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Abstract

Fetal Alcohol Spectrum Disorders (FASD), which results from gestational ethanol (a short-chain primary alcohol) exposure, is the most common form of preventable intellectual disability. Individuals with FASD have a variety of Central Nervous System dysfunctions, including impulsivity, difficulties with abstract thinking, problems with memory, and learning disabilities. FASD is highly prevalent throughout the world; in the United States alone, it is estimated that 24-48 in 1,000 individuals have FASD. While the mechanisms underlying the response of the developing brain to gestational ethanol exposure are not fully understood, a potential mechanism is tissue plasminogen activator (tPA), which is upregulated by ethanol, both in vivo and in vitro. The experiments in this dissertation examined the hypothesis that gestational ethanol exposure alters neuronal morphology, and that this alteration is, in part, due to astrocyte-mediated increases in tPA caused by ethanol.

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