Abstract
Background The precise mechanisms of nerve regeneration remain unclear. The potential of facial nerve regeneration and probable mechanisms involved following chronic facial nerve injury should be further studied. Methods Adult male Wistar rats were used to model either (i) facial nerve injury (axotomy) or (ii) reinjury (chronic axotomy followed by a second axotomy within 5 months). The rats were housed in the animal facility of the Eye and ENT Hospital of Shanghai Medical School, Fudan University (Shanghai, China). Expression of Shh (sonic hedgehog) and growth-associated protein 43 (GAP43, a neuronal marker) was detected in bilateral facial nuclei using reverse transcriptase PCR, western blotting analysis, and immunohistochemistry. The number of surviving motoneurons was quantified, and facial nerve regeneration was examined using transmission electron microscopy. Results Reinjury of the facial nerve 12 weeks after the first axotomy resulted in upregulation of GAP43 mRNA and protein expression in neurons ipsilateral to the axotomy; immunohistochemistry revealed that Shh expression was higher compared with control side facial nuclei at the same time point. GAP43 expression subsequently decreased. Conclusion The greatest regeneration potential of the facial nerve occurred within 5 months following chronic axotomy in rats, and regeneration may involve the Shh signaling pathway.
Highlights
Peripheral facial paralysis was characterized by paralysis of all facial expression muscles in the affected side, and facial muscle movement disorder was the main characteristic, which caused great psychological stress, mental trauma to the patients
We investigated the potential of facial nerve regeneration and whether it was affected by activation of the sonic hedgehog (Shh) signaling pathways
In Group II, at 12, 20, 28, and 36 weeks (w) after the initial facial nerve axotomy, the proximal 1 mm nerve stump was reaxotomized and the distal stump was ligated with 3-0 silk thread
Summary
Peripheral facial paralysis was characterized by paralysis of all facial expression muscles in the affected side, and facial muscle movement disorder was the main characteristic, which caused great psychological stress, mental trauma to the patients. Some scholars believed the facial nerve had a greater capacity for regeneration than any other neuron in the central nervous system; in this regard, the facial nerve was very similar to peripheral motor nerves [5,6,7,8]. Reinjury of the facial nerve 12 weeks after the first axotomy resulted in upregulation of GAP43 mRNA and protein expression in neurons ipsilateral to the axotomy; immunohistochemistry revealed that Shh expression was higher compared with control side facial nuclei at the same time point. The greatest regeneration potential of the facial nerve occurred within 5 months following chronic axotomy in rats, and regeneration may involve the Shh signaling pathway
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