Abstract
To assess whether phospholipase A2 (PLA2) plays a role in the pathogenesis of spinal cord injury (SCI), we compared lesions either induced by PLA2 alone or by a contusive SCI. At 24-h post-injury, both methods induced a focal hemorrhagic pathology. The PLA2 injury was mainly confined within the ventrolateral white matter, whereas the contusion injury widely affected both the gray and white matter. A prominent difference between the two models was that PLA2 induced a massive demyelination with axons remaining in the lesion area, whereas the contusion injury induced axonal damage and myelin breakdown. At 4 weeks, no cavitation was found within the PLA2 lesion, and numerous axons were myelinated by host-migrated Schwann cells. Among them, 45% of animals had early transcranial magnetic motor-evoked potential (tcMMEP) responses. In contrast, the contusive SCI induced a typical centralized cavity with reactive astrocytes forming a glial border. Only 15% of rats had early tcMMEP responses after the contusion. BBB scores were similarly reduced in both models. Our study indicates that PLA2 may play a unique role in mediating secondary SCI likely by targeting glial cells, particularly those of oligodendrocytes. This lesion model could also be used for studying demyelination and remyelination in the injured spinal cord associated with PLA2-mediated secondary SCI.