Department of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, OH, USA.
Adv Neurobiol. 2022;28:111-130. doi: 10.1007/978-3-031-07167-6_5.
The mammalian neuromuscular junction (NMJ) is an ideal preparation to study synaptic plasticity. Its simplicity- one input, one postsynaptic target- allows experimental manipulations and mechanistic analyses that are impossible at more complex synapses. Homeostatic synaptic plasticity attempts to maintain normal function in the face of perturbations in activity. At the NMJ, 3 aspects of activity are sensed to trigger 3 distinct mechanisms that contribute to homeostatic plasticity: Block of presynaptic action potentials triggers increased quantal size secondary to increased release of acetylcholine from vesicles. Simultaneous block of pre- and postsynaptic action potentials triggers an increase in the probability of vesicle release. Block of acetylcholine binding to acetylcholine receptors during spontaneous fusion of single vesicles triggers an increase in the number of releasable vesicles as well as increased motoneuron excitability. Understanding how the NMJ responds to perturbations of synaptic activity informs our understanding of its response to diverse neuromuscular diseases.
哺乳动物的神经肌肉接头（NMJ）是研究突触可塑性的理想准备。其简单性——一个输入，一个突触后靶标——允许进行实验操作和机制分析，这在更复杂的突触中是不可能的。 自稳态突触可塑性试图在活动受到干扰的情况下维持正常功能。在 NMJ 中，有 3 个方面的活动被感知为触发 3 种不同的机制，这些机制有助于自稳态可塑性： 突触前动作电位的阻断会触发囊泡中乙酰胆碱释放增加，从而导致量子大小增加。 同时阻断突触前和突触后动作电位会增加囊泡释放的概率。 在单个囊泡自发融合期间阻断乙酰胆碱与乙酰胆碱受体的结合会触发可释放囊泡的数量增加以及运动神经元兴奋性增加。 了解 NMJ 如何响应突触活动的干扰，可以帮助我们了解其对各种神经肌肉疾病的反应。
