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HINDBRAIN NEURAL TRACKING AND CONTROL OF FOOD INTAKE

Kreisler, Alison (2015) HINDBRAIN NEURAL TRACKING AND CONTROL OF FOOD INTAKE. Doctoral Dissertation, University of Pittsburgh. (Unpublished)

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Abstract

Food intake is the product of meal size and frequency. Meal size is determined by sensory feedback signals that arise from the gastrointestinal (GI) tract and other digestive organs during feeding. Hindbrain glucagon-like peptide-1 (GLP-1) and prolactin-releasing peptide-positive noradrenergic A2 neurons (PrRP-positive) are anatomically poised to receive multimodal ingestive/metabolic-related information and engage local oral motor circuits that govern feeding. Moreover, multiple lines of evidence support a role for signaling from these populations in the suppression of food intake, while a role in the day-to-day control of meal size is less clear. Considering this, we hypothesized that GLP-1 and PrRP A2 neurons participate in satiation.
Results from studies conducted herein demonstrated that the proportion of GLP-1 and A2 neurons that were activated by food intake closely reflects both the volume and caloric value of the food consumed, and this activation was modulated by experience with consuming unusually large meals. Among GLP-1 neurons, those in the caudal nucleus of the solitary tract (cNTS) were more sensitive than those in the neighboring medullary reticular formation (MRF), supporting direct vagal afferents as an important route by which sensory information recruits these neurons. PrRP-positive A2 neurons were more sensitive than PrRP-negative A2 neurons to feeding-related sensory signals, suggesting that PrRP may be a particularly important among the many neuropeptide products of A2 neurons in the context of feeding control. In Chapter 4, we demonstrated that blocking central GLP-1 receptors produced larger and longer meals consumed during the latter phases of the feeding period, without changing meal frequency or the interval between meals. These results indicated a causal role for central GLP-1 signaling in satiation specifically.

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Details

Item Type: University of Pittsburgh ETD
Status: Unpublished
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Kreisler, Alisonadk45@pitt.eduADK45
ETD Committee:
TitleMemberEmail AddressPitt UsernameORCID
Committee ChairSved, Alan Fsved@pitt.eduSVED
Committee MemberRinaman, Lindarinaman@pitt.eduRINAMAN
Committee MemberCard, J Patrickcard@pitt.eduCARD
Committee MemberSesack, Susansesack@pitt.eduSESACK
Committee ChairHorn, Charles C.chorn@pitt.eduCHORN
Date: 26 September 2015
Date Type: Publication
Defense Date: 16 July 2015
Approval Date: 26 September 2015
Submission Date: 1 August 2015
Access Restriction: 2 year -- Restrict access to University of Pittsburgh for a period of 2 years.
Number of Pages: 166
Institution: University of Pittsburgh
Schools and Programs: Dietrich School of Arts and Sciences > Neuroscience
Degree: PhD - Doctor of Philosophy
Thesis Type: Doctoral Dissertation
Refereed: Yes
Uncontrolled Keywords: glucagon-like peptide-1, prolactin-releasing peptide, caudal nucleus of the solitary tract, food intake
Date Deposited: 27 Sep 2015 01:32
Last Modified: 26 Sep 2017 05:15
URI: http://d-scholarship.pitt.edu/id/eprint/25877

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