Nociceptor Hyper-Responsiveness during Vincristine-Induced Painful Peripheral Neuropathy in the Rat

摘要: Neuropathic pain accompanies peripheral nerve injury after a wide variety of insults including metabolic disorders, traumatic injury, and neurotoxic drugs. Chemotherapy-induced neuropathic pain, caused by drugs such as vincristine taxol, occurs in cancer patients who receive these antineoplastic agents. Although remediations have been attempted, the absence knowledge concerning mechanisms chemotherapy-induced has hindered development treatment strategies. Vincristine, widely used chemotherapeutic agent, produces painful neuropathy humans mechanical hyperalgesia rats. To test hypothesis that alterations C-fiber nociceptor function occur during vincristine-induced neuropathy, we performed vivo extracellular recordings single neurons from saphenous vincristine-treated Forty-one percent nociceptors were significantly hyper-responsive to suprathreshold stimulation. As population, mechanically also had greater responses heat stimulation; however, hyper-responsiveness was found only subset never detected hyper-responsiveness. In addition, mean conduction velocities A-fibers C-fibers rats slowed. Mean activation thresholds nociceptors, their distribution among subclasses, percentage spontaneously active not statistically different controls. Vincristine does not, therefore, cause generalized impairment but rather specifically interferes with underlying responsiveness stimuli. Furthermore, may involve mechanotransduction some general cellular adaptation others.