ETHANOL DECREASES EXPRESSION OF DEVELOPING NEURONS, BUT NOT NEURONAL VIABILITY, IN A CULTURED RAT HIPPOCAMPUS
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Master of Science (MS)
Arts and Sciences
Dr. Mark A. Prendergast
As of 2019, alcohol use disorders (AUDs) affect roughly 14.1 million individuals over the age of 18 and cost up to $249 billion in economic burden in the United States. In addition to central nervous system (CNS), those affected by AUDs can present with cognitive and behavioral abnormalities. Specifically, those affected by AUDs experience deficits in memory consolidation and retrieval as well as executive functioning, which may be due to cellular changes within the hippocampus. There are at least two prominent and contended theories which explain the mechanism of functional impairment caused by alcohol: 1) alcohol induces excitotoxic neuronal death in the hippocampus and/or 2) alcohol diminishes neurogenesis, reducing production and proliferation of new neuronal cells. Determining the relative involvement of neuronal death and neuronal production in alcohol-induced hippocampal dysfunction is necessary to inform potential therapeutic targets aiming to restore cognitive deficits caused by alcohol exposure. The purpose of this experiment is to examine the effects of continuous alcohol exposure and explore the relative contributions of each of these processes in the conformational changes in the hippocampus after chronic alcohol exposure and establish organotypic hippocampal slice culture as a viable method to continue exploring these changes.
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This study was supported by Grant no. 3R44AA025804-03S1 in collaboration with Naprogenix Inc. in 2020-2022.
Count, Cassidy, "ETHANOL DECREASES EXPRESSION OF DEVELOPING NEURONS, BUT NOT NEURONAL VIABILITY, IN A CULTURED RAT HIPPOCAMPUS" (2023). Theses and Dissertations--Psychology. 231.