The neuromuscular junction (NMJ) is the chemical synapse connecting motor neurons and skeletal muscle fibers. NMJs allow all voluntary movements, and ensure vital functions like breathing. Changes in the structure and function of NMJs are hallmarks of numerous pathological conditions that affect muscle function including sarcopenia, the age-related loss of muscle mass and function. However, the molecular mechanisms leading to the morphological and functional perturbations in the pre- and post-synaptic compartments of the NMJ remain poorly understood. Here, we discuss the role of the metabolic pathway associated to the kinase TOR (Target of Rapamycin) in the development, maintenance and alterations of the NMJ. This is of particular interest as the TOR pathway has been implicated in aging, but its role at the NMJ is still ill-defined. We highlight the respective functions of the two TOR-associated complexes, TORC1 and TORC2, and discuss the role of localized protein synthesis and autophagy regulation in motor neuron terminals and sub-synaptic regions of muscle fibers and their possible effects on NMJ maintenance.

神经肌肉接头（NMJ）是连接运动神经元和骨骼肌纤维的化学突触。 NMJ 允许所有自主运动，并确保呼吸等重要功能。 NMJ 结构和功能的变化是影响肌肉功能的多种病理状况的标志，包括肌肉减少症（与年龄相关的肌肉质量和功能丧失）。然而，导致 NMJ 突触前和突触后区室形态和功能扰动的分子机制仍然知之甚少。在这里，我们讨论与激酶 TOR 相关的代谢途径的作用（雷帕霉素靶点）参与 NMJ 的开发、维护和变更。这是特别有趣的，因为 TOR 通路与衰老有关，但它在 NMJ 中的作用仍然不明确。我们重点介绍了两个 TOR 相关复合物 TORC1 和 TORC2 各自的功能，并讨论了运动神经元末梢和肌纤维突触亚区中局部蛋白质合成和自噬调节的作用及其对 NMJ 维持的可能影响。