Shi R, Pryor J D
Department of Basic Medical Sciences, Center for Paralysis Research, School of Veterinary Medicine, Purdue University, IN 47907, West Lafayette, USA.
Neuroscience. 2000;98(1):157-66. doi: 10.1016/s0306-4522(00)00096-8.
Using an in vitro sucrose-gap recording chamber, sealing of cut axons in isolated strips of white matter from guinea pig spinal cord was measured by recording the "compound membrane potential". This functional sealing was found to correlate well with anatomical resealing, measured by a horseradish peroxidase uptake assay. Near-complete functional and anatomical recovery of the axonal membrane occurred routinely within 60 min following transection at 37 degrees C in regular Krebs' solution. The rate of membrane potential recovery is exponential, with a time-constant of 20+/-5 min. The sealing process at 31 degrees C was similar to that at 37 degrees C, and was effectively blocked at 25 degrees C, under which condition most axons continued to take up horseradish peroxidase for more than 1h, and failed to substantially recover their membrane potential. Seventy-five percent of the cords transected at 40 degrees C had similar sealing behavior to those at 37 degrees C and 31 degrees C. The balance failed to seal the cut end. Two-dimensional morphometric analysis has shown that raising the temperature from 25 degrees C to above 31 degrees C significantly decreases axonal permeabilization to horseradish peroxidase (increases the sealing of transected ends) across all areas of a transverse section of spinal cord. Moreover, this enhancement of sealing exists across all axon calibers. Since severe cooling compromises membrane resealing, caution needs to be taken when hypothermic treatment (below 25 degrees C) is applied within the first 60 min following mechanical injury. In summary, we have found that at normal temperature (37 degrees C), nerve fibers repair their damaged membrane following physical injury with an hour. This is similar at mildly lower (31 degrees C) and relatively higher (40 degrees C) temperature, although some fibers tend to collapse under this febrile temperature. Moreover, severely low temperature (25 degrees C) hindered the repair of damaged membranes. Based on our study, caution is needed in treating spinal cord injury with low temperatures.
使用体外蔗糖间隙记录室，通过记录“复合膜电位”来测量豚鼠脊髓白质分离条带中切断轴突的封闭情况。发现这种功能封闭与通过辣根过氧化物酶摄取试验测量的解剖学重新封闭密切相关。在37℃的常规 Krebs 溶液中横断后，轴突膜通常在60分钟内实现近乎完全的功能和解剖学恢复。膜电位恢复速率呈指数形式，时间常数为20±5分钟。31℃时的封闭过程与37℃时相似，而在25℃时被有效阻断，在此条件下大多数轴突在1小时以上持续摄取辣根过氧化物酶，且未能基本恢复其膜电位。40℃横断的脊髓中，75% 的情况与37℃和31℃时具有相似的封闭行为。其余情况未能封闭切断端。二维形态计量分析表明，将温度从25℃升高至31℃以上，可显著降低脊髓横切面所有区域轴突对辣根过氧化物酶的通透性（增加切断端的封闭）。此外，这种封闭增强在所有轴突管径中均存在。由于严重低温会损害膜的重新封闭，因此在机械损伤后的最初60分钟内应用低温治疗（低于25℃）时需谨慎。总之，我们发现，在正常温度（37℃）下，神经纤维在物理损伤后1小时内修复其受损膜。在略低（31℃）和相对较高（40℃）温度下情况类似，尽管在这种发热温度下一些纤维容易塌陷。此外，严重低温（25℃）阻碍受损膜的修复。基于我们的研究，在低温治疗脊髓损伤时需谨慎。
