# Investigating how long-term signals modulate brainstem satiation circuits

> **NIH NIH F31** · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2024 · $44,892

## Abstract

Project Abstract:
The size of a meal is carefully regulated to prevent over- or under-feeding. Direct control of meal size is
attributed by brainstem areas, such as the caudal nucleus of the solitary tract (cNTS), that directly receive
short-term sensory feedback from the GI tract during feeding. In contrast, the indirect controls, which include
hypothalamic circuits and leptin, are hypothesized to encode long-term energy balance and regulate meal
termination by modulating the potency of these short-term signals sensed in the brainstem. Interactions
between these long-term and short-term systems are critical for the control of food intake, but how it is
encoded in the dynamics of the underlying brainstem circuits remains unknown. The cNTS contains many cell
types that are involved in controlling food intake. Among these cell types, prolactin releasing hormone (PRLH)
and glucagon (GCG) neurons are particularly important for meal termination. In my recent studies, I performed
the first neural recordings of these two cell types in awake behaving mice. I found unexpectedly that these cells
were rapidly activated at the start of a meal by feedforward signals such as taste. These technical and
conceptual advances create an opportunity for me to investigate the longstanding question of how signals of
long-term energy balance modulate brainstem circuits to control meal termination. I propose here to address
this question by investigating how two regulators of long-term energy balance – Agouti-related peptide (AgRP)
neurons and leptin – modulate PRLH or GCG neuron dynamics or their control of feeding behavior. Together
these results will reveal how long-term systems modulate brainstem circuits to regulate meal size, which is an
important determinant of overall food intake and can be dysregulated in conditions like obesity.

## Key facts

- **NIH application ID:** 10876927
- **Project number:** 5F31DK137586-02
- **Recipient organization:** UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
- **Principal Investigator:** Truong Ly
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $44,892
- **Award type:** 5
- **Project period:** 2023-07-01 → 2026-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10876927

## Citation

> US National Institutes of Health, RePORTER application 10876927, Investigating how long-term signals modulate brainstem satiation circuits (5F31DK137586-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10876927. Licensed CC0.

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