Journal of oral & facial pain and headache · 2016
Peripheral Brain-Derived Neurotrophic Factor Modulates Regeneration Following Inferior Alveolar Nerve Injury in Rats.
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Yoshikawa Hiroyuki, Yamada Yurie, Kurose Masayuki, Yamamura Kensuke, Maeda Takeyasu, Seo Kenji
Аннотация
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 real-time 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.
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 real-time 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.