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Cone Photoreceptor Loss in Light-Damaged Albino Rats

We investigated the etiology of decreased cone-driven vision in a light damage (LD) model of retinal degeneration. To induce slow, moderate degeneration, albino rats underwent low-intensity light exposure for 10 days. Electroretinography was utilized to assess physiologic function of the rod- and co...

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Detalles Bibliográficos
Autores principales: Benthal, Molly C., McKeown, Alex S., Kraft, Timothy W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8999964/
https://www.ncbi.nlm.nih.gov/pubmed/35409336
http://dx.doi.org/10.3390/ijms23073978
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author Benthal, Molly C.
McKeown, Alex S.
Kraft, Timothy W.
author_facet Benthal, Molly C.
McKeown, Alex S.
Kraft, Timothy W.
author_sort Benthal, Molly C.
collection PubMed
description We investigated the etiology of decreased cone-driven vision in a light damage (LD) model of retinal degeneration. To induce slow, moderate degeneration, albino rats underwent low-intensity light exposure for 10 days. Electroretinography was utilized to assess physiologic function of the rod- and cone-driven retinal function in LD and control rats. Immunohistochemistry targeting cone arrestin allowed for quantification of cone density and for comparison of the decline in function. Photoreceptor loss was quantified by outer nuclear layer thickness decreases, as observed by optical coherence tomography and histology. The LD rats showed decreased rod- and cone-driven function with partial recovery 30 days after cessation of light exposure. In addition, LD rats showed decreased cone photoreceptor densities in the central retinal region compared to control rats. Our results demonstrate that the loss of cone-driven visual function induced by light damage is at least partially due to the death of cone photoreceptors.
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spelling pubmed-89999642022-04-12 Cone Photoreceptor Loss in Light-Damaged Albino Rats Benthal, Molly C. McKeown, Alex S. Kraft, Timothy W. Int J Mol Sci Article We investigated the etiology of decreased cone-driven vision in a light damage (LD) model of retinal degeneration. To induce slow, moderate degeneration, albino rats underwent low-intensity light exposure for 10 days. Electroretinography was utilized to assess physiologic function of the rod- and cone-driven retinal function in LD and control rats. Immunohistochemistry targeting cone arrestin allowed for quantification of cone density and for comparison of the decline in function. Photoreceptor loss was quantified by outer nuclear layer thickness decreases, as observed by optical coherence tomography and histology. The LD rats showed decreased rod- and cone-driven function with partial recovery 30 days after cessation of light exposure. In addition, LD rats showed decreased cone photoreceptor densities in the central retinal region compared to control rats. Our results demonstrate that the loss of cone-driven visual function induced by light damage is at least partially due to the death of cone photoreceptors. MDPI 2022-04-02 /pmc/articles/PMC8999964/ /pubmed/35409336 http://dx.doi.org/10.3390/ijms23073978 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Benthal, Molly C.
McKeown, Alex S.
Kraft, Timothy W.
Cone Photoreceptor Loss in Light-Damaged Albino Rats
title Cone Photoreceptor Loss in Light-Damaged Albino Rats
title_full Cone Photoreceptor Loss in Light-Damaged Albino Rats
title_fullStr Cone Photoreceptor Loss in Light-Damaged Albino Rats
title_full_unstemmed Cone Photoreceptor Loss in Light-Damaged Albino Rats
title_short Cone Photoreceptor Loss in Light-Damaged Albino Rats
title_sort cone photoreceptor loss in light-damaged albino rats
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8999964/
https://www.ncbi.nlm.nih.gov/pubmed/35409336
http://dx.doi.org/10.3390/ijms23073978
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