HCN1 Channels Enhance Rod System Responsivity in the Retina under Conditions of Light Exposure.

Vision originates in rods and cones at the outer retina. Already at these early stages, diverse processing schemes shape and enhance image information to permit perception over a wide range of lighting conditions. In this work, we address the role of hyperpolarization-activated and cyclic nucleotide...

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Main Authors: Vithiyanjali Sothilingam, Stylianos Michalakis, Marina Garcia Garrido, Martin Biel, Naoyuki Tanimoto, Mathias W Seeliger
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2016-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4725747?pdf=render
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author Vithiyanjali Sothilingam
Stylianos Michalakis
Marina Garcia Garrido
Martin Biel
Naoyuki Tanimoto
Mathias W Seeliger
author_facet Vithiyanjali Sothilingam
Stylianos Michalakis
Marina Garcia Garrido
Martin Biel
Naoyuki Tanimoto
Mathias W Seeliger
author_sort Vithiyanjali Sothilingam
collection DOAJ
description Vision originates in rods and cones at the outer retina. Already at these early stages, diverse processing schemes shape and enhance image information to permit perception over a wide range of lighting conditions. In this work, we address the role of hyperpolarization-activated and cyclic nucleotide-gated channels 1 (HCN1) in rod photoreceptors for the enhancement of rod system responsivity under conditions of light exposure.To isolate HCN1 channel actions in rod system responses, we generated double mutant mice by crossbreeding Hcn1-/- mice with Cnga3-/- mice in which cones are non-functional. Retinal function in the resulting Hcn1-/- Cnga3-/- animals was followed by means of electroretinography (ERG) up to the age of four month. Retinal imaging via scanning laser ophthalmoscopy (SLO) and optical coherence tomography (OCT) was also performed to exclude potential morphological alterations.This study on Hcn1-/- Cnga3-/- mutant mice complements our previous work on HCN1 channel function in the retina. We show here in a functional rod-only setting that rod responses following bright light exposure terminate without the counteraction of HCN channels much later than normal. The resulting sustained signal elevation does saturate the retinal network due to an intensity-dependent reduction in the dynamic range. In addition, the lack of rapid adaptational feedback modulation of rod photoreceptor output via HCN1 in this double mutant limits the ability to follow repetitive (flicker) stimuli, particularly under mesopic conditions.This work corroborates the hypothesis that, in the absence of HCN1-mediated feedback, the amplitude of rod signals remains at high levels for a prolonged period of time, leading to saturation of the retinal pathways. Our results demonstrate the importance of HCN1 channels for regular vision.
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spelling doaj.art-37dc61ff7c1e463c97f9cb7ed30532da2022-12-22T03:19:38ZengPublic Library of Science (PLoS)PLoS ONE1932-62032016-01-01111e014772810.1371/journal.pone.0147728HCN1 Channels Enhance Rod System Responsivity in the Retina under Conditions of Light Exposure.Vithiyanjali SothilingamStylianos MichalakisMarina Garcia GarridoMartin BielNaoyuki TanimotoMathias W SeeligerVision originates in rods and cones at the outer retina. Already at these early stages, diverse processing schemes shape and enhance image information to permit perception over a wide range of lighting conditions. In this work, we address the role of hyperpolarization-activated and cyclic nucleotide-gated channels 1 (HCN1) in rod photoreceptors for the enhancement of rod system responsivity under conditions of light exposure.To isolate HCN1 channel actions in rod system responses, we generated double mutant mice by crossbreeding Hcn1-/- mice with Cnga3-/- mice in which cones are non-functional. Retinal function in the resulting Hcn1-/- Cnga3-/- animals was followed by means of electroretinography (ERG) up to the age of four month. Retinal imaging via scanning laser ophthalmoscopy (SLO) and optical coherence tomography (OCT) was also performed to exclude potential morphological alterations.This study on Hcn1-/- Cnga3-/- mutant mice complements our previous work on HCN1 channel function in the retina. We show here in a functional rod-only setting that rod responses following bright light exposure terminate without the counteraction of HCN channels much later than normal. The resulting sustained signal elevation does saturate the retinal network due to an intensity-dependent reduction in the dynamic range. In addition, the lack of rapid adaptational feedback modulation of rod photoreceptor output via HCN1 in this double mutant limits the ability to follow repetitive (flicker) stimuli, particularly under mesopic conditions.This work corroborates the hypothesis that, in the absence of HCN1-mediated feedback, the amplitude of rod signals remains at high levels for a prolonged period of time, leading to saturation of the retinal pathways. Our results demonstrate the importance of HCN1 channels for regular vision.http://europepmc.org/articles/PMC4725747?pdf=render
spellingShingle Vithiyanjali Sothilingam
Stylianos Michalakis
Marina Garcia Garrido
Martin Biel
Naoyuki Tanimoto
Mathias W Seeliger
HCN1 Channels Enhance Rod System Responsivity in the Retina under Conditions of Light Exposure.
PLoS ONE
title HCN1 Channels Enhance Rod System Responsivity in the Retina under Conditions of Light Exposure.
title_full HCN1 Channels Enhance Rod System Responsivity in the Retina under Conditions of Light Exposure.
title_fullStr HCN1 Channels Enhance Rod System Responsivity in the Retina under Conditions of Light Exposure.
title_full_unstemmed HCN1 Channels Enhance Rod System Responsivity in the Retina under Conditions of Light Exposure.
title_short HCN1 Channels Enhance Rod System Responsivity in the Retina under Conditions of Light Exposure.
title_sort hcn1 channels enhance rod system responsivity in the retina under conditions of light exposure
url http://europepmc.org/articles/PMC4725747?pdf=render
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