Research articleDifferential expression of ryanodine receptor isoforms after spinal cord injury

- RyR2 and RyR3 are upregulated in dorsal root ganglion neurons acutely after SCI.
- RyR2 and RyR3 are upregulated in the lesion site after SCI.
- RyR1 remained unchanged acutely following SCI.
- RyR2 and RyR3 spatially overlap with dystrophic axons after SCI.

Ryanodine receptors (RyRs) are highly conductive intracellular Ca2+ release channels and are widely expressed in many tissues, including the central nervous system. RyRs have been implicated in intracellular Ca2+ 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. Quantitative RT PCR analysis revealed that RyR3 was significantly increased in lumbar DRGs and at the lesion site at 1 and 2 d post contusion compared to sham (laminectomy only) controls. Additionally, RyR2 expression was increased at 1 d post injury within the lesion site. RyR2 and -3 protein expression was localized to lumbar DRG neurons and their spinal projections within the lesion site acutely after SCI. In contrast, RyR1 expression within the DRG and lesion site remained unaltered following trauma. Our study shows that SCI initiates acute differential expression of RyR isoforms in DRG and spinal cord.