PUBLICATION

A novel light damage paradigm for use in retinal regeneration studies in adult zebrafish

Authors
Thomas, J.L., and Thummel, R.
ID
ZDB-PUB-131203-27
Date
2013
Source
Journal of visualized experiments : JoVE   (80): e51017 (Journal)
Registered Authors
Thomas, Jennifer, Thummel, Ryan
Keywords
none
MeSH Terms
  • Animals
  • Disease Models, Animal*
  • Light
  • Regeneration/physiology*
  • Retina/physiology*
  • Retinal Cone Photoreceptor Cells/physiology*
  • Retinal Degeneration/etiology*
  • Retinal Degeneration/pathology*
  • Retinal Rod Photoreceptor Cells/physiology*
  • Zebrafish
PubMed
24192580 Full text @ J. Vis. Exp.
Abstract

Light-induced retinal degeneration (LIRD) is commonly used in both rodents and zebrafish to damage rod and cone photoreceptors. In adult zebrafish, photoreceptor degeneration triggers Müller glial cells to re-enter the cell cycle and produce transient-amplifying progenitors. These progenitors continue to proliferate as they migrate to the damaged area, where they ultimately give rise to new photoreceptors. Currently, there are two widely-used LIRD paradigms, each of which results in varying degrees of photoreceptor loss and corresponding differences in the regeneration response. As more genetic and pharmacological tools are available to test the role of individual genes of interest during regeneration, there is a need to develop a robust LIRD paradigm. Here we describe a LIRD protocol that results in widespread and consistent loss of both rod and cone photoreceptors in which we have combined the use of two previously established LIRD techniques. Furthermore, this protocol can be extended for use in pigmented animals, which eliminates the need to maintain transgenic lines of interest on the albino background for LIRD studies.

Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping