Biology Reference
In-Depth Information
induction of neuronal death. Thus, this single glial transcription factor
appears to be of extreme importance in this context (
Arthur-Farraj et al.,
2012
). The c-Jun is also a negative regulator of the myelination
(
Parkinson et al., 2008
). Interestingly, ATF3 expression may be dependent
on the c-Jun appearance, particularly observed in sensory neurons (
Lindwall
et al., 2004
).
The knowledge about single transection pathways that are involved in
cell death by apoptosis after nerve injury is incompletely known
(
Mantuano et al., 2011
). Apoptosis does occur in some neurons, particularly
among sensory neurons, and appears also in satellite cells and in Schwann
cells. Those sensory neurons that project to the skin seem to be more vul-
nerable to apoptosis than those sensory neurons that project to a muscle
(
Welin, Novikova, Wiberg, Kellerth, & Novikov, 2008
). Furthermore,
the apoptotic mechanism(s) may be different in Schwann cells and satellite
cells compared to motor and sensory neurons, since a marker of apoptosis,
cleaved caspase 3, is not observed in neurons after injury, but is clearly
expressed in Schwann cells and in some satellite cells (
Saito, Kanje, &
Dahlin, 2009
).
2. THE TIMING OF NERVE REPAIR AND
RECONSTRUCTION
As pointed out earlier, there are large numbers of factors that influence
the functional outcome after nerve injury and repair and reconstruction;
some of them are not possible to influence by the surgeon, like the age of
the patient (
Chemnitz, Bjorkman, Dahlin, & Rosen, 2013
). The timing
of nerve repair or reconstruction is an important point in nerve regenera-
tion. It is one of the factors that the surgeon can guide and thereby improve
functional outcome. In an interesting clinical paper, it was clearly demon-
strated that the results after reconstruction of a brachial plexus nerve injury in
adults were considerably better, with respect to motor functional recovery, if
the delay of the nerve reconstruction procedure was shorter than 2 weeks
(
Jivan, Kumar, Wiberg, & Kay, 2009
). This clinical observation should
be put into perspective with the described mechanisms in signal transduc-
tion. An injured neuron with its transected axon can probably be reactivated
if a secondary nerve reconstruction procedure is done by “refreshing” the
proximal nerve end during surgery through the retransection of the axon.
By such a procedure, the described intraneuronal activation mechanisms
can probably be reinitiated with a further outgrowth of the axons. However,
