Salmonid fishes have been reported to have a remarkable ontogeny of cone photoreceptors in their retina. The ultraviolet-sensitive (UVS) cones are of particular interest, as they disappear from, and reappear into, the retina. These events occur at times associated with migration to marine waters, and the return migration to freshwater spawning grounds, respectively. The primary goal of this thesis was to discover the mechanisms underlying this ontogeny of UVS cones by studying a salmonid, the rainbow trout (Oncorhynchus mykiss). Two hypotheses were considered: 1) UVS cones become dormant, similar to speculations regarding light damage of rod photoreceptors in albino trout; 2) UVS cones die and subsequently regenerate from stem cells known to robustly proliferate in trout retina. I cloned partial cDNAs of each opsin from trout and used them to develop in sjtu hybridization labelling of photoreceptors. I introduced the ability to assess UV sensitivity utilizing electroretinograms, and developed a polyclonal antibody against the UVS opsin, to label UVS cones in immunohistochemistry. I combined these tools to examine trout UVS cones during natural development, and found that it was similar to events during thyroid hormone (TH) treatment. I used labels and inhibitors of programmed cell death to determine that UVS cone death is a major mechanism of UVS cone disappearance. UVS cones reappeared into the retina following termination of TH treatment. Application of cell fate markers indicates that reappearing UVS cones can be generated from proliferating stem cells. Electroretinograms demonstrated that these regenerated UVS cones sufficiently integrate into the retina to pass signals onto second order neurons. This represents the only known example of cone photoreceptors regenerating from stem cells during natural development. I speculate on the adaptive value of the ontogeny of UVS cones. I also investigated mechanisms underlying the apparent survival of rod photoreceptors when albino trout retina receive light-induced damage. Previous conclusions in this area had been influential in forming the hypotheses of UVS cone ontogeny. Two hypotheses were envisioned: 1) rod photoreceptors were surviving light damage; 2) rods were being killed by light but quickly replaced by proliferating retinal cells. My results support the latter hypothesis.
| Identifer | oai:union.ndltd.org:uvic.ca/oai:dspace.library.uvic.ca:1828/347 |
| Date | 10 April 2008 |
| Creators | Allison, William Edward |
| Contributors | Hawryshyn, Craig W. |
| Source Sets | University of Victoria |
| Detected Language | English |
| Format | application/pdf |
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