BDNF contributes to animal model neuropathic pain after peripheral nerve transection.

The outcome of peripheral nerve injury is often impaired by neuropathic pain, which is resistant to most analgesics and presents a serious clinical problem. The mechanisms underlying post-traumatic neuropathic pain remain unclear, but they are likely associated with the regeneration processes. Brain-derived neurotrophic factor (BDNF) is known to enhance peripheral nerve regeneration and is also considered to be an endogenous modulator of nociceptive responses following spinal cord lesion. The aim of this work was to examine the local effect of BDNF in a neuropathic pain model. Sciatic nerves of adult male rats were transected and supplied with connective tissue chambers filled with (1) fibrin only, (2) fibrin with BDNF, or (3) fibrin with antibodies against BDNF. In control animals the nerve was transected and no chamber was applied. During follow-up, autotomy behavior was assessed. Seven weeks after the operation, the number of surviving and regenerating neurons in dorsal root ganglia was counted and the neuroma incidence was examined. We found that local inactivation of BDNF decreased the incidence as well as severity of autotomy and neuroma formation, but did not influence neuron regeneration into the chambers. These results indicate that BDNF plays a locally crucial role in neuropathic pain development after peripheral nerve injury.