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人类视锥细胞通路中暗适应的特征描述:等效背景假说的应用

Characterisation of dark adaptation in human cone pathways: an application of the equivalent background hypothesis.

作者信息

Pianta M J, Kalloniatis M

机构信息

Department of Optometry and Vision Sciences, University of Melbourne, Victoria 3010, Australia.

出版信息

J Physiol. 2000 Nov 1;528(Pt 3):591-608. doi: 10.1111/j.1469-7793.2000.00591.x.

DOI:10.1111/j.1469-7793.2000.00591.x
PMID:11060133
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2270158/
Abstract

It is well accepted that in rod photoreceptors the photoproducts generated by a bleach cause desensitisation during dark adaptation. We examine whether this notion holds for cones. A model of cone dark adaptation is developed based on the equivalent background concept. The underlying theory of the model relies on a series of assumptions that link psychophysically determined detection thresholds to cone phototransduction. Correction of thresholds for the reduced quantum-catching ability of the cones (due to the depletion of photopigment caused by a bleaching light) is an important aspect of the model. Foveal detection thresholds were measured for a small test flash presented on a large steady background field or presented alone after adapting to the background field. Test and background fields were monochromatic, with wavelengths closely matched to promote detection by the luminance mechanism. The model provided a good description of the data collected under these conditions. Parameters of the model were similar for all wavelengths and each observer, as were the derived equivalent background relationships. Analysis of previously published data for Stiles' pi5 mechanism gave analogous results. The model is made up of two components. The early (fast) component is likely to be due to the direct action of the cone equivalent of inactivated Rh* on the G-protein cascade and/or the reverse reaction of the cone equivalent of inactivated Rh* to Rh*. The later (slow) component may be due to the direct action of cone opsin on the G-protein cascade.

摘要

人们普遍认为,在视杆光感受器中,漂白产生的光产物会在暗适应过程中引起脱敏。我们研究了这一概念是否适用于视锥细胞。基于等效背景概念建立了视锥细胞暗适应模型。该模型的基础理论依赖于一系列假设,这些假设将心理物理学确定的检测阈值与视锥细胞光转导联系起来。对视锥细胞量子捕获能力降低(由于漂白光导致光色素耗尽)的阈值校正,是该模型的一个重要方面。在大的稳定背景场中呈现一个小测试闪光,或在适应背景场后单独呈现时,测量中央凹检测阈值。测试场和背景场是单色的,波长紧密匹配,以促进通过亮度机制进行检测。该模型很好地描述了在这些条件下收集的数据。所有波长和每个观察者的模型参数相似,推导的等效背景关系也相似。对之前发表的关于斯泰尔斯(Stiles)的π5机制的数据进行分析,得到了类似的结果。该模型由两个部分组成。早期(快速)部分可能是由于失活的视紫红质(Rh*)的视锥细胞等效物对G蛋白级联反应的直接作用和/或失活的视紫红质(Rh*)的视锥细胞等效物与视紫红质(Rh*)的反向反应。后期(缓慢)部分可能是由于视锥细胞视蛋白对G蛋白级联反应的直接作用。