title: Retinal compensatory changes after light damage in albino mice.
abstract: OBJECTIVE
  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.
authors.affiliation: Departamento de Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica, Facultad de Medicina, Universidad de Murcia, Murcia, Spain.
authors.forename: Luis
authors.initials: L
authors.lastname: Montalbán-Soler
authors.forename: Luis
authors.initials: L
authors.lastname: Alarcón-Martínez
authors.forename: Manuel
authors.initials: M
authors.lastname: Jiménez-López
authors.forename: Manuel
authors.initials: M
authors.lastname: Salinas-Navarro
authors.forename: Caridad
authors.initials: C
authors.lastname: Galindo-Romero
authors.forename: Fabrízio
authors.initials: F
authors.lastname: Bezerra de Sá
authors.forename: Diego
authors.initials: D
authors.lastname: García-Ayuso
authors.forename: Marcelino
authors.initials: M
authors.lastname: Avilés-Trigueros
authors.forename: Manuel
authors.initials: M
authors.lastname: Vidal-Sanz
authors.forename: Marta
authors.initials: M
authors.lastname: Agudo-Barriuso
authors.forename: Maria P
authors.initials: MP
authors.lastname: Villegas-Pérez
mesh_terms: D000417:Albinism; D000818:Animals; D017209:Apoptosis / Q000528:radiation effects; D004596:Electroretinography; D004801:Eosine Yellowish-(YS); D005260:Female; D006416:Hematoxylin; D008027:Light / Q000009:adverse effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D010786:Photoreceptor Cells / Q000166:cytology / Q000378:metabolism / Q000528:radiation effects*; D051571:Protein Kinase C-alpha / Q000096:biosynthesis; D020127:Recovery of Function / Q000502:physiology*; D012162:Retinal Degeneration / Q000378:metabolism / Q000473:pathology; D012165:Retinal Ganglion Cells / Q000166:cytology / Q000378:metabolism / Q000528:radiation effects*; D012171:Retinal Vessels / Q000378:metabolism / Q000528:radiation effects*; D016708:Synaptophysin; D015854:Up-Regulation; D033921:Vesicular Transport Proteins / Q000096:biosynthesis
chemical_list: D016708:Synaptophysin; C569015:Syp protein, mouse; D033921:Vesicular Transport Proteins; D051571:Protein Kinase C-alpha; D004801:Eosine Yellowish-(YS); D006416:Hematoxylin