Graduation Date

Spring 5-4-2024

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Programs

Neuroscience

First Advisor

Matthew Van Hook

Abstract

The brain has the remarkable ability to compensate for damage and maintain physiological set points. In the visual system where even after significant damage has been done, the brain fills in visual gaps because of this compensation. This thesis attempts to understand several components of visual changes after damage in disorders such as glaucoma. This was accomplished by using several models of vision loss in mice including the DBA/2J (D2) and silicone oil (SO) models of glaucoma, the RD10 model of retinitis pigmentosa, and a retina-specific knockout of brain-derived neurotrophic factor (BDNF)— the Chx10-cre; BDNFfl/fl mouse. Through these models we discovered that the cause of the well-known D2 electroretinogram abnormalities were due to a combination of pupil dilation deficits and likely sectorial photoreceptor damage causing a shift in the photoreceptor response curve and decreased amplitude, respectively, compared to strain-matched controls. Additionally, while there are compensatory effects in the excitability of thalamocortical (TC) neurons in the dorsolateral geniculate nucleus for loss of retinal input as a result of IOP increases, we did not find any changes in the superior colliculus in the silicone oil model for glaucoma. Finally, we found that when the neurotrophin BDNF was selectively deleted from the retina, that there were visual deficits in the optomotor response, decreased TC neuron dendritic complexity, and increased single vesicular release events as measured by mEPSCs and mIPSCs. Together, these findings show the ability of visual system to respond to changes in retinal input.

Comments

2024 Copyright, the authors

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