Effects of a bupivacaine nerve block on the axonal transport of Tumor Necrosis Factor-alpha (TNF-α) in a rat model of carrageenan-induced inflammation

Abstract Many pro-inflammatory cytokines are involved in the process of inflammatory pain. Bi directional axonal transport of Tumor Necrosis Factor-alpha (TNF-α) occurs in case of neuropathic pain induced by nerve ligation. We used an in vivo preparation with injection of carrageenan and fluorescent TNF-α in the territory of the saphenous nerve of rats to study this transport. We have shown that retrograde transport of TNF-α occurs after an inflammatory insult caused by the injection of carrageenan. This transport was likely mediated by the TNF receptor 1. A nerve block with bupivacaine totally abolishes the expression of the receptor in the dorsal root ganglion and the retrograde transport of TNF-α. In addition, bupivacaine at low concentrations (1–10 μM) was able to stop the axonal transport ex vivo . Tetrodotoxin was less efficacious for inhibiting the TNF-α transport and the rise in receptor expression and for inhibiting the axonal transport ex vivo . This may partly explain the efficacy of nerve blocks with bupivacaine to decrease the neurogenic inflammation and in a lower extent the long-term inhibition of hyperalgesic phenomenon observed in animals and in humans.