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视杆光转导的失活机制:科根讲座。

Deactivation mechanisms of rod phototransduction: the Cogan lecture.

机构信息

Department of Ophthalmology and Vision Science and Center for Neuroscience, University of California, Davis, California, USA

出版信息

Invest Ophthalmol Vis Sci. 2010 Mar;51(3):1282-8. doi: 10.1167/iovs.09-4366.

Abstract

The absorption of photons in rods and cones of the retina activate homologous biochemical signaling cascades that lead to the electrical changes that subserve the first steps in vision. Persistent activity of the cascade interferes with the ability of the photoreceptor to signal the absorption of subsequent photons, ultimately limiting the photoreceptor's sensitivity and temporal resolution. This article summarizes recent work on transgenic and knockout mouse rods that has revealed the deactivation mechanisms essential for normal response recovery and how each of these processes contributes to the overall time course of the flash response of rods.

摘要

视网膜中的视杆和视锥细胞吸收光子会激活同源的生化信号级联反应,从而导致支持视觉初始步骤的电变化。级联反应的持续活动会干扰光感受器对后续光子吸收的信号传递能力,最终限制光感受器的灵敏度和时间分辨率。本文总结了最近在转基因和敲除小鼠视杆细胞上的研究工作,这些工作揭示了正常响应恢复所必需的失活动力学机制,以及这些过程中的每一个如何共同影响视杆细胞闪光反应的整体时程。

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