Date of Award

Spring 5-20-2020

Document Type

Undergraduate Honors Thesis

Degree Name

Bachelor of Arts in Behavioral Neuroscience

Department

Psychological Sciences

Advisor

Dr. Callen Hyland

Abstract

Fragile X syndrome (FXS) is a neurodevelopmental disorder characterized by intellectual disabilities, disruptions in sleep, and autism in humans. Mutations in Fragile X Mental Retardation gene 1 (FMR1), which codes for a protein that modifies the expression of many target proteins, are primarily responsible for this disorder. Genetic modifications of FMR1 can increase or decrease the overall amount of sleep in humans. A potential pharmaceutical target of FXS is dopamine, a critical neurotransmitter in the regulation of sleep and wakefulness. In fruit flies (Drosophila melanogaster) dopamine has been shown to alter sleep. The mushroom body, a structure in the Drosophila brain that regulates sleep and memory, is innervated by dopaminergic neurons and is heavily impacted by low expression of dFMR1. In this study, a Drosophila Activity Monitoring system (DAMs) was used to measure sleep and locomotor activity in Drosophila models of FXS. We found that fruit flies with underexpression of dFMR1 slept more than their control but in shorter periods, which may lead to impaired memory consolidation. Furthermore, the activity of these flies when they are awake is reduced, leaving them with fewer chances to feed, court, and mate. In addition, the mushroom body specific overexpression of dFMR1 in a null background was able to rescue sleep deficits. Further studies on dFMR1 in Drosophila will help us understand how sleep is disrupted and how these changes lead to modifications in behavior.

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