Chronic Remyelination After Spinal Cord Injury
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Date
2020-02
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Abstract
Spinal cord injury (SCI) renders motor and sensory deficits below the level of injury, in part, due to severed axons and extensive axon demyelination. Demyelination slows conduction through spared axons, leading to functional impairments. This is due to node of Ranvier disruption as highly organized proteins around the node of Ranvier spread along axons. After SCI, demyelinated axons are spontaneously remyelinated which re-establishes nodal organization and restores proper conduction in axons. Therefore, promoting remyelination is often a therapeutic strategy to restore motor function after SCI. However, the capacity for remyelination after injury remains debated in the field. Here, we tested the hypothesis that remyelination of spared axons occurs chronically after SCI. For this, we collected spinal cords from naïve and SCI reporter mice to quantify the amount of new myelin formed during specific periods of recovery. In naïve mice, only ~5% of axons were wrapped in new myelin. After SCI, remyelination peaked during the 3rd month post-injury (mpi) when over 15% of axons were remyelinated. Interestingly, spared axons continued to be remyelinated for at least 6mpi, although at a lower rate. Overall this work shows for the first time that axon remyelination persists for at least 6mpi, suggesting that the injured spinal cord remains capable of repair long-term.
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Biological Sciences: 1st Place (The Ohio State University Edward F. Hayes Graduate Research Forum)
Keywords
Spinal cord injury, Remyelination, Oligodendrocyte, Transgenic mice