Glazer E J, Baker T, Riker W F
J Neurocytol. 1978 Dec;7(6):741-58. doi: 10.1007/BF01205148.
The fine structure of the cat soleus neuromuscular junction was studied following a single intra-arterial injection of di-isopropylfluorophosphate (DFP) into the right femoral artery. DFP induced separate subacute and delayed morphologic changes in soleus non-myelinated motor nerve terminals. Three days after DFP administration motor nerve terminals were reduced in number. Subacute DFP damage was also noted in the subneural apparatus and in the immediate subjacent muscle. Both pre- and post-junctional subacute changes were resolved two weeks post-DFP. One week following this initial regeneration, soleus motor nerve terminals underwent a delayed transient degeneration, followed by reinnervation of damaged endplates 6--8 weeks following DFP. Quantitative analysis of methylene blue-stained intramuscular nerves indicated that both subacutely and chronically denervated soleus muscle fibres were reinnervated by regeneration of the original motor axon. Reinnervation by means of collateral sprouting was insignificant. This mechanism of reinnervation and the rapidity with which it occurred suggests that both subacute and delayed soleus motor nerve damage is initiated from local actions of DFP on the non-myelinated terminal. The subacute reaction probably results from a direct cytotoxic action of DFP at pre- and post-junctional sites. The delayed nerve terminal degeneration may also stem from an acute effect not immediately detrimental to nerve function.
通过向右侧股动脉单次动脉内注射二异丙基氟磷酸酯(DFP),研究了猫比目鱼肌神经肌肉接头的精细结构。DFP在比目鱼肌无髓运动神经末梢引起了单独的亚急性和延迟性形态学变化。DFP给药三天后,运动神经末梢数量减少。在神经下装置和紧邻的肌肉中也观察到亚急性DFP损伤。DFP给药两周后,神经节前和节后的亚急性变化均得到缓解。在这一初始再生一周后,比目鱼肌运动神经末梢经历了延迟性短暂变性,随后在DFP给药后6 - 8周对受损终板进行了重新支配。对亚甲蓝染色的肌内神经进行定量分析表明,亚急性和慢性去神经支配的比目鱼肌纤维均通过原始运动轴突的再生进行了重新支配。通过侧支芽生进行的重新支配并不显著。这种重新支配的机制及其发生的速度表明,比目鱼肌运动神经的亚急性和延迟性损伤均由DFP对无髓末梢的局部作用引发。亚急性反应可能是由于DFP在神经节前和节后部位的直接细胞毒性作用所致。延迟性神经末梢变性也可能源于一种对神经功能无立即损害的急性效应。