Abstract
Purpose :
The high sensitivity of rod photoreceptors has led to the notion that they saturate when exposed to moderate light intensities, thus contributing little to vision in bright light. Recent studies have challenged this view and suggest that rods are able to avoid saturation under some conditions of bright persistent illumination. We tested the hypothesis that the light-dependent translocation of the G protein, transducin, causes a reduction in gain, allowing rods to escape saturation during prolonged illumination.
Methods :
We recorded mouse rod photoresponses en masse using ex vivo electroretinogram (ERG) as well as single-cell suction electrode recording in the presence of steady, bright background light. Cone contributions were eliminated from ERGs by the use of Gnat2-/- mice. In addition, we recorded from Gnat2-/- Gnat1-/-A3C+ mice in which the alpha subunit of transducin has an additional S-palmitoylation site that anchors it more tightly to cell membranes and thus impedes its translocation. The amount of pigment bleaching under experimental conditions was quantified using microspectrophotometry to measure spectral absorbance.
Results :
During prolonged exposure to bright light (104 - 106 effective photons μm-2 s-1) rods recovered responsiveness from initial saturation, increasing their response amplitude and sensitivity over a period of 30 - 90 minutes. In the A3C+ mouse, responses in the presence of the background light were almost undetectable immediately after turning on background light and continued to be smaller, growing much more slowly in amplitude than in control retinas. In addition, control rods remained responsive even after light exposures that were calculated to bleach nearly all the rhodopsin. This finding was confirmed in both whole retina recording as well as single-cell recording, indicating that a mechanism of pigment regeneration within the rods themselves is required to sustain responsiveness during prolonged bright light exposure.
Conclusions :
The reduction in outer-segment transducin and a novel mechanism of visual-pigment regeneration within the rod itself together 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 channel closure, which is known to cause photoreceptor death.
This is a 2021 ARVO Annual Meeting abstract.