Synaptic function crucially relies on the constant supply and removal of neuronal membranes. The morphological complexity of neurons poses a significant challenge for neuronal protein transport since the machineries for protein synthesis and degradation are mainly localized in the cell soma. In response to this unique challenge, local micro-secretory systems have evolved that are adapted to the requirements of neuronal membrane protein proteostasis. However, our knowledge of how neuronal proteins are synthesized, trafficked to membranes, and eventually replaced and degraded remains scarce. Here, we review recent insights into membrane trafficking at synaptic sites and into the contribution of local organelles and micro-secretory pathways to synaptic function. We describe the role of endoplasmic reticulum specializations in neurons, Golgi-related organelles, and protein complexes like retromer in the synthesis and trafficking of synaptic transmembrane proteins. We discuss the contribution of autophagy and of proteasome-mediated and endo-lysosomal degradation to presynaptic proteostasis and synaptic function, as well as nondegradative roles of autophagosomes and lysosomes in signaling and synapse remodeling. We conclude that the complexity of neuronal cyto-architecture necessitates long-distance protein transport that combines degradation with signaling functions.

中文翻译：

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突触的需求——局部细胞器如何服务于突触蛋白质稳态。

突触功能关键依赖于神经元膜的持续供应和去除。神经元的形态复杂性对神经元蛋白质的转运提出了重大挑战，因为蛋白质合成和降解的机制主要位于细胞体中。为了应对这一独特的挑战，已经进化出适应神经元膜蛋白蛋白质稳态要求的局部微分泌系统。然而，我们对神经元蛋白质如何合成、运输到膜以及最终被替换和降解的知识仍然很少。在这里，我们回顾了最近对突触部位膜运输以及局部细胞器和微分泌途径对突触功能的贡献的见解。我们描述了内质网特化在神经元中的作用，高尔基相关的细胞器和蛋白质复合物如逆转录酶在突触跨膜蛋白的合成和运输中。我们讨论了自噬和蛋白酶体介导的和内溶酶体降解对突触前蛋白质稳态和突触功能的贡献，以及自噬体和溶酶体在信号传导和突触重塑中的非降解作用。我们得出结论，神经元细胞结构的复杂性需要将降解与信号功能相结合的长距离蛋白质转运。以及自噬体和溶酶体在信号传导和突触重塑中的非降解作用。我们得出结论，神经元细胞结构的复杂性需要将降解与信号功能相结合的长距离蛋白质转运。以及自噬体和溶酶体在信号传导和突触重塑中的非降解作用。我们得出结论，神经元细胞结构的复杂性需要将降解与信号功能相结合的长距离蛋白质转运。