Spinal cord injury (SCI) results in the rupture of blood vessels and bleeding inside the spinal cord, as well as the release of alarmins from necrotic cells, leading to neuroinflammation and disruption of blood-spinal cord barriers. This increased permeability of the blood vessel walls allows for the entry of blood substances into the spinal cord parenchyma. Among these substances is immunoglobulin G (IgG). To understand the role of IgG, we performed immunofluorescence (IF) against IgG at 1 hour, 24 hours, and 7 days post-injury, both near and far from the lesion, in a mouse model of T9-T10 spinal cord contusion. We observed that IgG diffuses into areas near the site of SCI and, to a lesser degree, in more distant regions of the spinal cord using the central canal as a major invasion route. Notably, IgG signal was detected extending to the cervical spinal cord level, and we observed that neurons throughout the rostro-caudal spinal cord axis internalized IgG. At 1 hour after injury, IgG internalization was localized in neurons adjacent to the lesion site and around the central canal in more distant tissue sections. By 24 hours, most neurons proximal to the lesion colocalized with IgG IF staining. Interestingly, the presence of IgG in neurons completely disappeared 7 days post-SCI. Future work will aim to investigate the mechanisms by which IgG internalization occurs in neurons, as well as determining whether this internalization has a harmful or protective impact on the spinal cord.