Comparative study of wild-type and rd10 mice reveals transient intrinsic optical signal response before phosphodiesterase activation in retinal photoreceptors

野生型和 rd10 小鼠的比较研究揭示了视网膜光感受器中磷酸二酯酶激活前的瞬态内在光信号响应

阅读:18
作者:Yiming Lu, Tae-Hoon Kim, Xincheng Yao

Abstract

Transient intrinsic optical signal (IOS) has been observed in stimulus-evoked retinal photoreceptors. This study is to compare IOS changes in wild-type and retinal degeneration 10 (rd10) mouse retinas, to evaluate the effect of cyclic guanosine monophosphate phosphodiesterase on photoreceptor-IOS. Time-lapse near-infrared light microscopy was employed to monitor the spatiotemporal dynamics of the IOS responses in freshly isolated retinas activated by visible light stimulation. Comparative IOS recordings were conducted at postnatal days 14 (P14) and P16. At P14, intrinsic optical signal magnitudes and spatiotemporal dynamics in wild-type and rd10 retinas were similar, indicating that the phosphodiesterase deficiency in rd10 did not affect the formation of photoreceptor-IOS. At P16, IOS magnitude in rd10 significantly decreased compared to that in wild-type, suggesting the IOS sensitivity to the photoreceptor degeneration in rd10. Our experimental results and theoretical analysis indicate that early disc-based stages of the phototransduction cascade before the activation of phosphodiesterase may contribute to the formation of the photoreceptor-IOS responses; and the IOS can be a sensitive biomarker for objective assessment of retinal function. Impact statement: Comparative study of wild-type and rd10 mice was implemented to reveal that transient intrinsic optical signal (IOS) was initiated before the phosphodiesterase activation in stimulus-activated photoreceptors and the IOS magnitude was sensitive to photoreceptor degeneration. The photoreceptor-IOS promises a noninvasive biomarker for objective assessment of age-related macular degeneration, retinitis pigmentosa, and other eye diseases that can produce photoreceptor dysfunctions.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。