Fox, Donald A.2015-08-242015-08-24August 2012013-08http://hdl.handle.net/10657/1041PURPOSE: Gestational lead exposure (GLE) increased and prolonged retinal progenitor cell proliferation in mice, resulting in a dose-dependent increase in two late-born retinal neurons: rod photoreceptors and bipolar cells. The present goals were to examine: 1) the spatiotemporal differentiation and functional development of these two cell types, 2) the profile of glutamatergic responses in developing retina prior to canonical synaptic function, and 3) the structural integrity of aging retinas after GLE. METHODS: RT-qPCR, immunohistochemistry, confocal microscopy, agmatine probe labeling, and pharmacological assays. RESULTS: GLE decreased the relative expression of rod specific genes at PN2; delayed the differentiation and functional development of rod photoreceptors and bipolar cells by 2-3 days; increased and prolonged the glutamatergic response of post-mitotic rod and bipolar precursors in the ventricular zone of developing retina; and increased and accelerated the age-related degeneration of rod photoreceptors and bipolar cells. CONCLUSIONS: Gestational exposure to environmental toxicants such as lead can produce differential age-dependent effects on the developing and aging retina. Furthermore, the lifespan effect of increased proliferation can result in degeneration later in life.application/pdfengThe author of this work is the copyright owner. UH Libraries and the Texas Digital Library have their permission to store and provide access to this work. Further transmission, reproduction, or presentation of this work is prohibited except with permission of the author(s).Retinal developmentToxicologyLeadBiochemistry2015-08-24Thesisborn digital