Synapses are fundamental structures of neural circuits that transmit information between neurons. Thus, the process of neural circuit formation via proper synaptic connections shapes the basis of brain functions and animal behavior. Synapses continuously undergo repeated formation and elimination throughout the lifetime of an organism, reflecting the dynamics of neural circuit function. The structural transformation of synapses has been described mainly in relation to neural activity-dependent strengthening and weakening of synaptic functions, that is, functional plasticity of synapses. An increasing number of studies have unveiled the roles of microglia, brain-resident immune cells that survey the brain parenchyma with highly motile processes, in synapse formation and elimination as well as in regulating synaptic function. Over the past 15 years, the molecular mechanisms underlying microglia-dependent regulation of synaptic plasticity have been thoroughly studied, and researchers have reported that the disruption of microglia-dependent regulation causes synaptic dysfunction that leads to brain diseases. In this review, we will broadly introduce studies that report the roles of microglia in synaptic plasticity and the possible underlying molecular mechanisms.

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小胶质细胞调节突触发育和可塑性

突触是在神经元之间传递信息的神经回路的基本结构。因此，通过适当的突触连接形成神经回路的过程形成了大脑功能和动物行为的基础。突触在有机体的整个生命周期中不断地重复形成和消除，反映了神经回路功能的动态。突触的结构转变主要与突触功能的神经活动依赖性增强和减弱有关，即突触的功能可塑性。越来越多的研究揭示了小胶质细胞（一种大脑驻留免疫细胞）在突触形成和消除以及调节突触功能中的作用，这些细胞以高度运动的过程调查大脑实质。在过去的 15 年里，小胶质细胞依赖性突触可塑性调节的分子机制已被彻底研究，研究人员报告说，小胶质细胞依赖性调节的破坏会导致突触功能障碍，从而导致脑部疾病。在这篇综述中，我们将广泛介绍报告小胶质细胞在突触可塑性中的作用以及可能的潜在分子机制的研究。