Ye, Buttigieg, Wan, Wan And Fehlings’s paper “Expression and functional
role of BK channels in chronically injured spinal cord white matter” is very
different from the findings in the paper by Laiene, Perlmutter and Horner “No
evidence for chronic demyelingation in spared axons after spinal cord injury in
a mouse”. Ye et al claim in their paper that decrease in axonal conduction
after spinal cord injury is due to the demyelination of the axons and the over
exposure of the ion channels. It is commonly believed amongst the scientific
community that chronic demyelination occurs after spinal cord injury, followed
by incomplete remyelination. That is why there is so much research done in cell
replacement and stem cell research, in order to find a way to fully
remyelinated the injured spinal cord axons. Lasiene et al found evidence that
contradicts these common scientific beliefs. They found that given 12 weeks
after the spinal cord injury the spared axons of a mouse will fully remyelinate
on its own. This conclusion then suggests that maybe the problem with axonal
conduction isn’t a result of incomplete remyelination, but is a result of some
other issue after spinal cord injury. The remyelinated axons are obviously
thinner then the myelin on the uninjured spinal cord axons. But Lasiene claims
that the axon is still fully remyelinated, because even though the myelin is
thinner, the axonal diameter and also thinner, meaning that they G ratio is
still in the normal range.
Lasiene et al suggest that any issue with axonal conduction may be due to
the shortened internode length, and not the thinness of the myelin. On the
other hand, the majority of researchers see that the remyelinated axon is much
thinner then the unjuried axon, and immediately come to the conclusion that the
axon is not fully remyelinated.
Some
difference in the research done by Ye and Lasiene, was that Lasiene et al
didn’t actually measure the conductance of the axon after the remyelination.
But, Lasiene did do some really nice fluorescent imagery of the axons, that was
lacking in Ye’s paper.
Lasiene J, Shupe L, Perlmutter S, Horner P. No evidence for chronic
demyelination in spared axons after spinal cord injury in a mouse. J
Neurosci. 2008 Apr 9;28(15):3887-96.
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