# Neural circuit mechanisms controlling non-homeostatic feeding

> **NIH NIH R00** · MAX PLANCK FLORIDA CORPORATION · 2022 · $249,000

## Abstract

PROJECT SUMMARY
Compulsive eating is a major contributor to the obesity epidemic in the US, as over 35% of adults are now
classified as overweight or obese. Behavioral outcomes such as compulsive eating derive from a complex
interaction of genetics, innate behaviors and learning about previous experiences. Cue-food associations (e.g.
advertising, eating in front of the television, etc.) that are formed during periods of hunger lead to long-lasting
memories that control non-homeostatic overconsumption. However, the neural circuitry, and specifically the
molecular cell types, governing this behavior are not well defined. Using an original paradigm that induced
overconsumption in sated mice with contextual cues, I have established a role of the insular cortex, and
specifically Nos1 neurons within the insular cortex, as critical mediators of learned overconsumption. These
neurons do not play a role in homeostatic feeding itself and are therefore hypothesized to provide top down
control of homeostatic feeding circuitry to control food intake. Moreover, a projection from the insular cortex to
the central amygdala is necessary to generate this overconsumption response.
Under the primary mentorship of Dr. Jeffrey Friedman at the Rockefeller University and the co-mentorship of Dr.
Denise Cai at the Icahn School of Medicine at Mount Sinai, I will continue to build on my behavioral and molecular
neuroscience expertise while developing my training in optogenetics and in vivo calcium imaging. In the
mentored K-phase of this grant, I will analyze the role of a molecularly defined cortical-amygdalar circuit in
overconsumption using optogenetics and calcium imaging techniques. I will also determine the amygdala targets
of insular cortex Nos1 neurons. In the independent phase (R00), I will utilize retrograde tracing techniques to
examine the regions and molecularly profile the cell types that directly project to the insular cortex neurons that
control overconsumption, and test causally how they are functionally involved in non-homeostatic feeding.
Together, these data will establish a cell-type specific circuit through the insular cortex that controls
overconsumption in response to environmental stimuli. This data will expand the knowledge of higher-order brain
regions involved in feeding behavior and may lead to the development of novel therapeutic avenues to control
overeating. At the same time, the research and training plans proposed in this application will enable me to
develop my technical and professional skills in order to transition to an independent research position. With the
successful completion of this project, I will have developed a platform for a fully independent research program
aimed at understanding how the brain coordinates the interplay between innate and learned behaviors that drive
maladaptive choices.

## Key facts

- **NIH application ID:** 10327339
- **Project number:** 5R00DA048749-03
- **Recipient organization:** MAX PLANCK FLORIDA CORPORATION
- **Principal Investigator:** Sarah Stern
- **Activity code:** R00 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $249,000
- **Award type:** 5
- **Project period:** 2020-03-01 → 2023-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10327339

## Citation

> US National Institutes of Health, RePORTER application 10327339, Neural circuit mechanisms controlling non-homeostatic feeding (5R00DA048749-03). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10327339. Licensed CC0.

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