Salgado-Ceballos H, Guizar-Sahagun G, Feria-Velasco A, Grijalva I, Espitia L, Ibarra A, Madrazo I
Unit of Medical Research in Neurological Diseases, Instituto Mexicano del Seguro Social, México, DF, México.
Brain Res. 1998 Jan 26;782(1-2):126-35. doi: 10.1016/s0006-8993(97)01252-3.
The capability of the central nervous system to remyelinate axons after a lesion has been well documented, even though it had been described as an abortive and incomplete process. At present there are no long-term morphometric studies to assess the spinal cord (S.C.) remyelinative capability. With the purpose to understand this phenomenon better, the S.C. of seven lesionless rats and the S.C. of 21 rats subjected to a severe weight-drop contusion injury were evaluated at 1, 2, 4, 6, and 12 months after injury. The axonal diameter and the myelination index (MI = axolemmal perimeter divided by myelinated fiber perimeter) were registered in the outer rim of the cord at T9 SC level using a transmission electron microscope and a digitizing computer system. The average myelinated fiber loss was 95.1%. One month after the SC, 64% of the surviving fibers were demyelinated while 12 months later, only 30% of the fibers had no myelin sheath. The MI in the control group was 0.72 +/- 0.07 (X +/- S.D.). In the experimental groups, the greatest demyelination was observed two months after the lesion (MI = 0.90 +/- 0.03), while the greatest myelination was observed 12 months after the injury (MI = 0.83 +/- 0.02). There was a statistical difference (p < 0.02) in MI between 2 and 12 months which means that remyelination had taken place. Remyelination was mainly achieved because of Schwann cells. The proportion of small fibers (diameter = 0.5 micron or less) considered as axon collaterals, increased from 18.45% at 1 month to 27.66% a year after the contusion. Results suggest that remyelination is not an abortive phenomenon but in fact a slow process occurring parallel to other tissue plastic phenomena, such as the emission of axon collaterals.
中枢神经系统在损伤后重新髓鞘化轴突的能力已有充分记录，尽管这一过程曾被描述为一个失败且不完整的过程。目前尚无长期形态学研究来评估脊髓的再髓鞘化能力。为了更好地理解这一现象，我们对7只无损伤大鼠的脊髓以及21只遭受严重重物坠落挫伤的大鼠脊髓在损伤后1、2、4、6和12个月进行了评估。使用透射电子显微镜和数字化计算机系统，在T9脊髓节段水平的脊髓外周记录轴突直径和髓鞘形成指数（MI = 轴膜周长除以有髓纤维周长）。平均有髓纤维损失为95.1%。脊髓损伤后1个月，64%存活的纤维发生脱髓鞘，而12个月后，只有30%的纤维没有髓鞘。对照组的MI为0.72±0.07（X±标准差）。在实验组中，损伤后2个月观察到最大程度的脱髓鞘（MI = 0.90±0.03），而损伤后12个月观察到最大程度的髓鞘形成（MI = 0.83±0.02）。2个月和12个月之间的MI存在统计学差异（p < 0.02），这意味着发生了再髓鞘化。再髓鞘化主要是由雪旺细胞实现的。被视为轴突侧支的小纤维（直径 = 0.5微米或更小）的比例从损伤后1个月的18.45%增加到挫伤后1年的27.66%。结果表明，再髓鞘化不是一个失败的现象，而是一个与其他组织可塑性现象（如轴突侧支的发出）并行发生的缓慢过程。
