Anika Puttaiah
Pronouns: she/her
Research Mentor(s): Martin Myers Jr
Research Mentor School/College/Department: / Medicine
Program: UROPF
Session: Session 5 (2:40pm – 3:30pm)
Authors:
Abstract
Previous studies in our lab have shown that liraglutide (GLP-1R agonist) reduces food intake, reduces body weight and incites taste aversion (e.g., nausea)- potentially by a set of area postrema (AP) neurons termed GLU4, which activate aversive lPBN CGRP neurons. In contrast, amylin reduces food intake without causing aversive responses, potentially via activating a distinct set of AP neurons (termed GLU10) that contain the amylin receptor (a complex of Calcr/RAMP3). We hypothesized that physiological nutrient signals activate AP Calcr/RAMP expressing GLU4 cells, which do not activate CGRP neurons. To begin to test this hypothesis, we artificially activated AP Calcr neurons in rats and examined food intake and potential aversive responses. We measured conditioned taste avoidance (CTA) by pairing a novel palatable taste with injections of liraglutide, CNO (to activate AP Calcr neurons) or saline. This causes the rat to learn to associate the palatable novel taste to gut malaise or no gut malaise. To measure aversion, the amount of consumption and preference for the novel tastant after recovery from the stimulus. Our results show that artificial activation of AP Calcr cells in the rat does not induce a conditioned taste aversion (CTA) and does not induce long-term suppression or weight loss but promotes acute food suppression. In the future, we will examine pica (eating inert clay) in response to the activation of these neurons as an additional test of aversive signaling.
