Juntunen J, Linnoila I, Haltia M
Scand J Work Environ Health. 1977 Mar;3(1):36-42. doi: 10.5271/sjweh.2792.
Myoneural junctions in the tibialis anterior muscle of rats with clinical signs of polyneuropathy induced with carbon disulfide were studied by light and electron microscopy. Histochemically demonstrable acetylcholinesterase (AChE; E.C. 3.1.1.7) activity was distributed similarly in the myoneural junctions of both the exposed and the control rats. In both groups intense enzyme activity was localized at the level of the post-synaptic membrane of the myoneural junction. The postsynaptic infoldings of the myoneural junctions of the exposed rats appeared normal. No enzyme activity was seen outside the zone of the myoneural junctions. The ultrastructure of the sub-sarcolemmal space, as well as the postsynaptic membranes of the myoneural junctions of the exposed animals, was normal. In the terminal axons signs of various degrees of degeneration were present, e.g., disappearance of the preterminal axoplasmic neurotubules, partial disappearance of synaptic vesicles, appearance of dense bodies, and even total disappearance or destruction of the terminal axons. Synaptic clefts were often widened with Schwann cell interposition. It thus seems that systemic carbon disulfide poisoning primarily alters the presynaptic structures of the myoneural junctions, while the postsynaptic side remains relatively intact, especially since the histochemical distribution of AChE in myoneural junctions was normal.
通过光学显微镜和电子显微镜对患有二硫化碳诱发的多神经病临床症状的大鼠胫前肌中的肌神经接头进行了研究。组织化学可证实的乙酰胆碱酯酶(AChE;E.C. 3.1.1.7)活性在暴露组和对照组大鼠的肌神经接头中分布相似。在两组中,强烈的酶活性都定位于肌神经接头突触后膜水平。暴露组大鼠肌神经接头的突触后褶皱看起来正常。在肌神经接头区域之外未见酶活性。暴露动物的肌膜下间隙以及肌神经接头的突触后膜的超微结构正常。在终末轴突中存在不同程度的退变迹象,例如,终末前轴浆神经微管消失、突触小泡部分消失、致密体出现,甚至终末轴突完全消失或破坏。突触间隙常因施万细胞插入而增宽。因此,似乎全身性二硫化碳中毒主要改变肌神经接头的突触前结构,而突触后部分相对保持完整,特别是因为AChE在肌神经接头中的组织化学分布是正常的。