Scientists Discover “Meal Memory” Neurons That Control When and How Much We Eat

Researchers have discovered “meal memory” neurons in laboratory rats that may explain why forgetting lunch can lead to overeating.

Scientists have identified a unique population of brain cells responsible for forming memories of meals, capturing both what was eaten and when it occurred. The research, published in Nature Communications, may help explain why individuals with memory difficulties are more prone to overeating and why forgetting a recent meal can heighten hunger and contribute to unhealthy eating behaviors.

As eating takes place, neurons in a part of the brain called the ventral hippocampus become active, creating what the researchers describe as “meal engrams.” These are specialized memory traces that record details of eating experiences. Although engrams have long been known to store general memories and experiences, this study is the first to reveal a set of engrams specifically linked to meals.

“An engram is the physical trace that a memory leaves behind in the brain,” said Scott Kanoski, professor of biological sciences at the USC Dornsife College of Letters, Arts and Sciences and corresponding author of the study. “Meal engrams function like sophisticated biological databases that store multiple types of information such as where you were eating, as well as the time that you ate.”

Distracted eating implications

The discovery has immediate relevance for understanding human eating disorders. Patients with memory impairments, such as those with dementia or brain injuries that affect memory formation, may often consume multiple meals in quick succession because they cannot remember eating.

Furthermore, distracted eating — such as mindlessly snacking while watching television or scrolling on a phone — may impair meal memories and contribute to overconsumption.

Based on the experiment’s findings, meal engrams are formed during brief pauses between bites when the brain of laboratory rats naturally survey the eating environment. These moments of awareness allow specialized hippocampal neurons to integrate multiple streams of information.

Kanoski said it can be assumed that a human’s brain would undergo a similar phenomenon. When someone’s attention is focused elsewhere — on phone or television screens — these critical encoding moments are compromised. “The brain fails to properly catalog the meal experience,” said Lea Decarie-Spain, postdoctoral scholar at USC Dornsife and the study’s first author, “leading to weak or incomplete meal engrams.”

Mechanism of ‘meal memories’

The research team used advanced neuroscience techniques to observe the brain activity of laboratory rats as they ate, providing the first real-time view of how meal memories form.

The meal memory neurons are distinct from brain cells involved in other types of memory formation. When researchers selectively destroyed these neurons, lab rats showed impaired memory for food locations but retained normal spatial memory for non-food-related tasks, indicating a specialized system dedicated to meal-related information processing. The study revealed that meal memory neurons communicate with the lateral hypothalamus, a brain region long known to control hunger and eating behavior. When this hippocampus-hypothalamus connection was blocked, the lab rats overate and could not remember where meals were consumed.

Eating management implications

Kanoski said the findings could eventually inform new clinical approaches for treating obesity and weight management. Current weight management strategies often focus on restricting food intake or increasing exercise, but the new research suggests that enhancing meal memory formation could be equally important.

“We’re finally beginning to understand that remembering what and when you ate is just as crucial for healthy eating as the food choices themselves,” Kanoski said.

Reference: “Ventral hippocampus neurons encode meal-related memory” by Léa Décarie-Spain, Cindy Gu, Logan Tierno Lauer, Keshav S. Subramanian, Samar N. Chehimi, Alicia E. Kao, Serena X. Gao, Iris Deng, Alexander G. Bashaw, Molly E. Klug, Jessica J. Rea, Alice I. Waldow, Ashyah Hewage Galbokke, Olivia Moody, Kristen N. Donohue, Mingxin Yang, Guillaume de Lartigue, Kevin P. Myers, Richard C. Crist, Benjamin C. Reiner, Matthew R. Hayes and Scott E. Kanoski, 11 June 2025, Nature Communications.
DOI: 10.1038/s41467-025-59687-1

The study was supported by a Quebec Research Funds Postdoctoral Fellowship (315201), an Alzheimer’s Association Research Fellowship (AARFD-22-972811), a National Science Foundation Graduate Research Fellowship (DK105155), and a National Institute of Diabetes and Digestive and Kidney Diseases grant (K104897).

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