面神经损伤后星形胶质细胞塑形活动的实验研究

目的 研究面神经损伤修复过程中面神经核内胶质塑形活动的变化。方法 大鼠面神经断伤吻合后1、7、21、60天时，观察面部运动情况，同时用神经逆行示踪结合免疫荧光组织化学的双重标记技术以及透射电镜技术，观察外周损伤后面神经核内胶质原纤维酸性蛋白（glial fibrillary acidic protein，GFAP）表达以及星形胶质细胞超微结构的塑形变化。结果 面神经再生修复后面部运动功能逐渐恢复，但难以完全恢复正常，且常伴有联带后遗症。荧光金逆行示踪标记出面神经核内面运动神经元有严格的躯体定位分布特征。正常状态下面神经核内GFAP表达强度极弱，术后7天时患侧表达强度显著增强，至再生修复晚期减弱，但仍高于健侧水平。超微结构观察显示，术后50天时塑形活化的星形胶质细胞形成板层状突起包裹隔绝面运动神经元。结论 本研究观察了外周损伤后面运动神经元周围星形胶质细胞塑形活动的一些规律性变化，其晚期塑形活动很可能与联带等后遗症的产生机制关系密切。

Plastic changes of astrocytes in facial nucleus following facial nerve anastomosis

OBJECTIVE To observe the glial reac- tions surrounding the facial motor neurons following fa- cial nerve anastomosis. METHODS At day 1, 7, 21 and 60 following facial nerve anastomosis, the recovery process of facial movement was observed and the ex- pression of glial fibrillary acidic protein (GFAP) was de- tected by a combined fluorescent retrograde tracing and immunofluorescent histochemical staining method. The ultrastructure of astrocytes was also observed under transmission electron microscope (TEM). RESULTS The function of facial muscle improved gradually after facial nerve anastomosis, but couldn't reach the normal state. The facial muscles movement often ac- companied with synkinesis. Fluoro-gold (FG) retrograde tracing labeled every motor neuron of facial subnucleus, which showed an evident somatotopic organization. Normally there was a considerable number of GFAP- positive cells in some non-nucleus areas and few in the facial nucleus. Postoperatively the GFAP immunore- activity of the anastomosis side increased more than that of the control side, but which gradually decreased at late time. The ultrastructure of astrocytes showed that the sheet-like process of astrocytes invested and protected the injured facial motor neurons moderately. The apoptotic appearance was not found in astrocytes and motor neurons. CONCLUSION The present study shows some characteristic changes of astrocytes re- action during the process of facial nerve injury and regeneration. The plastic change at late time may in- volve the mechanism of synkinesis.