Differential expression of ryanodine receptor isoforms after spinal cord injury.

Ryanodine receptors (RyRs) are highly conductive intracellular Ca release channels and are widely expressed in many tissues, including the central nervous system. RyRs have been implicated in intracellular Ca overload which can drive secondary damage following traumatic injury to the spinal cord (SCI), but the spatiotemporal expression of the three isoforms of RyRs (RyR1-3) after SCI remains unknown. Here, we analyzed the gene and protein expression of RyR isoforms in the murine lumbar dorsal root ganglion (DRG) and the spinal cord lesion site at 1, 2 and 7 d after a mild contusion SCI.

Intracellular calcium release through IPR or RyR contributes to secondary axonal degeneration.

Severed CNS axons often retract or dieback away from the injury site and fail to regenerate. The precise mechanisms underlying acute axonal dieback and secondary axonal degeneration remain poorly understood. Here we investigate the role of Ca store mediated intra-axonal Ca release in acute axonal dieback and secondary axonal degeneration.

The toll-like receptor 2 agonist Pam3CSK4 is neuroprotective after spinal cord injury.

Microglia/macrophage activation and recruitment following spinal cord injury (SCI) is associated with both detrimental and reparative functions. Stimulation of the innate immune receptor Toll-like receptor-2 (TLR2) has shown to be beneficial following SCI, and it increases axonal regeneration following optic nerve crush. However, the mechanism(s) remain unclear.