Thrombospondin-4 contributes to spinal cord injury-induced changes in nociception.

摘要: Background: Our previous data have indicated that nerve injury-induced up-regulation of thrombospondin-4 (TSP4) proteins in dorsal spinal cord plays a causal role neuropathic pain state development ligation model. To investigate whether TSP4 also contribute to the centrally mediated changes nociception after injury (SCI), we investigated SCI induced dysregulation, and if so, this change correlated with T9 contusion Methods: Behavioural sensitivity mechanical, thermal stimuli locomotor function recovery were tested blindly or sham rats post-injury. Intrathecal antisense mismatch control oligodeoxynucleotides used treat nociceptive hyperreflexia, Western blots measure protein levels samples. Results: below-level hindpaw hypersensitivity stimuli. are up-regulated but not without hyperreflexia. There was no significant difference motor post-injury between treatment antisense, control, led reversal hyperreflexia rats. Conclusions: leads lumbar may play critical mediating behavioural hypersensitivity. Blocking pathway be helpful management SCI-induced nociception. © 2013 European Federation International Association for Study Pain Chapters.