The recently assembled growth cone
starts to reuse material creating a prompt supply for the axon, process
facilitated by the action of the local synthesised proteins, inducing the
beginning of the regeneration process. Moreover, recently it has been outlined
the importance of protein expression control during the triggering of precise
signalling factors throughout the axonal reconstruction (Park, M. et. al 2013).

In addition, one more signalling
wave is perceived a few hours postinjury, usually between 4 and 6 hours, aiming
to comprise the principal injury signal composed of proteins that are locally
synthesised and translated in the wounded axon. Furthermore, JNK associating
protein joins axon vesicles to the damaged site and transport back the injury
signal by a retrograde pathway along the microtubules. Whilst the resting
potential of the membrane is re-established, the axon may form a growth cone or
a retraction bulb, this last one considered to be the non-growing counterparts
of the growth cones where the growth failure is associated to the non-stabilization
of the microtubules (Erturk, A. et. al 2007).

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Immediately after the PNS is injured
a prompt deluge of calcium happens at a harm axon tip that scopes over 1 Mm in
concentration (Bradke, F. et. al 2012). This intense ascent in intracellular
calcium is fundamental for activating axon recovery as neurons in a
free-calcium condition neglect to start axon outgrowth (Spira M.E. et.al 1997).
The calcium wave induces chromatin rebuilding leading to the first connection
between the damaged tip and the soma (Cho, Y. et. al 2013) and, as the
cytoskeleton endure restoration, it has been determined that its sealing rate
is proportional to the calcium-regulated proteins that take part in the process.
As a consequence of this series of events, the soma experiences chromatolysis
eliminating, therefore, the excitatory inputs preserving just the inhibitory
ones that would communicate with the damaged soma (Spejo, A., Oliveira, A.

Immediately after an injury is produced,
the regeneration pathway begins stimulating chemical changes and the
upregulation of a large number of genes, known as RAGs in the PNS -some of them
directly involved in neuronal regeneration-. It is also undergone the local synthesis
of proteins, alterations in the membrane excitability and signals communication
reaching the soma are also expected (Erna A. et.al 2016).


Conversely, PNS regeneration is robust due to the stimulatory
response Schwann cells develop on the axonal regeneration, which contrasts the
inhibitory reaction of oligodendroglia (Siegel G. J. et. al 1999). Scavenger
cells play a really important role in the axon reconstruction as it clears away
the debris, along with the macrophages, in a relatively small amount of time and
excrete factors that stimulate Schwann cells to secrete growth factors in order
to start the neurodegenerative process, re-establishing connections towards the
old pathway and remyelinating the isolation sheets that were lost during
injury, restoring both motor and sensory functions (Müller J. 2013).


CNS neuronal regeneration fails
because the habitat that surrounds the lesion inhibits the axon’s
reconstruction not enabling thus the plasticity process to take place (Fawcett,
JW. et. al 2012), and, moreover, the regrowth response provided by CNS axons is
weak and uncertain). It’s immune and glial cells would aggravate the
deterioration throughout the time the oligodendrocytes and growth factors would
produce inhibitory material on one hand and, the astrocytes actions would lead
to an obstruction at the lesion site not allowing neuronal processes to pass
through and execute its functions on the other hand. Furthermore, the debris
that results from isolated materials as a contusion consequence requires a great
amount of time to be cleared away, inhibiting, therefore, the axon repair
system (Zhao R.R. et. al 2013).


Chromatolysis is also found in
both structures and induces the reorganization of the principal structures
which includes nucleus and endoplasmic reticulum as well as an increase in
their volume not allowing consequently Nissl bodies organization to function
correctly by disrupting its placement as Nissl body-free axonal cytoskeleton
assemble in the middle of the axon and nucleus structures. It is more commonly
appreciated in the CNS rather than in the PNS as neurodegeneration leading to
death is contemplated (Mcllwain, D.L, Hoke, V. B. 2005) although, it may be a
reversible process if neuronal death has not been reached yet, being therefore
able to restore its distal structure (Boron, F., Boulpaep, L. 2017).

One of the principal factors that
can be found both in the CNS and PNS is the Wallerian degeneration where its
molecular activity, as well as its cellular composition, promote the
restoration of axons into targeted tissues by an innate immune response acting
on the contusion section and producing likeways loss of distal structure due to
the lesion site. The post-traumatic events and results that Wallerian
degeneration endure varies regarding cells type, as Schwann cells -possessors
of an amazing remyelination efficacy – amongst others, are present in the PNS whereas
microglia and oligodendrocytes are found taking part of the CNS regeneration mechanism
respectively. Although Wallerian degeneration is found in both sites of the
nervous system, the process is not as effective in the CNS as in the PNS
(Rotshenker, J. 2011).


Both CNS and PNS possess the
ability to regenerate after a trauma is produced, each one undertaking a
specific pathway leading to some main differences between them such as, for
example, the existing long-distance and almost instantaneous recovery of the
PNS nerve deterioration and the extremely limitation of an axon reconstruction
in the CNS (Huebner and Strittmattern 2010). Despite the contrast that may be
found between these two routes, there are also a few essential similarities
between them that may be crucial to understanding how they function and which pathways
are required in order to undertake them, even if the repair course would differ

he axon regeneration following an
injury of the central nervous system (CNS) and peripheral nervous system (PNS)
is of particular importance since its neurological functional capacity and
effective functionality can be recovered.

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