IP₃R-mediated intra-axonal Ca²⁺ release contributes to secondary axonal degeneration following contusive spinal cord injury.

ABSTRACT: Secondary axonal loss contributes to the persistent functional disability following trauma. Consequently, preserving axons following spinal cord injury (SCI) is a major therapeutic goal to improve neurological outcome; however, the complex molecular mechanisms that mediate secondary axonal degeneration remain unclear. We previously showed that IP₃R-mediated Ca²⁺ release contributes to axonal dieback and axonal loss following an ex vivo laser-induced SCI. Nevertheless, targeting IP₃R in a clinically relevant in vivo model of SCI and determining its contribution to secondary axonal degeneration has yet to be explored. Here we used intravital two-photon excitation microscopy to assess the role of IP₃R in secondary axonal degeneration in real-time af

SUBMITTER: Orem BC 

PROVIDER: S-EPMC7686917 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature