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Open Access Publications from the University of California

GABAA Receptor-Expressing Neurons in Drosophila melanogaster Promote Consumption of Appetitive and Non-Appetitive Substances

  • Author(s): Cheung, Samantha Ka-Yan
  • Advisor(s): Scott, Kristin
  • et al.
No data is associated with this publication.

Animals must regulate the amount of food consumed to ensure the appropriate intake of nutrients. This decision making process is highly plastic, heavily influenced by the internal state of the animal, external sensory signals most prominently from taste and olfactory input, and associations with past food-related experiences. Often times, these cues are competing and contribute different weights toward the feeding decision process. The neural mechanisms by which taste detection, internal states influence feeding are under heavy investigation. Here, I used Drosophila melanogaster as a model system to study the underlying neural mechanisms by which feeding behavior is regulated.

Previous studies indicate that four GABAergic interneurons (DSOG1) in the Drosophila melanogaster brain are necessary to inhibit overconsumptive behavior. This thesis examines the role of GABAergic receptors and GABAergic receptor expressing neurons in consumption behavior. Here we find Resistance to dieldrin (RDL), a GABAA receptor, is required for proper control of ingestion in Drosophila. Knockdown of Rdl in VT16839-Gal4 neurons causes overconsumption of tastants, indicating that the line contains a set of neurons that regulates consumption in Drosophila melanogaster. These neurons are sufficient to drive consumption, as acute activation promotes consumption in flies. Complementary, acute silencing of these neurons causes decreased consumption of appetitive substances in motivated flies. Additionally, we find that there are VT16839-Gal4 neurons in the higher brain region that are responsive to sucrose and water stimulation. Our study identifies neurons that are necessary and sufficient for Drosophila ingestive behavior.

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This item is under embargo until April 2, 2021.