Food choice is a modifiable health factor which involves neural, hormonal, and metabolic signals. The lateral parabrachial nucleus is a brain structure in the pons that integrates multiple aspects of food choice. It receives information from the homeostatic melanocortin hypothalamic system and projects to the mesolimbic dopamine reward system. The lateral parabrachial is molecularly diverse and expresses the acetylcholine synthesis enzyme: choline acetyltransferase (ChAT). In this study, we used ChAT-CRE mice to investigate the anatomical projections, the calcium dynamics, and the causal role of the LPBN ChAT neurons. Anatomical projection results were produced using CRE dependent viral vectors to express mRuby tagged synaptophysin, the highest output being the central amygdala. Calcium dynamics were measured at the amygdala using the genetically encoded calcium indicator GCaMP. The dynamics around the decision to consume food were seen to be different between fasted and sated satiety states. Activation of the circuit showed a pronounced latency to food consumption and time to finish for a single calorie of food. These data demonstrate a possible node that integrates homeostatic feeding information and relays it to higher order brain systems that modify reward value. / Master of Science / Health can be impacted by the food an individual decides to eat, and this choice is controlled by the brain. There are many regions of the brain that are recruited when an individual decides to eat, but the two major circuits recruited are the homeostatic feeding circuit and the reward feeding circuit. The homeostatic feeding circuit involves the hypothalamus, the structure that controls basic essential functions of the body and circulating hunger hormones to signal energy availability. The second circuit is the reward circuitry which uses the neurotransmitter dopamine to signal pleasure and motivation for food. At the middle of the two circuits sits the parabrachial nucleus which expresses choline acetyltransferase, the enzyme that creates the neurotransmitter acetylcholine. To harness the molecular and anatomical specificity, we employed viral dependent protein expression to measure the anatomical output, the activity when a mouse is engaged in feeding behavior, and the causal role of the identified circuit during feeding behavior. The results showed the anatomical output to be the central amygdala, a modifier of food reward and value. The activity of the cells while feeding was seen to be higher when sated, and the activation of the circuit saw an increased latency to eat food and increased the time to consume a calorie. Together, we have demonstrated a circuit from the parabrachial nucleus the amygdala which integrates homeostatic information and projects to a brain structure that modifies food value and reward.
| Identifer | oai:union.ndltd.org:VTETD/oai:vtechworks.lib.vt.edu:10919/115421 |
| Date | 13 June 2023 |
| Creators | Tatera, Walter James |
| Contributors | Graduate School, Howe, William Matthew, Vijayan, Sujith, Chappell, John Christopher |
| Publisher | Virginia Tech |
| Source Sets | Virginia Tech Theses and Dissertation |
| Language | English |
| Detected Language | English |
| Type | Thesis |
| Format | ETD, application/pdf |
| Rights | In Copyright, http://rightsstatements.org/vocab/InC/1.0/ |
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