Repository logo
 

Mechanism of neuronal cell death in canine glaucoma

Simple item page
dc.contributor.authorAlyahya, Khaleel I., author
dc.contributor.authorMadl, James E., advisor
dc.date.accessioned2024-03-13T18:14:55Z
dc.date.available2024-03-13T18:14:55Z
dc.date.issued2009
dc.description.abstractGlaucoma is one of the most important causes of blindness in human and dogs. Glaucoma is characterized by a progressive loss of retinal ganglion cells that is often associated with increased intraocular pressure and decreased retinal blood flow. In previous investigations, we found that changes in glutamate distribution occur selectively in damaged areas of retinas of dogs with primary glaucoma. This glutamate redistribution is consistent with high levels of extracellular glutamate (↑GluE) contributing to excitotoxic damage to neurons. In this dissertation, we used immunohistochemical methods to test three mechanisms by which this glutamate redistribution may occur in retinas from clinical cases of canine glaucoma. First, we tested if ischemia due to microvessel loss causes the changes in glutamate distribution. We found significantly lower microvessel density in damaged regions, consistent with ischemia occurring in canine glaucoma. Second, we tested if loss of glutamine synthetase induces the glutamate redistribution. We have found significantly decreased amounts of glutamine synthetase in areas with neuronal damage and glutamate redistribution, consistence with decreased glutamate synthetase contributing to glutamate redistribution. Third, leakage of glutamate from blood vessels from inflamed areas may lead to glutamate redistribution. We found that there is albumin leakage from blood vessels in damaged regions with other inflammatory indicators in those areas. The smaller size of glutamate suggests that it should also diffuse out of blood into the extracellular fluid of the retina even more readily than albumin. Increase leakiness of blood vessels in canine glaucoma is consistent with glutamate leakage contributing to glutamate redistribution. In conclusion, our results are consistent with all three mechanisms contributing to glutamate redistribution in canine glaucoma. The dissertation includes further discussion of more refined hypotheses of the mechanisms by which glutamate redistribution and neuronal damage may occur.
dc.format.mediumborn digital
dc.format.mediumdoctoral dissertations
dc.identifierETDF_Alyahya_2009_3374674.pdf
dc.identifier.urihttps://hdl.handle.net/10217/237557
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.rights.licensePer the terms of a contractual agreement, all use of this item is limited to the non-commercial use of Colorado State University and its authorized users.
dc.subjectcanine
dc.subjecteye
dc.subjectglaucoma
dc.subjectglutamate
dc.subjectprimary angle
dc.subjectretina
dc.subjectneurosciences
dc.subjectophthalmology
dc.subjectphysiology
dc.titleMechanism of neuronal cell death in canine glaucoma
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.disciplineBiomedical Sciences
thesis.degree.grantorColorado State University
thesis.degree.levelDoctoral
thesis.degree.nameDoctor of Philosophy (Ph.D.)

Files

Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
ETDF_Alyahya_2009_3374674.pdf
Size:
3.85 MB
Format:
Adobe Portable Document Format
Download

Collections

2000-2019
Theses and Dissertations