Department of Ophthalmology and Jules Stein Eye Institute, University of California, Los Angeles, California 90095-7000.
Department of Ophthalmology and Jules Stein Eye Institute, University of California, Los Angeles, California 90095-7000
J Neurosci. 2021 Apr 14;41(15):3320-3330. doi: 10.1523/JNEUROSCI.2817-20.2021. Epub 2021 Feb 16.
Rod photoreceptors can be saturated by exposure to bright background light, so that no flash superimposed on the background can elicit a detectable response. This phenomenon, called increment saturation, was first demonstrated psychophysically by Aguilar and Stiles and has since been shown in many studies to occur in single rods. Recent experiments indicate, however, that rods may be able to avoid saturation under some conditions of illumination. We now show in electroretinogram and single-cell recordings that in continuous and prolonged exposure even to very bright light, the rods of mice from both sexes recover as much as 15% of their dark current and that responses can persist for hours. In parallel to recovery of outer segment current is an ∼10-fold increase in the sensitivity of rod photoresponses. This recovery is decreased in transgenic mice with reduced light-dependent translocation of the G protein transducin. The reduction in outer-segment transducin together with a novel mechanism of visual-pigment regeneration within the rod itself enable rods to remain responsive over the whole of the physiological range of vision. In this way, rods are able to avoid an extended period of transduction channel closure, which is known to cause photoreceptor degeneration. Rods are initially saturated in bright light so that no flash superimposed on the background can elicit a detectable response. Frederiksen and colleagues show in whole retina and single-cell recordings that, if the background light is prolonged, rods slowly recover and can continue to produce significant responses over the entire physiological range of vision. Response recovery occurs by translocation of the G protein transducin from the rod outer to the inner segment, together with a novel mechanism of visual-pigment regeneration within the rod itself. Avoidance of saturation in bright light may be one of the principal mechanisms the retina uses to keep rod outer-segment channels from ever closing for too long a time, which is known to produce photoreceptor degeneration.
视杆细胞可以通过暴露在明亮的背景光下而饱和,因此,没有叠加在背景光上的闪光可以引起可检测的反应。这种现象称为增量饱和,最早由 Aguilar 和 Stiles 在心理物理学上证明,并已在许多研究中表明在单个视杆细胞中发生。然而,最近的实验表明,在某些照明条件下,视杆细胞可能能够避免饱和。我们现在在视网膜电图和单细胞记录中表明,即使在持续和长时间暴露于非常亮的光线下,来自两性的小鼠视杆细胞也可以恢复多达 15%的暗电流,并且反应可以持续数小时。与外段电流恢复平行的是视杆光反应灵敏度增加了约 10 倍。这种恢复在光依赖性转导蛋白视紫红质转移减少的转基因小鼠中减少。外段转导蛋白的减少以及视杆细胞内视色素再生的新机制使视杆细胞能够在整个生理视觉范围内保持反应性。通过这种方式,视杆细胞能够避免延长的转导通道关闭期,已知这会导致光感受器变性。视杆细胞在强光下最初饱和,因此没有叠加在背景光上的闪光可以引起可检测的反应。Frederiksen 及其同事在整个视网膜和单细胞记录中表明,如果背景光延长,视杆细胞会缓慢恢复,并能够在整个生理视觉范围内继续产生显著的反应。反应恢复是通过 G 蛋白转导蛋白从视杆细胞外段到内段的易位以及视杆细胞内自身的一种新的视色素再生机制实现的。在明亮的光下避免饱和可能是视网膜用来防止视杆细胞外段通道长时间关闭的主要机制之一,已知这会导致光感受器变性。