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Articles 1 - 3 of 3
Full-Text Articles in Behavioral Neurobiology
Sleep Modifications In A Drosophila Melanogaster Model Of Fragile X Syndrome, Morgan Mclaughlin
Sleep Modifications In A Drosophila Melanogaster Model Of Fragile X Syndrome, Morgan Mclaughlin
Undergraduate Honors Theses
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 Role Of Dopamine In Decision Making Processes In Drosophila Melanogaster, Michelle C. Bowers
The Role Of Dopamine In Decision Making Processes In Drosophila Melanogaster, Michelle C. Bowers
Undergraduate Honors Theses
Understanding the neural processes that mediate decision making is a relatively new field of investigation in the scientific community. With the ultimate goal of understanding how humans decide between one path and another, simpler models such as Drosophila Melanogaster, the common fruit fly, are often utilized as a way of determining the neural circuits involved in these decision-making processes. One of the most important decisions flies make is the decision of where to lay their eggs (oviposit). Choosing the proper substrate upon which to lay eggs is a crucial decision that can ultimately impact their fecundity. This paper investigates the …
Activation Of The Sonic Hedgehog Effector Smoothened Counteracts L-Dopa Induced Dyskinesia By Restoring Cholinergic Interneuron Function, Lauren Malave
Dissertations, Theses, and Capstone Projects
Many types of neurons act as multimodal signaling centers. Yet, we have only limited insight into the regulation and functional consequences of neuronal co-transmission. For example, dopamine (DA) neurons, whose degeneration causes motor deficits characteristic of Parkinson’s Diseases (PD), communicate with all their targets by DA but only a selective subset of their targets using GABA, Glutamate, and the secreted cell signaling protein Sonic Hedgehog (Shh). It is unknown whether Levo-dopamine (L-Dopa) induced dyskinesia (LIDs), a severely debilitating side effect of DA supplementation in PD, might appear because DA neuron targets are exposed to high DA- but low Shh- signaling …