Abstract
As one of the most effective and frequently used antineoplastic agents, paclitaxel produces neuropathic pain during and often persists after chemotherapy. Previous studies have developed various rodent models of paclitaxel-induced pain syndrome; however, a clear cellular mechanism has yet to emerge. The aim of this study was to identify the molecular mechanisms underlying this dose-limiting side effect of paclitaxel in cellular models. We treated isolated dorsal root ganglion sensory neurons and DRG-like F11 cells with paclitaxel in a sub-apoptotic dose range (0.1-50 nM) which was verified not to induce apoptosis.
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