Cecchini T, Cuppini R, Ciaroni S, Guidi L, Ambrogini P, Del Grande P
Istituto di Scienze Morfologiche, Università di Urbino, Italy.
Ital J Anat Embryol. 1994 Apr-Jun;99(2):81-90.
Unmyelinated axons of normal and regenerated sciatic nerve were counted in controls and vitamin E-deficient rats. No significant change in the number of unmyelinated axons of uninjured nerve was found in the vitamin E deficiency in comparison to controls (12961 +/- 1591 and 12450 +/- 1290, respectively, mean +/- SEM). In regenerated nerve of control rats the number of unmyelinated axons was higher than in uninjured nerve (16971 +/- 1854 and 20786 +/- 1574 at 1 and 2 months after crush, respectively). In vitamin E-deficient rats the increase in number of unmyelinated axons was greater than in corresponding controls (21880 +/- 662) at 1 month after lesion, but the number returned to value found in uninjured nerve at 2 months after lesion (12536 +/- 659). These results suggest that sprouting at lesion may be enhanced but some regenerated axons does not survive at long term in vitamin E-deficiency.
在对照组和维生素E缺乏的大鼠中，对正常和再生坐骨神经的无髓轴突进行计数。与对照组相比，维生素E缺乏时未损伤神经的无髓轴突数量没有显著变化（分别为12961±1591和12450±1290，平均值±标准误）。在对照大鼠的再生神经中，无髓轴突数量高于未损伤神经（挤压后1个月和2个月时分别为16971±1854和20786±1574）。在维生素E缺乏的大鼠中，损伤后1个月时无髓轴突数量的增加大于相应对照组（21880±662），但损伤后2个月时数量恢复到未损伤神经中的值（12536±659）。这些结果表明，在维生素E缺乏时，损伤处的轴突发芽可能增强，但一些再生轴突不能长期存活。
