# Neural circuit mechanisms controlling non-homeostatic feeding

> **NIH NIH R00** · MAX PLANCK FLORIDA CORPORATION · 2021 · $50,628

## Abstract

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. In the mentored K-phase of this grant, I analyzed
the role of a molecularly defined cortical-amygdalar circuit in overconsumption and determined
the amygdala targets of insular cortex Nos1 neurons. In the independent phase (R00), I will
further this understanding by employing in vivo calcium imaging to the insula Nos1 to central
amygdala circuit during behavior. I will also 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.

## Key facts

- **NIH application ID:** 10429408
- **Project number:** 3R00DA048749-02S1
- **Recipient organization:** MAX PLANCK FLORIDA CORPORATION
- **Principal Investigator:** Sarah Stern
- **Activity code:** R00 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $50,628
- **Award type:** 3
- **Project period:** 2020-03-01 → 2023-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10429408

## Citation

> US National Institutes of Health, RePORTER application 10429408, Neural circuit mechanisms controlling non-homeostatic feeding (3R00DA048749-02S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10429408. Licensed CC0.

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