Spinal caspase-3 contributes to tibial fracture-associated postoperative allodynia via up-regulation of LRRTM1 expression in mice.

Spinal caspase-3 contributes to tibial fracture-associated postoperative allodynia via up-regulation of LRRTM1 expression in mice.

Model: Tibial fracture with intramedullary pinning as a model of postoperative pain

Spinal caspase-3 inhibition prevented fracture-associated mechanical and cold allodynia in a dose-dependent manner and reduced the spinal rise in LRRTM1, while intrathecal recombinant caspase-3 induced hypersensitivity that was reversed by LRRTM1 knockdown.

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