Fernandez H L, Stiles J R
Neurosci Lett. 1984 Aug 24;49(1-2):117-22. doi: 10.1016/0304-3940(84)90146-0.
Acetylcholinesterase (AChE) inhibitor treatments were used to study the temporal course of intra- versus extracellular 16S AChE recovery in endplate regions of adult rat anterior gracilis muscles previously exposed to a brief, in situ application of diisopropylfluorophosphate (DFP). Following such enzymatic inactivation (95-100%), extracellular 16S AChE recovery began significantly later than that of intracellular (onset at approximately 36 and 12 h, respectively) but, once begun, progressed at approximately the same rate (1.32%/h). The recovery of AChE molecular form activities subsequent to identical DFP-inactivation was blocked to a large extent (65-85%) by in vivo treatment with cycloheximide, a protein synthesis inhibitor. These results support the hypothesis that extracellular 16S AChE at mammalian skeletal muscle motor endplates is primarily derived from complete, previously assembled 16S molecules originating in myofibers.
使用乙酰胆碱酯酶（AChE）抑制剂处理来研究成年大鼠股薄肌前肌终板区域内16S AChE与细胞外16S AChE恢复的时间进程，这些肌肉先前已在原位短暂应用二异丙基氟磷酸酯（DFP）。在这种酶失活（95 - 100%）后，细胞外16S AChE的恢复开始时间明显晚于细胞内（分别在约36小时和12小时开始），但一旦开始，进展速度大致相同（1.32%/小时）。相同DFP失活后AChE分子形式活性的恢复在很大程度上（65 - 85%）被蛋白质合成抑制剂环己酰亚胺的体内处理所阻断。这些结果支持以下假设，即哺乳动物骨骼肌运动终板处的细胞外16S AChE主要来源于源自肌纤维的完整、先前组装好的16S分子。
