Abstract:AIM: Glial cell-derived neurotrophic factor (GDNF) was injected into the target muscle to observe its effects on functional recovery, neuromorphology and GDNF expression in central facial neurons in rats after facial nerve crush injury, so as to investigate the feasibility and mechanism of action of GDNF injection via the target muscle in the treatment of peripheral facial paralysis. METHODS: SD rats were randomly divided into sham-operated group (right facial nerve trunk exposed only), model group (facial nerve trunk pressed), experimental control group (facial nerve trunk pressed + buccal muscle injected with saline) and experimental group (facial nerve trunk pressed + buccal muscle injected with GDNF). The neurological recovery of rats was observed by buccal muscle electrophysiology, animal facial palsy score, morphological changes of buccal muscle fibres by Masson staining, morphological changes of facial nerve by toluidine blue staining and GDNF expression in facial neurons by Western Blot. RESULTS: ① The rats in the experimental group had basically recovered from facial palsy 28 days after surgery, while the rats in the model and control groups had improved to different degrees but not fully recovered from facial palsy, with a score of more than 3; ② Buccal muscle electrophysiology: the peak latency was prolonged to different degrees and the maximum amplitude decreased to different degrees in each group compared with the sham-operated group; over time, the peak latency was significantly shorter (P<0.05) and the maximum amplitude increased (P<0.05) in the experimental group compared with the model group and the experimental control group; ③Toluidine blue staining: the model group, the experimental control group and the experimental group all showed irregular nerve fiber morphology, discontinuous and unclear outer membrane and reduced number of axons after surgery. 28 days after surgery, the facial nerve morphology of the experimental group was not significantly different from that of the sham operation, and there was significant recovery compared with the model group and the experimental control group; ④Masson staining: the number of muscle fibers decreased and the area occupied by muscle tissue decreased in each group; the morphology of muscle fibers in the experimental group recovered faster than that of the model group and the experimental control group, and by 28 days postoperatively, the morphology of muscle fibers was close to normal (P<0.05); ⑤Western Bolt assay: the protein expression of central facial neurons decreased in each group after modelling. The protein expression of GDNF in the central facial neuron tissues decreased in each group after modelling and gradually increased during the observation period; compared with the model group and the experimental control group, the protein expression of GDNF in the central facial neuron tissues was significantly enhanced in the experimental group at each time point after surgery (P<0.01). CONCLUSION: GDNF can be used as one of the effective modes of administration to improve peripheral nerve injury, promoting nerve fibre repair, recovery of target muscle function and repair of peripherally injured nerves by the central nervous system.