Abstract
Several axonal growth inhibitors have already been identified following spinal cord injury, the most known being myelin-derived proteins, such as Nogo-A. The present study aimed to correlate the formation of glial scar with the beginning of growth inhibitor, Nogo-A, release in rats previously submitted to compressive spinal cord injury. For this, 12 male and female Wistar rats (250 ± 50g) were divided into 3 groups of 4 animals each, according to the animals' euthanasia time after spinal cord injury (G3 - three days; G5 - five days; G7 - seven days). Spinal cord injuries were induced by means of dorsal laminectomy of the T10 vertebra and epidural compression. Histopathological evaluation and immunoreactivity of the Nogo-A axonal growth inhibitor were performed. It was observed that there was the release of the axonal inhibitor Nogo-A after 24h after the occurrence of spinal cord injury, and that the glial scar must be maintained, in this time interval, in order to guarantee the rebalancing of the post-trauma environment. Thus, it is suggested that the glial scar should be maintained in the acute phase of the lesion, guaranteeing its numerous benefits for the rebalancing of the post-injured environment and, after 24 hours, when the release of the studied axonal growth inhibitor begins, it should be removed.
Highlights
Spinal cord injuries occur through traumatic or non-traumatic pathways, with progression almost always catastrophic, especially when there are locomotor deficits such as paraplegia or quadriplegia (Lee et al, 2014, Alibardi, 2020)
The present study aims to contribute to the understanding of the pathophysiological processes of spinal cord injury, through the correlation between the formation of the glial scar and the beginning of the release of the Nogo-A axonal growth inhibitor
The proposed methodology aimed to elucidate the understanding of the pathophysiological processes of spinal cord injury, through the correlation between the formation of the glial scar and the beginning of the release of the Nogo-A axonal growth inhibitor
Summary
Spinal cord injuries occur through traumatic or non-traumatic pathways, with progression almost always catastrophic, especially when there are locomotor deficits such as paraplegia or quadriplegia (Lee et al, 2014, Alibardi, 2020). Axonal growth inhibitors have been identified following spinal cord injury, with myelin-derived proteins being more well-known, such as Nogo-A, myelin-associatedglycoprotein (MAG) and oligodendrocytemyelinglycoprotein (OMG). These inhibitors are associated with the formation of the glial scar, following the spinal cord injury process (Huang et al, 2012; Adams and Gallo, 2018). The elimination of the glial scar is one of the main objectives in the treatment of spinal cord injury, for many years it was believed that the glial scar was a solely limiting factor, since it induced the production of axonal growth inhibitors important in the regeneration process. The present study aims to contribute to the understanding of the pathophysiological processes of spinal cord injury, through the correlation between the formation of the glial scar and the beginning of the release of the Nogo-A axonal growth inhibitor
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