中国神经再生研究(英文版) ›› 2025, Vol. 20 ›› Issue (5): 1244-1257.doi: 10.4103/NRR.NRR-D-23-01620

• 综述:神经损伤修复保护与再生 • 上一篇    下一篇

神经轴突引导分子在癫痫发病中的作用

  

  • 出版日期:2025-05-15 发布日期:2024-10-29

The role of axon guidance molecules in the pathogenesis of epilepsy

Zheng Liu, Chunhua Pan, Hao Huang*   

  1. Department of Neurology, Afffliated Hospital of Zunyi Medical University, Zunyi, Guizhou Province, China
  • Online:2025-05-15 Published:2024-10-29
  • Contact: Hao Huang, PhD, haohuang325@163.com.
  • Supported by:
    This work was supported by the Nattonal Natural Science Foundatton of China, Nos. 81760247, 82171450; the Scienttffc Research Foundatton for Doctors of the Afffliated Hospital of Zunyi Medical University, No. (2016)14 (all to HH). 

摘要:

目前治疗癫痫的方法只能控制发病症状,而无法改变发病和抑制病情发展。因此,需要发现具有新的细胞和分子靶点及作用机制的药物。有研究表明,轴突导向分子可影响神经网络的结构和功能改变,不同的同轴导向分子变异与癫痫易感性之间具有相关性。为此,文章主要阐述了轴突导向分子在癫痫发病机制中的作用,包括轴突导向分子对癫痫各方面的影响,如神经元连接、脑网络和结构重塑之间的关系,以及神经炎症性发作活动。①轴突导向分子(如semaphorins和ephrins)在引导神经元轴突生长和突触连接的形成方面发挥着至关重要的作用,这些分子的表达或功能异常会导致神经元连接出现问题,并导致癫痫发作。②神经网络的重塑也是癫痫的一个主要特征,轴突导向分子参与神经回路的动态重组,影响突触的形成和消除,这些分子的失调会破坏神经元网络中兴奋和抑制之间的平衡,导致过度兴奋和癫痫易感性增加。③炎症信号可调节轴突导向分子的表达和功能,从而影响轴突生长、导向和突触可塑性,而神经炎症失调可加剧神经元功能障碍并导致癫痫发作。④文章通过阐明轴突导向分子在癫痫发病中的病理机制,为研究人员研究癫痫的治疗靶点提供了参考依据,为癫痫的治疗策略提供了新的视角。

https://orcid.org/0000-0001-7739-275X (Hao Huang)

关键词: 癫痫, 神经元, 轴突指导, 神经元可塑性, 突触重塑, 耐药性癫痫, 神经炎症性疾病, 神经通路, 神经系统疾病, 神经再生

Abstract: Current treatments for epilepsy can only manage the symptoms of the condition but cannot alter the initial onset or halt the progression of the disease. Consequently, it is crucial to identify drugs that can target novel cellular and molecular mechanisms and mechanisms of action. Increasing evidence suggests that axon guidance molecules play a role in the structural and functional modifications of neural networks and that the dysregulation of these molecules is associated with epilepsy susceptibility. In this review, we discuss the essential role of axon guidance molecules in neuronal activity in patients with epilepsy as well as the impact of these molecules on synaptic plasticity and brain tissue remodeling. Furthermore, we examine the relationship between axon guidance molecules and neuroinflammation, as well as the structural changes in specific brain regions that contribute to the development of epilepsy. Ample evidence indicates that axon guidance molecules, including semaphorins and ephrins, play a fundamental role in guiding axon growth and the establishment of synaptic connections. Deviations in their expression or function can disrupt neuronal connections, ultimately leading to epileptic seizures. The remodeling of neural networks is a significant characteristic of epilepsy, with axon guidance molecules playing a role in the dynamic reorganization of neural circuits. This, in turn, affects synapse formation and elimination. Dysregulation of these molecules can upset the delicate balance between excitation and inhibition within a neural network, thereby increasing the risk of overexcitation and the development of epilepsy. Inflammatory signals can regulate the expression and function of axon guidance molecules, thus influencing axonal growth, axon orientation, and synaptic plasticity. The dysregulation of neuroinflammation can intensify neuronal dysfunction and contribute to the occurrence of epilepsy. This review delves into the mechanisms associated with the pathogenicity of axon guidance molecules in epilepsy, offering a valuable reference for the exploration of therapeutic targets and presenting a fresh perspective on treatment strategies for this condition.

Key words: axon guidance, drug-resistant epilepsy, epilepsy, nerve regeneration, nervous system diseases, neural pathways, neuroinflammatory diseases, neuronal plasticity, neurons, synaptic remodeling