Study on the mechanism of visual dysfunction and pathological changes in mice with acute hepatic encephalopathy
10.16557/j.cnki.1000-7547.2024.05.001
- VernacularTitle:急性肝性脑病小鼠视觉功能障碍的机制研究
- Author:
Kenan LI
1
;
Yunhu BAI
;
Zhenhua WANG
;
Ziwei NI
;
Changlei ZHU
;
Hui LIU
;
Yanling YANG
;
Yayun WANG
Author Information
1. 空军军医大学基础医学院国家级基础医学教学示范中心,西安 710032
- Publication Type:Journal Article
- Keywords:
acute hepatic encephalopathy(AHE);
retina;
visual electrophysiology;
ventrolateral thalamic nucleus(VL);
visual cortex;
mouse
- From:
Chinese Journal of Neuroanatomy
2024;40(5):533-540
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the changes in visual function and its mechanism in mice with acute hepatic enceph-alopathy(AHE)model.Method:Twelve male mice were divided into experimental and control groups,with six mice in each.A mouse model of AHE was created using TAA,and serum ALT,AST,and ammonia levels were measured using ELISA and colorimetric assays.Behavioral tests,including open-field and elevated cross maze experiments,were conducted,and neurological function scores were evaluated.HE staining was used to evaluate visual function scores in mice.Behavioural tests were conducted to assess neurological function scores.HE staining was used for pathological examination of the liver and retina.Visual electrophysiology was used to test visual function in both eyes.Retrograde tracer adeno-associated virus was used to label the ventrolateral thalamic nucleus(VL)of thalamus in c-Fos-CreERT2 mice.Results:Compared to the control group,the AHE mice had abnormal liver function and neurological changes.The HE results showed liver tissue damage.The retinal tissues were not significantly different from the control group.The visual electrophysiological results showed changes in visual function in both eyes of the AHE mice.The retrograde tracer virus injections revealed no significant difference in VL activation between the AHE model and the control group.In the AHE model,VL nucleus accumbens neurons primarily received input from ipsilateral visual cortical neurons.Conclusion:The visual deficits in AHE mice caused by TAA were primarily functional rather than organic changes,and were associated with the activation of the visual cortex-to-VL pathway.
