Centre for Synaptic Plasticity, School of Biochemistry, University of Bristol, Bristol BS8 1TD, United Kingdom.
Centre for Synaptic Plasticity, School of Biochemistry, University of Bristol, Bristol BS8 1TD, United Kingdom.
Semin Cell Dev Biol. 2018 May;77:3-9. doi: 10.1016/j.semcdb.2017.09.007. Epub 2017 Sep 7.
One of the most interesting features of Arc-dependent synaptic plasticity is how multiple types of synaptic activity can converge to alter Arc transcription and then diverge to induce different plasticity outcomes, ranging from AMPA receptor internalisation that promotes long-term depression (LTD), to actin stabilisation that promotes long-term potentiation (LTP). This diversity suggests that there must be numerous levels of control to ensure the temporal profile, abundance, localisation and function of Arc are appropriately regulated to effect learning and memory in the correct contexts. The activity-dependent transcription and post-translational modification of Arc are crucial regulators of synaptic plasticity, fine-tuning the function of this key protein depending on the specific situation. The extensive cross-talk between signalling pathways and the numerous routes of Arc regulation provide a complex interplay of processes in which Arc-mediated plasticity can be broadly induced, but specifically tailored to synaptic activity. Here we provide an overview what is currently known about these processes and potential future directions.
Arc 依赖性突触可塑性的一个最有趣的特征是，多种类型的突触活动如何汇聚来改变 Arc 转录，然后发散以诱导不同的可塑性结果，范围从促进长时程抑制 (LTD) 的 AMPA 受体内化，到促进长时程增强 (LTP) 的肌动蛋白稳定。这种多样性表明，必须有许多层次的控制来确保 Arc 的时间特性、丰度、定位和功能得到适当调节，以便在正确的情况下实现学习和记忆。Arc 的活性依赖性转录和翻译后修饰是突触可塑性的关键调节剂，根据具体情况微调这种关键蛋白的功能。信号通路之间的广泛串扰和 Arc 调节的众多途径提供了一个复杂的相互作用过程，其中 Arc 介导的可塑性可以广泛诱导，但专门针对突触活动进行调整。在这里，我们概述了目前对这些过程的了解以及未来的潜在方向。
