Habig W H, Bigalke H, Bergey G K, Neale E A, Hardegree M C, Nelson P G
J Neurochem. 1986 Sep;47(3):930-7. doi: 10.1111/j.1471-4159.1986.tb00700.x.
The clinical course of tetanus is notable, in addition to its often dramatic clinical presentation, by the long duration of the neuromuscular symptoms. Survivors may have tetanic manifestations for several weeks after the onset of the disease. In this article we correlate the duration of specific electrophysiologic effects produced by tetanus toxin with the degradation of cell-associated toxin in primary cultures of mouse spinal cord neurons. From these studies we can conclude that the toxin has a half-life of 5-6 days. Both the heavy and the light chains of tetanus toxin degrade at similar rates. Labeled toxin, visualized by radioautography, is associated with neuronal cell bodies and neurites, and its distribution is not altered during a 1-week period following toxin exposure. Blockade of synaptic activity persists for weeks at the concentration of radiolabeled toxin used in these studies. This blockade of transmission is reversed as the toxin is degraded, suggesting that degradation of toxin may be a sufficient mechanism for recovery from tetanus.
破伤风的临床病程值得关注,除了其往往引人注目的临床表现外,神经肌肉症状持续时间也很长。幸存者在疾病发作后数周可能仍有破伤风表现。在本文中,我们将破伤风毒素产生的特定电生理效应的持续时间与小鼠脊髓神经元原代培养物中细胞相关毒素的降解情况进行了关联。从这些研究中我们可以得出结论,该毒素的半衰期为5 - 6天。破伤风毒素的重链和轻链降解速率相似。通过放射自显影观察到的标记毒素与神经元细胞体和神经突相关,并且在毒素暴露后的1周内其分布没有改变。在这些研究中使用的放射性标记毒素浓度下,突触活动的阻断会持续数周。随着毒素降解,这种传递阻断会被逆转,这表明毒素的降解可能是从破伤风恢复的充分机制。