Psychology ETDs

Publication Date

Spring 5-15-2021


Prenatal alcohol exposure (PAE) is among the most common developmental insults to the nervous system and is characterized by spatial memory disruption. There is a pressing need to identify physiological alterations that help explain this memory impairment. The hippocampal (HPC) formation and connected regions are a compelling candidate for this purpose as they are vital for navigation, spatial memory, and memory consolidation. This document is broken up into 3 main parts, a detailed review of the prior literature followed by several experiments. First, It starts out with a comprehensive review on spatial behavioral impairments following PAE and the synaptic & circuit-level changes that might explain this impairment. Second, I test the hypothesis that HPC place cells are negatively impacted by PAE. Third, I test the hypothesis that the HPC mechanisms of memory consolidation, via the phenomena of sharp-wave ripples, are negatively affected by PAE. The review of the previous literature shows that there are clear dose-dependent negative impacts to spatial memory and hippocampal synaptic and cellular function as a result of alcohol exposure. Next, the investigation into place cell function revealed several differences associated with PAE, such as reduced spatial tuning, decreased orthogonalization, disrupted theta rhythmicity, and disrupted theta phase precession. These results established a clear linkage between moderate PAE and deficits in the spatial and rhythmic firing of HPC cell populations. Finally, the findings from the investigation of sharp-wave ripples suggest that the strength and diversity of neurons recruited to sharp-wave ripples are reduced, which indicates that the HPC mechanisms of memory consolidation are altered by PAE. All of these findings and details discussed throughout this dissertation provide a critical step in the characterization of hippocampal neural dynamics following PAE, which furthers our understanding of the neurobiological basis of deficits observed in spatial learning and memory. Following this groundwork, future studies should be newly equipped the further investigate the impacts of prenatal alcohol exposure.

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First Committee Member (Chair)

Benjamin J. Clark

Second Committee Member

Derek A. Hamilton

Third Committee Member

Jeremy Hogeveen

Fourth Committee Member

David N. Linsenbardt




Hippocampal, prenatal alcohol

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