Characterization of multiple light damage paradigms reveals regional differences in photoreceptor loss
- Authors
- Thomas, J.L., Nelson, C.M., Luo, X., Hyde, D.R., and Thummel, R.
- ID
- ZDB-PUB-120326-8
- Date
- 2012
- Source
- Experimental Eye Research 97(1): 105-116 (Journal)
- Registered Authors
- Hyde, David R., Luo, Xixia, Nelson, Craig, Thomas, Jennifer, Thummel, Ryan
- Keywords
- neuroD, transgene, zebrafish, retina, photoreceptor regeneration, light damage, light-induced retinal degeneration
- MeSH Terms
-
- Animals
- Biomarkers/metabolism
- Blotting, Western
- Cell Cycle/physiology
- Cell Proliferation
- Dark Adaptation
- Eye Proteins/metabolism
- Fluorescent Antibody Technique, Indirect
- Light
- Microscopy, Confocal
- Neuroglia/pathology
- Photoreceptor Cells, Vertebrate/physiology
- Photoreceptor Cells, Vertebrate/radiation effects*
- Radiation Injuries, Experimental/etiology*
- Radiation Injuries, Experimental/metabolism
- Radiation Injuries, Experimental/pathology
- Regeneration
- Retinal Degeneration/etiology*
- Retinal Degeneration/metabolism
- Retinal Degeneration/pathology
- Ultraviolet Rays
- Zebrafish
- PubMed
- 22425727 Full text @ Exp. Eye. Res.
Zebrafish provide an attractive model to study the retinal response to photoreceptor apoptosis due to its remarkable ability to spontaneously regenerate retinal neurons following damage. There are currently two widely-used light-induced retinal degeneration models to damage photoreceptors in the adult zebrafish. One model uses constant bright light, whereas the other uses a short exposure to extremely intense ultraviolet light. Although both models are currently used, it is unclear whether they differ in regard to the extent of photoreceptor damage or the subsequent regeneration response. Here we report a thorough analysis of the photoreceptor damage and subsequent proliferation response elicited by each individual treatment, as well as by the concomitant use of both treatments. We show a differential loss of rod and cone photoreceptors with each treatment. Additionally, we show that the extent of proliferation observed in the retina directly correlates with the severity of photoreceptor loss. We also demonstrate that both the ventral and posterior regions of the retina are partially protected from light damage. Finally, we show that combining a short ultraviolet exposure followed by a constant bright light treatment largely eliminates the neuroprotected regions, resulting in widespread loss of rod and cone photoreceptors and a robust regenerative response throughout the retina.