NOGO‐A immunolabeling is present in glial cells and some neurons of the recovering lumbar spinal cord in lizards

Abstract

The transected lumbar spinal cord of lizards was studied for its ability to recover after paralysis. At 34 days post‐lesion about 50% of lizards were capable of walking with a limited coordination, likely due to the regeneration of few connecting axons crossing the transection site of the spinal cord. This region, indicated as “bridge”, contains glial cells among which oligodendrocytes and their elongation that are immunolabeled for NOGO‐A. A main reactive protein band occurs at 100–110 kDa but a weaker band is also observed around 240 kDa, suggesting fragmentation of the native protein due to extraction or to physiological processing of the original protein. Most of the cytoplasmic immunolabeling observed in oligodendrocytes is associated with vesicles of the endoplasmic reticulum. Also, the nucleus is labeled in some oligodendrocytes that are myelinating sparse axons observed within the bridge at 22–34 days post‐transection. This suggests that axonal regeneration is present within the bridge region. Immunolabeling for NOGO‐A shows that the protein is also present in numerous reactive neurons, in particular motor‐neurons localized in the proximal stump of the transected spinal cord. Ultrastructural immunolocalization suggests that NOGO is synthesized in the ribosomes of these neurons and becomes associated with the cisternae of the endoplasmic reticulum, probably following a secretory pathway addressed toward the axon. The present observations suggest that, like for the regenerating spinal cord of fish and amphibians, also in lizard NOGO‐A is present in reactive neurons and appears associated to axonal regeneration and myelination.

Correlation of Nogo A release with glia scar formation in spinal cord injury

“…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. Spinal trauma can have an extrinsic origin, including fractures and dislocations secondary to bone diseases, such as congenital vertebral anomalies, neoplasms of vertebrae and nutritional alterations, and traumatic disc herniation, and extrinsic ones through fractures, dislocations and vertebral subluxations, resulting from traumatic events (Glass;Kent, 2007;Zhang et al, 2020).…”