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WT Allison, SG Dann, CW Hawryshyn; Cone Photoreceptor Death and Regeneration in the Context of Natural Development . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2689.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Ultraviolet-sensitive (UV-) cones disappear from the retina of salmonid fishes during the metamorphosis that prepares them for marine life. At sexual maturity, when migratory populations of these fish return to freshwater, a population of putative UV-cones reappears into the retina. Thyroid hormone mediates these events during natural development. Our aim is to clarify the mechanisms of this natural ontogeny by examining the effects of thyroid hormone on UV-cone distribution. Methods: We have developed a polyclonal antibody against the rainbow trout UV-opsin. We have combined this with in situ hybridization labeling of photoreceptors, as well as electroretinograms, to examine cone distributions. Thyroid hormone and/or caspase inhibitors were applied to examine their effects on UV-cone distribution. Results: Polyclonal antibody robustly labeled UV-cones in a variety of salmonids (including rainbow trout) as well as cones in goldfish and damselfish. UV-cones disappeared from the retina of rainbow trout during thyroid hormone treatment. This disappearance was blocked by the application of caspase inhibitors. Removal of thyroid hormone treatment resulted in the reappearance of UV-cones. Conclusion: Inhibition of caspases blocks UV-cone disappearance, which is consistent with our previous results that indicate the events are mediated by programmed cell death. The findings also represent the first confirmation that cones expressing UV-opsin can reappear into the retina. These observations are consistent with the hypothesis that the reappearance of UV-cones occurs through the proliferation of precursor/stem cells, which are known to reside in teleost retinae. The programmed cell death and regeneration of UV-cones occur during natural retinal development in salmonid fishes. This provides a powerful model of cone photoreceptor death in which individually identifiable neurons can be induced to degenerate. This also allows an examination of signals and gene expression inducing regeneration of cones from proliferating stem cells. Importantly, such studies can be conducted in vivo, without confounds of retinal damage, which is normally utilized to study such events. This work was supported by Fellowships from the Alzheimer Society of B.C./Canada (WTA) and NSERC (SGD), and by operating and equipment grants from NSERC (CWH).
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