中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (3): 1236-1248.doi: 10.4103/NRR.NRR-D-24-00394

• 原著:神经损伤修复保护与再生 • 上一篇    

慢性高眼压小鼠初级视皮质突触和树突棘减少

  

  • 出版日期:2026-03-15 发布日期:2025-07-05

Synapses and dendritic spines are eliminated in the primary visual cortex of mice subjected to chronic intraocular pressure elevation

Xinyi Zhang1 , Deling Li1 , Weiting Zeng1, 2, Yiru Huang1 , Zongyi Zhan1, 3, Yuning Zhang1 , Qinyuan Hu1 , Lianyan Huang4, *, Minbin Yu1, *   

  1. 1 State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, Guangdong Province, China; 2 Department of Ophthalmology, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People’s Hospital, Shenzhen, Guangdong Province, China; 3 Department of Ophthalmology, Shenzhen Eye Hospital, Jinan University, Shenzhen Eye Institute, Shenzhen, Guangdong Province, China; 4 Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong Province, China
  • Online:2026-03-15 Published:2025-07-05
  • Contact: Lianyan Huang, MD, PhD, Huangly55@mail.sysu.edu.cn; Minbin Yu, MD, PhD, yuminbin@mail.sysu.edu.cn.
  • Supported by:
    This study was supported by the National Natural Science Foundation of China, No. 82271115 (to MY).

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摘要：

突触可塑性对于维持中枢神经系统神经元功能至关重要，也是中枢神经系统神经退行性疾病的关键指标。最近有证据表明，青光眼也是一种中枢神经系统退行性疾病，会对整个视通路造成损害。然而，青光眼引起的初级视皮质内突触可塑性的变化尚不清楚。此次实验通过前房注射磁性微珠的方式构建单侧慢性高眼压小鼠模型，可见高眼压持续4周后，高压眼对侧的上丘和外侧膝状体中神经元的胞体缩小，并伴有胶质细胞活化和炎症因子表达增加。而高眼压持续8周可导致高压眼对侧初级视皮质的兴奋性和抑制性突触、树突棘和活化的神经胶质细胞减少。上述结果表明，青光眼不仅可直接损害视网膜，还会导致初级视皮质突触和树突棘发生变化，这为青光眼的发病机制提供了新见解。

https://orcid.org/0000-0001-8663-6197 (Lianyan Huang); https://orcid.org/0000-0002-3938-7164 (Minbin Yu)

关键词: 青光眼, 慢性高眼压, 视皮质, 视觉通路, 视网膜神经节细胞, 神经元, 突触可塑性, 树突棘, 胶质细胞, 神经炎症

Abstract: Synaptic plasticity is essential for maintaining neuronal function in the central nervous system and serves as a critical indicator of the effects of neurodegenerative disease. Glaucoma directly impairs retinal ganglion cells and their axons, leading to axonal transport dysfuntion, subsequently causing secondary damage to anterior or posterior ends of the visual system. Accordingly, recent evidence indicates that glaucoma is a degenerative disease of the central nervous system that causes damage throughout the visual pathway. However, the effects of glaucoma on synaptic plasticity in the primary visual cortex remain unclear. In this study, we established a mouse model of unilateral chronic ocular hypertension by injecting magnetic microbeads into the anterior chamber of one eye. We found that, after 4 weeks of chronic ocular hypertension, the neuronal somas were smaller in the superior colliculus and lateral geniculate body regions of the brain contralateral to the affected eye. This was accompanied by glial cell activation and increased expression of inflammatory factors. After 8 weeks of ocular hypertension, we observed a reduction in the number of excitatory and inhibitory synapses, dendritic spines, and activation of glial cells in the primary visual cortex contralateral to the affected eye. These findings suggest that glaucoma not only directly damages the retina but also induces alterations in synapses and dendritic spines in the primary visual cortex, providing new insights into the pathogenesis of glaucoma.

Key words: chronic ocular hypertension, dendritic spines, glaucoma, glial cells, neuroinflammation, neuron, retinal ganglion cells, synaptic plasticity, visual cortex, visual pathway