Monday, December 10, 2012

Do Axons Fully Demyelinate after SCI?



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.



 Hui Ye, Josef Buttigieg, Yudi Wan, Jian Wan and Michael G. Fehlings (2012). The effect of BK channel activation on axonal conduction following spinal cord injury. Neurobiology of Disease 2012 Apr 17. [Epub ahead of print] PMID: 22534235

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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