Theses and Dissertations from UMD

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New submissions to the thesis/dissertation collections are added automatically as they are received from the Graduate School. Currently, the Graduate School deposits all theses and dissertations from a given semester after the official graduation date. This means that there may be up to a 4 month delay in the appearance of a give thesis/dissertation in DRUM

More information is available at Theses and Dissertations at University of Maryland Libraries.

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Subject: search.filters.subject.Amblyopia

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    EARLY CHRONIC MONOCULAR VISUAL DEPRIVATION COMPROMISES THE RETINAL FUNCTION OF THE DEPRIVED EYE
    (2020) Ara, Jawshan; Quinlan, Elizabeth M.; Neuroscience and Cognitive Science; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Amblyopia is caused by abnormal visual experience during early childhood such as unilateral cataract, strabismus, and anisometropia. The misalignment of the images in the case of strabismus or blurriness/haziness of the image quality originating from the defective eye results in reduced visual acuity and contrast sensitivity in the deprived eye (Volkers et al., 1987) in comparison to the non-deprived eye and limits stereopsis in humans (Husk et al., 2012). Most clinical treatments for amblyopia penalize the fellow eye to bias the visual system towards the input from the amblyopic eye. Unfortunately, current clinical treatments for amblyopia are most effective in children younger than 7 years old (Cotter et al., 2012). Works in animal models of amblyopia are beginning to identify ways to improve vision in adult amblyopes. They have focused almost exclusively on deficits in the functions of the visual cortex. However, dark rearing can reduce the amplitude of the photopic Electroretinogram indicating reduced functions of cone-mediated retinal functions and alter the mGluR6 distribution and intensity in the first synapses between cone photoreceptors and ON bipolar cells (Dunn et al., 2013). It is predicted but not yet tested, that monocular deprivation will have a similar impact on retinal functions. Here we characterize various aspects of the effect of chronic monocular deprivation (cMD) on retinal functions in adult mice. We observed that chronic monocular deprivation significantly reduced electroretinogram (ERG) response originating from the inner retinal plexiform layer of the deprived eye retina in comparison to the non-deprived eye retina. Our observation suggests that early chronic visual deprivation compromises the retinal function of the deprived eye of the adult mice.
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    CHARACTERIZATION OF CHRONIC MONOCULAR DEPRIVATION AND ESTROGEN ADMINISTRATION IN ADULT RODENTS
    (2018) Sengupta, Deepali Clare; Quinlan, Elizabeth M; Neuroscience and Cognitive Science; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Reduced synaptic plasticity and excitatory synapse density contribute to age-related cognitive decline, and constrain recovery of function from injury in adults. A parallel reduction in circulating sex hormones in both sexes, particularly estrogens, exacerbates this decline in synaptic plasticity. Conversely, estrogen therapy in aged members of many species restores synapse density, promotes synaptic plasticity, and improves learning/memory. Importantly, acute estrogen administration can promote rapid synaptogenesis, and these new synapses can be stabilized by activity. Here I ask if estrogen treatment can promote synaptic plasticity in the primary visual cortex (V1) of aged rats. I demonstrate robust expression of estrogen receptors (ERs) in V1 of adult male and female rats, suggesting an opportunity to enhance plasticity with estrogens. I test this hypothesis following the induction of amblyopia by chronic monocular deprivation (cMD). I show that cMD reduces thalamic innervation from the deprived eye, and increases molecular markers which constrain plasticity, consistent with observations that the deficits induced by cMD are highly resistant to reversal. Surprisingly, cMD did not change markers for excitatory synapses, suggesting a homeostatic increase in synapses serving the non-deprived eye (NDE) to maintain synaptic density within an optimal range. Importantly, visually-evoked potentials (VEPs) induced by repetitive visual stimulation to the deprived eye depress more rapidly than those of the NDE, consistent with cMD inducing an increase in the probability of neurotransmitter release (Pr) at synapses in the cMD pathway. In contrast, treatment of cMD adults with a single dose of 17α estradiol significantly increased markers for excitatory synapses, and estradiol treatment followed by visual stimulation also increased markers for excitatory synapse activity. Repetitive estradiol treatments increased excitatory synapse markers, but not synaptic activity markers. Furthermore, one dose of estradiol enhanced VEP amplitude following repetitive visual stimulation, however this was observed only in response to stimulation of the NDE. As presynaptic ERs are known to increase Pr at glutamatergic synapses, this suggests that the effects of estradiol are specific to spared synapses where Pr has not been up-regulated by deprivation. Exploiting this selectivity may allow for receptive field remapping of spared inputs around a scotoma or cortical infarct