Objective
To investigate the neuropathic changes induced by nucleus pulposus and possible role of nitric oxide (NO) in the pathogenesis of painful radiculopathy.

Method
Autologous nucleus pulposus was harvested from the rat coccygeal intervertebral disc and grafted to the sciatic nerve. Pain behavior, neurophysiologic and pathologic changes were compared between autografted and sham operated group during 14-day-period. Western immunoblotting and immunohistochemistry with anti-nitrotyrosine mouse monoclonal antibody were used to compare the NO production and nerve damage in autografted and sham operated nerve tissues.

Results
Mechanical allodynia and thermal hyperalgesia were observed 2 days after autograft of nucleus pulposus and persisted during 14-day-period (p＜0.05). Motor nerve conduction latency was delayed and compound muscle action potential amplitude was decreased 5 days after autograft (p＜0.05). Histologically, nucleus pulposus induced severe inflammatory reaction with fibroblast proliferation and foamy macrophage infiltration, which were persisted during 14-day- period. More nitrated proteins were detected consistently in nerve tissues with autograft of nucleus pulposus and immunohistochemical staining of nitrotyrosine was prominent around foamy macrophages.

Conclusion
These data suggest that nucleus pulposus induce mechanical allodynia, thermal hyperalgesia and nerve dysfunction through inflammatory reaction with macrophage infiltration. NO and NO related tissue injury may play an important role in the pathogenesis of painful radiculopathy.