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Retinal compensatory changes after light damage in albino mice

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dc.contributor.authorMontalbán Soler, Luis
dc.contributor.authorJiménez López, Manuel
dc.contributor.authorBezerra de Sá, Fabrízio
dc.contributor.authorSalinas Navarro, Manuel Ángel
dc.contributor.authorAlarcón Martínez, Luis
dc.contributor.authorGalindo Romero, Caridad
dc.contributor.authorGarcía Ayuso, Diego
dc.contributor.authorAvilés Trigueros, Marcelino
dc.contributor.authorVidal Sanz, Manuel
dc.contributor.authorAgudo Barriuso, Marta
dc.contributor.authorVillegas Pérez, Maria Paz
dc.contributor.departmentAnatomía Humana y Psicobiología
dc.date.accessioned2026-03-05T10:03:19Z
dc.date.available2026-03-05T10:03:19Z
dc.date.copyright© 2012 Molecular Vision
dc.date.issued2012-03-24
dc.description.abstractPurpose: To investigate the anatomic and functional changes triggered by light exposure in the albino mouse retina and compare them with those observed in the albino rat. Methods: BALB/c albino mice were exposed to 3,000 lx of white light during 24 h and their retinas analyzed from 1 to 180 days after light exposure (ALE). Left pupil mydriasis was induced with topical atropine. Retinal function was analyzed by electroretinographic (ERG) recording. To assess retinal degeneration, hematoxylin and eosin staining, the TdT-mediated dUTP nick-end labeling (TUNEL) technique, and quantitative immunohistofluorescence for synaptophysin and protein kinase Cα (PKCα) were used in cross sections. Intravenous injection of horseradish peroxidase and Fluoro-Gold™ tracing were used in whole-mounted retinas to study the retinal vasculature and the retinal ganglion cell (RGC) population, respectively. Results: Light exposure caused apoptotic photoreceptor death in the central retina. This death was more severe in the dorsal than in the ventral retina, sparing the periphery. Neither retinal vascular leakage nor retinal ganglion cell death was observed ALE. The electroretinographic a-wave was permanently impaired, while the b-wave decreased but recovered gradually by 180 days ALE. The scotopic threshold responses, associated with the inner retinal function, diminished at first but recovered completely by 14 days ALE. This functional recovery was concomitant with the upregulation of protein kinase Cα and synaptophysin. Similar results were obtained in both eyes, irrespective of mydriasis. Conclusions: In albino mice, light exposure induces substantial retinal damage, but the surviving photoreceptors, together with compensatory morphological/molecular changes, allow an important restoration of the retinal function.
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dc.identifier.citationMontalbán-Soler, L., Alarcón-Martínez, L., Jiménez-López, M., Salinas-Navarro, M., Galindo-Romero, C., de Sá, F. B., ... & Villegas-Pérez, M. P. (2012). Retinal compensatory changes after light damage in albino mice. Molecular vision, 18, 675.
dc.identifier.eissn1090-0535
dc.identifier.urihttp://hdl.handle.net/10201/218382
dc.languageeng
dc.publisherMolecular Vision
dc.relationThis work was supported by research grants from Fundación Séneca 04446/GERM/07; Spanish Ministry of Education and Science SAF-22010–10385; Spanish Ministry of Science and Innovation and ISCIII-FEDER: PI10/00187, PI006/0780 and Red Temática de Investigación Cooperativa en Oftalmología RD07/0062/0001.
dc.relation.publisherversionhttp://www.molvis.org/molvis/v18/a73/
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.odsNo relacionado con ningún objetivo de desarrollo sostenible
dc.titleRetinal compensatory changes after light damage in albino mice
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
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