# Hippocampal Modulation of Energy Intake

> **NIH NIH R01** · GEORGIA STATE UNIVERSITY · 2020 · $373,466

## Abstract

PROJECT SUMMARY
Memory of a meal provides a record of recent intake that outlasts most signals generated by the meal.
Memory of a recent meal decreases intake in humans and interfering with meal-related memory encoding
increases later intake. The brain regions that mediate the inhibitory effects of memory on future intake are not
known. The long-term goal of this research is to elucidate the cognitive mnemonic mechanisms that control
food intake. Dorsal hippocampus (dHC) is critical for memories of personal experiences and ventral
hippocampus (vHC) is important for emotional memory. Both likely contribute to meal-related memory. dHC-
and vHC-dependent memory typically require synaptic plasticity in glutamatergic (Glu) synapses; thus, dHC
and vHC synaptic plasticity likely influences eating behavior. The melanocortin (MC) system is a strong
candidate for providing meal-related signals because it integrates the actions of numerous food-related
indicators and inhibits intake after ingestion. MC agonists and receptors (MCRs) are found in dHC CA1àCA3
synapses and promote Glu-dependent synaptic plasticity. The overarching hypothesis of this proposal is
that eating and food-related signals mediated by MCs induce synaptic plasticity in dCA1 neurons
necessary to inhibit subsequent intake, and that dHC neurons inhibit intake by activating vHC Glu
neurons, which project to several brain areas critical for eating behavior. AIM 1 will determine whether
dHC and vHC Glu neurons inhibit energy intake after ingestion and whether dHC Glu neurons inhibit intake by
activating vHC Glu neurons. It is predicted that postmeal optical inhibition of dHC or vHC Glu neurons or
dHCàvHC Glu projections will increase energy intake and that optical excitation will have the opposite effect.
Inclusion of both sexes will show whether dHC and vHC control of energy intake is sex-dependent. AIM 2 will
determine whether ingestion increases markers of synaptic plasticity in dHC or vHC neurons and whether
synaptic plasticity is necessary for dHC and vHC inhibition of energy intake. It is predicted that ingestion will
increase synaptic plasticity-associated protein activation and gene expression in dHC and vHC, optical
inhibition of dHC Glu neurons will attenuate these increases in vHC, that pharmacological inhibition of
synaptic plasticity will increase intake, and that long-term knock down of dHC or vHC synaptic plasticity-
associated genes will increase intake, body mass and adiposity. AIM 3 will determine whether dHC MCs
enhance meal-related synaptic plasticity and inhibit energy intake via Glu receptors (GluRs). It is expected
that dCA1 infusions of MCR antagonists will attenuate eating-induced increases in genes and protein
activation events necessary for synaptic plasticity and increase intake, body mass, and adiposity, that MCR
agonists will have the opposite effect, and that pharmacological inhibition of dCA1 GluRs will interfere with the
effects of MCR agonists. This project wi...

## Key facts

- **NIH application ID:** 10197298
- **Project number:** 3R01DK114700-03S1
- **Recipient organization:** GEORGIA STATE UNIVERSITY
- **Principal Investigator:** MARISE B PARENT
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $373,466
- **Award type:** 3
- **Project period:** 2018-09-03 → 2022-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10197298

## Citation

> US National Institutes of Health, RePORTER application 10197298, Hippocampal Modulation of Energy Intake (3R01DK114700-03S1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10197298. Licensed CC0.

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