UC Berkeley

Feeding behavior is essential for achieving metabolic homeostasis and is critical for survival. Animals adjust their food intake based on their physiological needs and food availability. How sensing deprivation signals and detection of taste gets converted to feeding behaviors remains poorly understood. Here I use the genetically tractable model organism Drosophila melanogaster to examine the neural mechanisms underlying feeding decisions. The genetic conservation of molecular signaling pathways, the simpler nervous system and the powerful genetic tools make it an excellent system to explore the organization and logic behind brain circuits controlling food intake.

This thesis investigates the neuronal mechanisms underlying inhibition in the Drosophila feeding circuit. Here I describe the identification of 4 GABA-ergic interneurons in the Drosophila brain that establish a central feeding threshold which is required for any taste and satiety dependent feeding decisions. I show that these neurons control consumption in an activity dependent manner. Inactivation of these cells results in indiscriminate and excessive ingestion, independent of taste quality or nutritional state. Conversely, acute activation of these neurons significantly reduces consumption of water and nutrients. I show that their output is acutely required to express any feeding preference and that these neurons are not regulated by taste processing pathways or satiety signals. This work reveals a new layer of inhibitory control in insect feeding circuits that is required to suppress a latent state of unrestricted and nonselective consumption. Furthermore I identify the recurrent nerve as a peripheral source of post-ingestive inhibition of nutrient intake in Drosophila and show that the two feeding inhibitory mechanisms are distinct and independent of each other. The work presented here opens the door to analyzing how central and peripheral inhibition regulates feeding behaviors in Drosophila melanogaster.