Dixon R W, Harris J B
School of Neurosciences and Psychiatry, Department of Neurobiology, Medical School, University of Newcastle upon Tyne, United Kingdom.
Am J Pathol. 1999 Feb;154(2):447-55. doi: 10.1016/s0002-9440(10)65291-1.
We report here original data on the biological basis of prolonged neuromuscular paralysis caused by the toxic phospholipase A2 beta-bungarotoxin. Electron microscopy and immunocytochemical labeling with anti-synaptophysin and anti-neurofilament have been used to show that the early onset of paralysis is associated with the depletion of synaptic vesicles from the motor nerve terminals of skeletal muscle and that this is followed by the destruction of the motor nerve terminal and the degeneration of the cytoskeleton of the intramuscular axons. The postjunctional architecture of the junctions were unaffected and the binding of fluorescein-isothiocyanate-conjugated alpha-bungarotoxin to acetylcholine receptor was not apparently affected by exposure to beta-bungarotoxin. The re-innervation of the muscle fiber was associated by extensive pre- and post-terminal sprouting at 3 to 5 days but was stable by 7 days. Extensive collateral innervation of adjacent muscle fibers was a significant feature of the re-innervated neuromuscular junctions. These findings suggest that the prolonged and severe paralysis seen in victims of envenoming bites by kraits (elapid snakes of the genus Bungarus) and other related snakes of the family Elapidae is caused by the depletion of synaptic vesicles from motor nerve terminals and the degeneration of the motor nerve terminal and intramuscular axons.
我们在此报告由毒性磷脂酶A2β-银环蛇毒素引起的长时间神经肌肉麻痹的生物学基础的原始数据。利用电子显微镜以及抗突触素和抗神经丝的免疫细胞化学标记来显示，麻痹的早期发作与骨骼肌运动神经末梢的突触小泡耗竭有关，随后是运动神经末梢的破坏以及肌内轴突细胞骨架的退化。连接处的突触后结构未受影响，异硫氰酸荧光素偶联的α-银环蛇毒素与乙酰胆碱受体的结合显然未受β-银环蛇毒素暴露的影响。肌纤维的重新神经支配在3至5天时伴有广泛的终末前和终末后芽生，但在7天时稳定下来。相邻肌纤维的广泛侧支神经支配是重新神经支配的神经肌肉接头的一个显著特征。这些发现表明，被银环蛇（眼镜蛇属的眼镜蛇科毒蛇）和其他相关眼镜蛇科蛇咬伤中毒的受害者出现的长时间严重麻痹是由运动神经末梢的突触小泡耗竭以及运动神经末梢和肌内轴突的退化引起的。
