Aims: To examine the effects of local brain-derived neurotrophic factor (BDNF) produced after nerve injury on the functional regeneration of the damaged nerve. Methods: The inferior alveolar nerve was transected in adult male rats and 1 μg or 10 μg of BDNF antibody was administered at the injury site; a third group of rats received saline and a fourth group underwent nerve ligation. BDNF mRNA was quantified in the transected tissue and trigeminal ganglion by using realtime polymerase chain reaction (PCR). Head withdrawal thresholds following mechanical (tactile) stimulation (with von Frey filaments) of the mental region were measured for 3 weeks postoperatively. Electromyographic activity of the jaw opening reflex (JOR) was recorded from the anterior belly of the digastric muscle. Results: Within 24 hours, transection induced significant elevation of BDNF mRNA expression in the injured tissue (unpaired t test, P .01). The head withdrawal threshold to mechanical stimulation increased at 1 day after transection and then decreased (two-way repeated measures analysis of variance [ANOVA], P .001). At 2 weeks after surgery, the head withdrawal threshold was higher than before surgery in the group that received a higher dose of BDNF antibody (ANOVA, P .001), but not in the group that received a smaller dose (ANOVA, P > .05). No significant differences were observed in the latency or threshold of the JOR between saline- and antibody-treated rats (unpaired t test, P > .05). Conclusion: These results suggest that locally administered BDNF antibody neutralizes nerve injury-induced BDNF at the injury site and thus influences sensorimotor recovery. Schlagwörter: jaw-opening reflex, neurotrophic factor, peripheral nerve injury, regeneration, withdraw reflex