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。