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Inducible photoreceptor degeneration model in goldfish

dc.contributor.authorVarland, Dezaray D., author
dc.contributor.authorVigh, Jozsef, advisor
dc.contributor.authorGionfriddo, Juliet, committee member
dc.contributor.authorIshii, Douglas, committee member
dc.contributor.authorMadl, James, committee member
dc.contributor.authorTobet, Stuart, committee member
dc.date.accessioned2007-01-03T05:34:26Z
dc.date.available2007-01-03T05:34:26Z
dc.date.issued2011
dc.description.abstractPhotoreceptor degenerative diseases are among the leading causes of vision loss and there is presently no known cure. The future success of biological and prosthetic vision rescue approaches following photoreceptor loss remains questionable, due to the morphological and functional changes occurring in the remaining retinal circuitry. In the current study we sought to establish a chemically-induced photoreceptor degenerative model in goldfish, based on the ability of teleost to regenerate their retina following damage. N-methyl-N-nitrosourea (MNU) was chosen to chemically induce the photoreceptor degeneration, because it has been found to be potent, and selective in mammalian studies. We hypothesized that MNU would induce selective and complete photoreceptor loss in the goldfish retina as well as the consequent morphological changes observed in mammalian retinas. Under anesthesia, fish received a direct, intraocular injection of MNU into the posterior chamber of one eye whereas the contralateral eye served as sham-injected control. The effects of MNU were determined by standard immunohistochemical methods using known, well-established molecular markers of retinal cells. The MNU induced unilateral, selective, and dose-dependent photoreceptor degeneration: up to ~60% of photoreceptors lost the injected eye of the goldfish within 7 days, followed by nearly complete regeneration by ~50 days post-injection. Repeated MNU treatments did not increase the magnitude of degeneration, but delayed the regeneration. Unlike in mammals, MNU did not destroy all of the photoreceptors in fish. The incomplete photoreceptor degeneration together with the quick regeneration may be responsible for preventing the development of chronic morphological and functional consequences. However, the regeneration observed after MNU treatment is promising. Inducing total photoreceptor degeneration in fish retina, possibly by combining MNU with other factors shown to destroy photoreceptors (i.e. strong light) could provide an all-encompassing natural model for studying the potential of stem cell-based vision rescue approaches after photoreceptor loss.
dc.format.mediumborn digital
dc.format.mediummasters theses
dc.identifierVarland_colostate_0053N_10504.pdf
dc.identifier.urihttp://hdl.handle.net/10217/48142
dc.languageEnglish
dc.language.isoeng
dc.publisherColorado State University. Libraries
dc.relation.ispartof2000-2019
dc.rightsCopyright and other restrictions may apply. User is responsible for compliance with all applicable laws. For information about copyright law, please see https://libguides.colostate.edu/copyright.
dc.subjectteleost
dc.subjectregeneration
dc.subjectretina
dc.subjectdegeneration
dc.subjectphotoreceptors
dc.titleInducible photoreceptor degeneration model in goldfish
dc.typeText
dcterms.rights.dplaThis Item is protected by copyright and/or related rights (https://rightsstatements.org/vocab/InC/1.0/). You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s).
thesis.degree.disciplineCell and Molecular Biology
thesis.degree.grantorColorado State University
thesis.degree.levelMasters
thesis.degree.nameMaster of Science (M.S.)

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