Anglister L
Department of Anatomy and Embryology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
J Cell Biol. 1991 Nov;115(3):755-64. doi: 10.1083/jcb.115.3.755.
Acetylcholinesterase (AChE) in skeletal muscle is concentrated at neuromuscular junctions, where it is found in the synaptic cleft between muscle and nerve, associated with the synaptic portion of the myofiber basal lamina. This raises the question of whether the synaptic enzyme is produced by muscle, nerve, or both. Studies on denervated and regenerating muscles have shown that myofibers can produce synaptic AChE, and that the motor nerve may play an indirect role, inducing myofibers to produce synaptic AChE. The aim of this study was to determine whether some of the AChE which is known to be made and transported by the motor nerve contributes directly to AChE in the synaptic cleft. Frog muscles were surgically damaged in a way that caused degeneration and permanent removal of all myofibers from their basal lamina sheaths. Concomitantly, AChE activity was irreversibly blocked. Motor axons remained intact, and their terminals persisted at almost all the synaptic sites on the basal lamina in the absence of myofibers. 1 mo after the operation, the innervated sheaths were stained for AChE activity. Despite the absence of myofibers, new AChE appeared in an arborized pattern, characteristic of neuromuscular junctions, and its reaction product was concentrated adjacent to the nerve terminals, obscuring synaptic basal lamina. AChE activity did not appear in the absence of nerve terminals. We concluded therefore, that the newly formed AChE at the synaptic sites had been produced by the persisting axon terminals, indicating that the motor nerve is capable of producing some of the synaptic AChE at neuromuscular junctions. The newly formed AChE remained adherent to basal lamina sheaths after degeneration of the terminals, and was solubilized by collagenase, indicating that the AChE provided by nerve had become incorporated into the basal lamina as at normal neuromuscular junctions.
骨骼肌中的乙酰胆碱酯酶（AChE）集中在神经肌肉接头处，在肌肉和神经之间的突触间隙中可以找到它，它与肌纤维基底层的突触部分相关联。这就引出了一个问题，即突触酶是由肌肉、神经还是两者共同产生的。对去神经和再生肌肉的研究表明，肌纤维可以产生突触AChE，并且运动神经可能起间接作用，诱导肌纤维产生突触AChE。本研究的目的是确定已知由运动神经产生和运输的一些AChE是否直接有助于突触间隙中的AChE。通过手术损伤青蛙肌肉，使其退化并将所有肌纤维从其基底层鞘中永久去除。同时，AChE活性被不可逆地阻断。运动轴突保持完整，并且在没有肌纤维的情况下，它们的终末几乎保留在基底层上的所有突触部位。手术后1个月，对有神经支配的鞘进行AChE活性染色。尽管没有肌纤维，但新的AChE以神经肌肉接头特有的分支模式出现，其反应产物集中在神经终末附近，使突触基底层模糊不清。在没有神经终末的情况下，AChE活性未出现。因此，我们得出结论，突触部位新形成的AChE是由持续存在的轴突终末产生的，这表明运动神经能够在神经肌肉接头处产生一些突触AChE。终末退化后，新形成的AChE仍附着在基底层鞘上，并被胶原酶溶解，这表明神经提供的AChE已像在正常神经肌肉接头处一样整合到基底层中。
