Synapses and dendritic spines are eliminated in the primary visual cortex of mice subjected to chronic intraocular pressure elevation
Xinyi Zhang1
Deling Li1
Weiting Zeng2
Yiru Huang1
Zongyi Zhan3
Yuning Zhang1
Qinyuan Hu1
Lianyan Huang4
Minbin Yu1
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,China2.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;Department of Ophthalmology,The First Affiliated Hospital of Shenzhen University,Shenzhen Second People's Hospital,Shenzhen,Guangdong Province,China3.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;Department of Ophthalmology,Shenzhen Eye Hospital,Jinan University,Shenzhen Eye Institute,Shenzhen,Guangdong Province,China4.Department of Pathophysiology,Zhongshan School of Medicine,Sun Yat-sen University,Guangzhou,Guangdong Province,China
摘要：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.
机标关键词：pressurecortexvisualmicechronicdendriticelevationeliminated
论文发表日期：2026-03-30
在线出版日期：2026-03-18（本平台首次上网日期，不代表文献的发表时间）
页数：13( 1236-1248 )
英文信息