中国神经再生研究(英文版) ›› 2021, Vol. 21 ›› Issue (5): 1698-1714.doi: 10.4103/NRR.NRR-D-24-01127

• 综述:神经损伤修复保护与再生 • 上一篇    下一篇

突触修剪机制和新兴图像技术在神经系统疾病中的应用

  

  • 出版日期:2026-05-15 发布日期:2025-08-20

Synaptic pruning mechanisms and application of emerging imaging techniques in neurological disorders

Yakang Xing1, 2, 3, Yi Mo1, 4, Qihui Chen1, 4, Xiao Li1, 2, 4, 5, *   

  1. 1 Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases of Ministry of Education, Gannan Medical University, Ganzhou, Jiangxi Province, China;  2 Institute for Department of Physiology, School of Basic Medical Sciences, Gannan Medical University, Ganzhou, Jiangxi Province, China;  3 Department of Pathology, Anyang Maternal and Child Health Hospital, Anyang, Henan Province, China;  4 Ganzhou Key Laboratory of Neuroinflammation Research, Gannan Medical University, Ganzhou, Jiangxi Province, China;  5 Jiangxi Province Key Laboratory of Pharmacology of Traditional Chinese Medicine, Gannan Medical University, Ganzhou, Jiangxi Province, China
  • Online:2026-05-15 Published:2025-08-20
  • Contact: Xiao Li, MD, 18970786303@gmu.edu.cn.
  • Supported by:
    This work was supported by the National Natural Science Foundation of China, No. 31760290, 82160688 and the Key Development Areas Project of Ganzhou Science and Technology, No. 2022B-SF9554 (all to XL).

摘要:

突触修剪是突触细化的一个关键过程,可消除神经回路中不稳定的突触连接。这一过程主要由自发神经活动和经验依赖机制触发和调节。突触修剪过程涉及多种分子信号和一系列调节 “吃我 ”和 “不吃我 ”状态的调控活动。在生理条件下,神经胶质细胞和神经元之间的相互作用会清除不必要的突触,通过突触修剪维持正常的神经回路功能。遗传和环境因素的改变会导致突触修剪失衡,从而可能导致神经系统疾病的发生和发展。此综述探讨了突触修剪的分子机制在神经发育中的关键作用。重点关注了突触修剪对神经回路的调控及其与神经系统疾病的关联。文章还讨论了新兴光学和成像技术在观察突触结构和功能方面的应用及其临床转化的潜力。目的是加深对神经发育过程中突触修剪的理解,包括突触功能调控的分子基础和突触密度的动态变化,并研究这些机制在神经系统疾病的病理生理学中的潜在作用,为神经系统疾病的治疗提供理论基础。

https://orcid.org/0000-0002-5411-5669 (Xiao Li)

关键词: 趋化因子, 补体, 经验依赖驱动的突触修剪, 成像技术, 神经胶质, 信号通路, 突触消除, 突触修剪

Abstract: Synaptic pruning is a crucial process in synaptic refinement, eliminating unstable synaptic connections in neural circuits. This process is triggered and regulated primarily by spontaneous neural activity and experience-dependent mechanisms. The pruning process involves multiple molecular signals and a series of regulatory activities governing the “eat me” and “don’t eat me” states. Under physiological conditions, the interaction between glial cells and neurons results in the clearance of unnecessary synapses, maintaining normal neural circuit functionality via synaptic pruning. Alterations in genetic and environmental factors can lead to imbalanced synaptic pruning, thus promoting the occurrence and development of autism spectrum disorder, schizophrenia, Alzheimer’s disease, and other neurological disorders. In this review, we investigated the molecular mechanisms responsible for synaptic pruning during neural development. We focus on how synaptic pruning can regulate neural circuits and its association with neurological disorders. Furthermore, we discuss the application of emerging optical and imaging technologies to observe synaptic structure and function, as well as their potential for clinical translation. Our aim was to enhance our understanding of synaptic pruning during neural development, including the molecular basis underlying the regulation of synaptic function and the dynamic changes in synaptic density, and to investigate the potential role of these mechanisms in the pathophysiology of neurological diseases, thus providing a theoretical foundation for the treatment of neurological disorders.

Key words: chemokine, complement, experience-dependent driven synaptic pruning, imaging techniques, neuroglia, signaling pathways, synapse elimination, synaptic pruning