Hergarden, Anne Christina (2011) The role of peptidergic neurons in the regulation of satiety in drosophila. Dissertation (Ph.D.), California Institute of Technology. http://resolver.caltech.edu/CaltechTHESIS:02272011-173157140
Understanding the neural mechanisms that motivate us to eat is important because of the increasing rates of obesity and the consequential increasing rates of diabetes and cardiovascular disease in our society. The aim of this dissertation is to gain insight into the neuromodulators and neural mechanisms that regulate satiety. To do this, we turned to Drosophila melanogaster, which has been a powerful model organism to study the molecular mechanisms underlying innate animal behaviors and which exhibits many conserved elements of feeding regulation and energy homeostasis found in mammals. A common theme in animal behavior is that food deprivation modifies behavioral responses, e.g., the likelihood that an animal will accept a low-nutrient food. I manipulated the parameters of a feeding assay to screen for animals that lacked several starvation-induced feeding behaviors: increased foraging for food, increased acceptance of low-nutrient food, and increased ingestion of low-quality food. Using this feeding assay, I identified a neuronal circuit manipulation that inhibits several starvation-induced behaviors. Activation of a subset of Allatostatin-A-expressing neurons, using a novel transgenic tool that we generated, inhibits starvation-induced changes in both the acceptance and the ingestion of low-quality foods. In contrast, this circuit manipulation did not affect starvation-induced metabolic changes or foraging behavior. This suggests that we tapped into a mechanism that regulates a specific subset of starvation-induced changes in feeding behavior that is independent from general starvation-induced behavioral responses and energy metabolism. Studies in blowflies have revealed that the primary mechanism that promotes satiety is inhibitory proprioceptive feedback from the gut, but whether such a mechanism operates in Drosophila is unclear. While Allatostatin A has been implicated as a satiety factor and as a myoinhibitor in several other insects, it has no known function in Drosophila. A mechanism that promotes satiety but that does not alter energy metabolism has not previously been identified in Drosophila. I have used this circuit manipulation to better understand how a state of satiety is achieved in Drosophila, by integrating the knowledge acquired from studies in other insects with the knowledge acquired from molecular genetic manipulations in Drosophila.
|Item Type:||Thesis (Dissertation (Ph.D.))|
|Subject Keywords:||Drosophila; Feeding; Neuropeptides; Neural Circuits|
|Degree Grantor:||California Institute of Technology|
|Thesis Availability:||Public (worldwide access)|
|Defense Date:||20 January 2011|
|Default Usage Policy:||No commercial reproduction, distribution, display or performance rights in this work are provided.|
|Deposited By:||Anne Hergarden|
|Deposited On:||24 Feb 2012 22:42|
|Last Modified:||26 Dec 2012 04:33|
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