglycans and uncleared debris leads
to an inadequate expression of supporting growth factors, which once again
restricts CNS axon regeneration capacity (Gaudet et al, 2011).