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ZFIN ID: ZDB-PUB-141018-2
Technical brief: Constant intense light exposure to lesion and initiate regeneration in normally pigmented zebrafish
Rajaram, K., Summerbell, E.R., Patton, J.G.
Date: 2014
Source: Molecular Vision   20: 1075-84 (Journal)
Registered Authors: Patton, James G.
Keywords: none
MeSH Terms:
  • Albinism, Ocular/pathology
  • Albinism, Ocular/physiopathology
  • Albinism, Ocular/radiotherapy
  • Animals
  • Animals, Genetically Modified
  • Apoptosis/radiation effects
  • Cell Dedifferentiation/radiation effects
  • Cell Proliferation/radiation effects
  • Disease Models, Animal
  • Ependymoglial Cells/pathology
  • Ependymoglial Cells/physiology
  • Ependymoglial Cells/radiation effects
  • Green Fluorescent Proteins/metabolism
  • Light
  • Neural Stem Cells/pathology
  • Neural Stem Cells/physiology
  • Neural Stem Cells/radiation effects
  • Photoreceptor Cells, Vertebrate/pathology
  • Photoreceptor Cells, Vertebrate/physiology
  • Photoreceptor Cells, Vertebrate/radiation effects
  • Recombinant Proteins/metabolism
  • Regeneration/physiology
  • Regeneration/radiation effects*
  • Retina/injuries*
  • Retina/physiopathology
  • Retina/radiation effects
  • Zebrafish/physiology*
PubMed: 25324680
Zebrafish are capable of robust and spontaneous regeneration of injured retina. Constant intense light exposure to adult albino zebrafish specifically causes apoptosis of rod and cone photoreceptor cells and is an excellent model to study the molecular mechanisms underlying photoreceptor regeneration. However, this paradigm has only been applied to lesion zebrafish of the nonpigmented albino genetic background, which precludes the use of numerous transgenic reporter lines that are widely used to study regeneration. Here, we explored the effectiveness of constant intense light exposure in causing photoreceptor apoptosis and stimulating regeneration in normally pigmented zebrafish retinas. We show that constant intense light exposure causes widespread photoreceptor damage in the dorsal-central retinas of pigmented zebrafish. Photoreceptor loss triggers dedifferentiation and proliferation of Müller glia as well as progenitor cell proliferation. We also demonstrate that the timeline of regeneration response is comparable between the albino and the pigmented retinas.