面神经核内塑形变化在面瘫后遗症发生中的作用

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目的观察外伤性面瘫后,面神经核内运动神经元的定位分布与轴索再生变化,探讨其在面瘫后遗症联带发生中的作用。方法大鼠32只,面神经断伤吻合建立面瘫模型,采用尼氏染色与神经逆行荧光示踪技术,观察面瘫60d后健患两侧面神经核内运动神经元的定位分布与轴索再生变化,用透射电镜技术观察面瘫后90d时面神经核内运动神经元的超微结构改变。结果1.面瘫后健患两侧尼氏染色神经元的数量及分布特征基本一致,仅有神经元分布区域的缩小趋势,尼氏染色与超微观察均未发现面神经核内运动神经元有坏死与凋亡样改变。但患侧代表轴索成功再生的荧光金(FG)标记神经元数目较健侧明显减少(P<0.05),提示核内存在未被FG逆行标记但被尼氏染色的未达靶神经元。2.面神经颞支与颊支的荧光红(FR)与FG逆行示踪发现,面神经核颊支支配区内错位分布支配颞支的神经元,患侧的错位神经元比例较健侧增加(P<0.05)。同时,患侧面神经核内还出现代表轴索芽生,同时支配颞颊支的荧光双标神经元。结论外伤性面瘫后面神经核内的塑形中,除轴索芽生与迷向再生影响瘫后功能恢复外,核内还存在未成功再生的面运动神经元,其在面瘫后遗症联带发生中的作用也值得深入研究。 Objective To observe the localization of motor neurons and the changes of axonal regeneration in facial nucleus after traumatic facial paralysis, and to explore its role in the occurrence of facial paralysis sequelae. Methods Thirty-two rats with facial nerve injury were established to establish facial paralysis model. Nissl staining and nerve retrograde fluorescence tracing technique were used to observe the location and axonal regeneration of motor neurons in facial nucleus of both sides of the affected area after 60 days of facial paralysis Transmission electron microscopy was used to observe the ultrastructural changes of motor neuron in facial nucleus 90 days after facial paralysis. The number and distribution of Nissl staining neurons on the two sides of the affected area were basically the same after facial paralysis, only the narrowing tendency of the distribution area of ​​neurons was observed. Neonatal staining and ultramicroscopy showed no necrosis of motor neurons in the facial nucleus Apoptosis-like changes. However, the number of labeled FG neurons on the ipsilateral axon significantly decreased compared with that on the contralateral side (P <0.05), suggesting that there were non-target neurons in the nucleus that were not retrogradely labeled but were stained with Nissl’s stain. The retrograde tracing of FR and FG with temporal branch and buccal branch of facial nerve showed that the neurons in the branch of temporal buccal branch dominated the temporal branch and the dislocation neurons in the buccal branch of facial nerve increased <0.05). At the same time, the affected side of the nucleus also appeared on behalf of axonal buds, while controlling the temporal buccal branch of double-labeled fluorescent neurons. Conclusions In the process of traumatic facial paralysis, the facial motor neurons that have not been successfully regenerated exist in the shape of the facial nucleus after the paraplegia, The role is worth further study.
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