Light exposure resulted in APPswe/PS1 transgenic mice retinal structural and functional disorder
10.13389/j.cnki.rao.2017.0080
- VernacularTitle:强光照致TgAPPswePS1转基因鼠视网膜功能障碍和结构损伤
- Author:
Zhizhang DONG
;
Juan LI
;
Xuerong SUN
;
Jian GE
- Keywords:
light insult;
electroretinography;
transgenic mouse;
Alzheimer's disease
- From:
Recent Advances in Ophthalmology
2017;37(4):317-320
- CountryChina
- Language:Chinese
-
Abstract:
Objective To research the functional and structural change in TgAP-PswePS1 transgenic mice after intensive light exposure insult.Methods APPswe/PS1 transgenic mice at the age of 6 months old were grouped for experiments,the transgenic mice were replaced by light insult device for 6 months,while the control mice were kept in normal conditions.After 6 months light exposure,the eyes of control and experimental mice were examined with electroretinography (ERG).The retinal morphology change was investigated with H&E staining.All of the results were quantified and statistically analyzed.Results In the control group,the amplitudes of a and b wave in the rod response were (18.33 ±3.53) μV and (107.58 ± 14.72) μV,while (64.80 ±7.57) μV and (178.76 ± 14.47) μV for the amplitudes of a and b wave in the maximum response;After treated by 6 months of intensive light exposure,in experimental group mice,the amplitudes of a and b wave in the rod response were (17.92 ±4.89) μV and (21.83 ± 5.51) μV;While in the maximum response a striking decrease was detected with a wave (18.23 ±4.44) μV and b wave (24.50 ± 4.49) μV,by compared with control group,the difference were statistical significant (all P < 0.05).Histopathological analysis found significant loss of outer nuclear layer,photoreceptor out segment,whereas controls remained little change in the retina.And the retinal thickness decreased significantly from (181.32 ± 13.47) μm in control group to (102.34 ±9.38) μm after light insults in experimental group,the difference was statistical significant (P =0.017).Conclusion Intensive light exposure can cause the retinal structural and functional disorder in the AP-Pswe/PS1 transgenic mouse.