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Updated: Sep 11, 2025
Facial Nerve Surgery in the Rat Model to Study Axonal Inhibition and Regeneration
Published on: May 5, 2020
Inhibition of the P2Y2 Receptor Promotes Facial Nerve Function by Enhancing Neuron Autophagy
Xianmin Song1, Yingna Gao1, Minhui Zhu1
1Department of Otolaryngology-Head & Neck Surgery, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China.
Objective:
Facial nerve injury induces autophagy and apoptosis in facial nerve nucleus motoneurons of the CNS, impairing nerve regeneration and functional recovery. The function of P2Y2R after facial nerve injury remains to be determined. This study hypothesizes that inhibiting P2Y2R may play a protective role in facial nerve injury by modulating the autophagy signaling pathway.
Methods:
An in vivo mouse model of facial nerve crush injury was utilized in this study. Mice received either a P2Y2R agonist or antagonist through intrathecal injections of 10 μL/daily for 4 weeks. This study measured facial nerve function, examined fibrogenesis, and analyzed expression of autophagy regulatory proteins. In an in vitro experiment, NSC34 cells were treated with a P2Y2R agonist or an antagonist, and changes in the levels of phosphorylated PI3K, Akt, and mTOR, as well as autophagy regulatory proteins determined.
Results:
Inhibition of P2Y2R significantly increased autophagy levels and enhanced facial nerve function. These protective outcomes were linked to the suppression of phosphorylated PI3K, Akt, and mTOR signaling pathways.
Conclusion:
The study suggests that P2Y2R inhibition may improve facial nerve function by improving autophagy, making it a promising therapeutic approach for treating facial nerve injury.
Insights
Inhibiting P2Y2R enhances facial nerve regeneration and function by promoting autophagy. This study reveals P2Y2R antagonism as a potential therapy for facial nerve injury.
Area of Science:
- Neuroscience
- Cell Biology
- Regenerative Medicine
Background:
- Facial nerve injury disrupts autophagy and apoptosis in motoneurons, hindering nerve regeneration and functional recovery.
- The role of the P2Y2 receptor (P2Y2R) in the context of facial nerve injury is not well understood.
- Autophagy modulation is a potential strategy to improve outcomes after facial nerve damage.
Purpose of the Study:
- To investigate the role of P2Y2R in facial nerve injury.
- To test the hypothesis that inhibiting P2Y2R offers neuroprotection by modulating autophagy.
- To evaluate P2Y2R antagonism as a therapeutic approach for facial nerve injury.
Main Methods:
- Established an in vivo mouse model of facial nerve crush injury.
- Administered P2Y2R agonist or antagonist via intrathecal injection for 4 weeks.
- Assessed facial nerve function, fibrogenesis, and autophagy-related protein expression; conducted in vitro experiments on NSC34 cells.
Main Results:
- P2Y2R inhibition significantly upregulated autophagy levels.
- Blocking P2Y2R enhanced facial nerve function and promoted nerve regeneration.
- These beneficial effects correlated with the suppression of phosphorylated PI3K/Akt/mTOR signaling pathways.
Conclusions:
- P2Y2R inhibition demonstrates a neuroprotective effect in facial nerve injury.
- Enhanced autophagy and improved facial nerve function are key outcomes of P2Y2R antagonism.
- Targeting P2Y2R represents a promising therapeutic strategy for facial nerve injury.
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