大鼠眼缺血综合征模型中视网膜内层神经元可塑性改变和视网膜重构

doi:10.6040/j.issn.1673-3770.1.2020.049

Journal of Otolaryngology and Ophthalmology of Shandong University ›› 2020, Vol. 34 ›› Issue (4): 80-86.doi: 10.6040/j.issn.1673-3770.1.2020.049

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Changes in the neural plasticity of neurons and retinal remodeling in the retinal inner nuclear layer of an ocular ischemic syndrome rat model CHEN Xi, LI Shanshan, YOU Ran, ZHAO Lu, WANG Yanling Department of Ophthalmology, Beijing Friendship Hospital, Capital Medical University, Beijing, China, 100050Abstract: Objective〓

To analyze the changes in the neurons of the retinal inner nuclear layer and in the visual function of rat models with ocular ischemia syndrome. MethodsAt the age of 8 weeks, Brown-Norway rats underwent bilateral common carotid artery occlusion(BCCAO)surgery as the model of ocular ischemia syndrome. After 1 and 2 months since the model was established, the retinal thickness was measured in eyeball slices. By applying immunofluorescence, changes in the morphology and synaptic plasticity of horizontal and bipolar cells in the retinal inner nuclear layer were observed. Changes in the visual function of rats were detected by electrophysiology. ResultsWith prolongation of the retinal ischemia time, the number of cells in each retinal layer decreased, and thicknesses of the inner and outer plexiform layers also decreased. Dendrites of horizontal and bipolar cells decreased or disappeared. The density of presynaptic membrane marker synaptophysin decreased. After 2 months since the modeling, the somatic positions of horizontal and bipolar cells migrated from the outer side to the basal side of the inner nuclear layer and formed new neurites. Synaptophysin was randomly distributed in the outer nuclear layer. Electrophysiology showed markedly reduced a- and b-wave amplitudes in BCCAO rats, indicating that the visual function of the BCCAO rats was impaired, and various retinal cell functions were affected. ConclusionIn rat models with ocular ischemia syndrome, the thickness of retinal layers and number of retinal cells decreased. Two months after the model was established, horizontal and bipolar cells migrated, and synaptic rewiring occurred, resulting in retinal remodeling.

Key words: Ocular ischemia syndrome;
Bipolar cells;
Horizontal cells;
Neural plasticity;
Retinal remodeling视网膜缺血通常会导致严重的视力损伤, 其主要原因是相关疾病引起的视网膜血液灌注不足, 如颈动脉狭窄等^［1］。在缺血损伤过程中, 视网膜的能量代谢下降, 导致一系列复杂的连锁反应, 如细胞离子稳态的丧失, 离子通道和转运体等功能障碍, 最终导致视网膜神经元的损伤, 特别是内层视网膜神经元的死亡^［2-5］。与缺血相关的疾病包括眼缺血综合征(ocular ischemic syndrome, OIS)、视网膜中央动脉阻塞、视网膜中央静脉阻塞、高血压性视网膜病变、糖尿病性视网膜病变和青光眼等^［6-8］。

Received:2020-05-26 Online:2020-07-20 Published:2020-08-28

Abstract

Abstract: Objective To analyze the changes in the neurons of the retinal inner nuclear layer and in the visual function of rat models with ocular ischemia syndrome. Methods At the age of 8 weeks, Brown-Norway rats underwent bilateral common carotid artery occlusion(BCCAO)surgery as the model of ocular ischemia syndrome. After 1 and 2 months since the model was established, the retinal thickness was measured in eyeball slices. By applying immunofluorescence, changes in the morphology and synaptic plasticity of horizontal and bipolar cells in the retinal inner nuclear layer were observed. Changes in the visual function of rats were detected by electrophysiology. Results With prolongation of the retinal ischemia time, the number of cells in each retinal layer decreased, and thicknesses of the inner and outer plexiform layers also decreased. Dendrites of horizontal and bipolar cells decreased or disappeared. The density of presynaptic membrane marker synaptophysin decreased. After 2 months since the modeling, the somatic positions of horizontal and bipolar cells migrated from the outer side to the basal side of the inner nuclear layer and formed new neurites. Synaptophysin was randomly distributed in the outer nuclear layer. Electrophysiology showed markedly reduced a- and b-wave amplitudes in BCCAO rats, indicating that the visual function of the BCCAO rats was impaired, and various retinal cell functions were affected. Conclusion In rat models with ocular ischemia syndrome, the thickness of retinal layers and number of retinal cells decreased. Two months after the model was established, horizontal and bipolar cells migrated, and synaptic rewiring occurred, resulting in retinal remodeling.

Key words: Ocular ischemia syndrome, Bipolar cells, Horizontal cells, Neural plasticity, Retinal remodeling

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