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DATE: May 14, 2026 at 12:00PM
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-------------------------------------------------TITLE: Brain cells store competing memories that drive or suppress alcohol relapse
URL: https://www.psypost.org/brain-cells-store-competing-memories-that-drive-or-suppress-alcohol-relapse/
A new study published in the journal Neuron provides evidence that the brain stores competing memories of alcohol use and the recovery from it within distinct networks of the same type of brain cell. The research suggests that the memory driving a return to drinking and the memory suppressing it exist side by side, competing for control over a person’s behavior. These findings offer a nuanced understanding of how addiction persists and point toward potential new ways to improve treatments for alcohol use disorder.
Addiction occurs when addictive substances hijack normal learning processes, leading to the formation of powerful memories that link certain actions and environments with the drug. Behavioral therapies, such as extinction training, attempt to reduce the urge to seek alcohol by repeatedly exposing individuals to drug-related cues without providing the alcohol reward. However, the clinical impact of these therapies tends to be limited because scientists do not fully understand the physical cellular structures that hold these opposing memories.
“Relapse is one of the most difficult challenges in alcohol use disorder, even after long periods of abstinence or treatment,” said Jun Wang, a professor in the Department of Neuroscience and Experimental Therapeutics at the Texas AM University Health Science Center’s College of Medicine. “Alcohol-associated cues and contexts can trigger powerful memories that drive renewed alcohol seeking. We wanted to understand where relapse-related memories are stored in the brain, and how extinction training reduces alcohol-seeking behavior by erasing the original alcohol memory or by creating a competing memory that suppresses relapse.”
Memories are thought to be physically stored in the brain through specific groups of cells called engrams. An engram is a physical change in the brain that represents a memory. It consists of a specific network of brain cells that activate together when an experience happens, and when the brain recalls that memory, the same group of cells fires again. Past research on engrams has mostly focused on fear learning in other parts of the brain, meaning less is known about the engrams that store habits and voluntary actions related to addictive substances.
The researchers designed the study to test whether the memories for alcohol use and the memories for extinction are stored in separate areas or within the same cell populations. They focused on a brain region called the dorsomedial striatum, which helps control goal-directed behaviors. Within this region, they examined a specific type of cell known as direct-pathway medium spiny neurons.
“We were surprised to find that these opposing memories were encoded within the same genetically defined cell type, direct-pathway medium spiny neurons, rather than being separated simply by different neuron types,” Wang said. “Traditionally, many models emphasize broad distinctions between direct- and indirect-pathway neurons, but our findings show that even within one cell type, distinct neuronal ensembles can have very different, even opposite, behavioral functions.”
The scientists conducted a series of experiments using genetically modified mice. They placed the mice in specialized testing boxes equipped with levers and lights. The mice learned that pressing an active lever three times would deliver a small amount of a twenty percent alcohol solution, which was accompanied by a specific tone and a yellow light. After several weeks of this training, the mice underwent nine days of extinction training, where pressing the lever no longer provided the alcohol or the cues.
To track the memory cells, the researchers used a specialized genetic tagging technique. They injected a drug that allowed them to permanently label the specific brain cells that were active either during the initial alcohol learning or during the later extinction training. Following the training phases, the researchers tested groups of four to seven mice to see which memory cells were reactivated during a simulated relapse event.
They found that the brain cells tagged during the initial alcohol learning were highly reactivated when the mice experienced the cues associated with alcohol. The cells tagged during extinction training were not reactivated during this simulated relapse, which provides evidence that alcohol use and extinction training recruit different sets of the same type of brain cell.
The researchers then looked at where these specific cell groups were located within the dorsomedial striatum. This brain region is divided into two distinct areas: the matrix, which generally promotes action, and the striosome, which generally discourages action. By analyzing brain tissue samples, the scientists found that the cells linked to extinction memories were heavily clustered in the striosome areas. These extinction-related cells strongly inhibited dopamine-producing neurons, which helps suppress the urge to seek alcohol. In contrast, the cells linked to alcohol use were spread broadly across the matrix and promoted reward-seeking behavior.
To test whether these distinct groups of cells actively control behavior, the researchers used a technique that allows them to turn specific neurons on or off using custom-made chemicals. They injected viral vectors into the brains of the mice, which safely delivered genetic instructions causing the tagged memory cells to produce specialized receptors. The researchers then injected a chemical that binds to these receptors to either turn the cells on or off.
In tests involving groups of seven to sixteen mice, the authors found that turning off the alcohol-learning cells successfully suppressed the simulated relapse. Activating the extinction-learning cells also reduced the animals’ attempts to seek alcohol. The scientists repeated these tests using sucrose instead of alcohol and found no effect. This suggests these particular memory cells are specific to alcohol and do not generalize to natural rewards.
The authors also wanted to understand exactly how the brain physicalizes the memory of alcohol use. Learning changes the brain by strengthening the synapses, which are the connections between different brain cells. The researchers focused on the connections coming from the medial prefrontal cortex, a brain area involved in complex decision-making. By taking electrical recordings from dozens of individual neurons across multiple mice, they found that alcohol use caused a long-lasting strengthening of the synapses connecting the medial prefrontal cortex to the specific cells involved in alcohol learning.
To see if this strengthened connection was the actual memory, the scientists used a technique that controls brain cells with light. They introduced light-sensitive proteins into the brain cells of a new group of mice, numbering seven to eleven per group, that had never consumed alcohol. By shining a specific wavelength of light into the brain through tiny optical fibers, the scientists forced the neurons to fire and strengthened their connections artificially.
This artificial stimulation was paired with specific lights and sounds in the testing chamber. Later, when the researchers played the lights and sounds again, the mice began pressing the lever as if they were seeking alcohol. This suggests that the researchers successfully created an artificial memory of alcohol relapse simply by strengthening a specific brain connection. The authors also replicated these behavioral findings in a small group of rats to ensure the results were not unique to mice.
“One important aspect of the study is that we were able to identify not only the neurons associated with alcohol relapse and extinction, but also a synaptic mechanism that helps store relapse-related memory,” Wang said. “Specifically, we found that communication from the medial prefrontal cortex to striatal neurons was strengthened after alcohol self-administration, and experimentally mimicking this strengthening was sufficient to drive relapse-like behavior. This provides evidence that alcohol-related memories can be physically embedded in specific brain connections.”
“The main takeaway is that relapse and recovery-related learning are not only abstract psychological processes; they are represented by specific groups of neurons in the brain,” Wang explained. “We found that two opposing alcohol-related memories, one that promotes relapse and one that suppresses alcohol seeking after extinction, can be encoded within the same broad type of striatal neuron. This suggests that recovery may depend not only on weakening relapse-driving circuits, but also on strengthening the brain circuits that support extinction and behavioral control.”
While the study provides a detailed look at how the brain stores alcohol-related memories, there are some limitations to consider. The timeline of alcohol exposure in the study was relatively short compared to human addiction, which tends to develop over years. It is possible that the physical nature of these memories changes over longer periods of chronic alcohol use.
“An important caveat is that this study was conducted in mouse models of alcohol self-administration, extinction, and relapse-like behavior,” Wang noted. “These models capture important aspects of alcohol seeking and relapse, but they do not fully reproduce the complexity of human alcohol use disorder. We also do not want readers to interpret the findings as meaning that relapse is controlled by a single brain region or a simple ‘on/off switch.’ Rather, our study identifies one specific circuit and cellular mechanism that contributes to alcohol-related memory and relapse-like behavior.”
Current medical treatments cannot selectively erase or enhance specific memory cells in human patients. However, understanding that recovery involves strengthening a competing extinction memory gives researchers a new conceptual target. Future therapeutic strategies might focus on finding medications or brain stimulation techniques that specifically boost the extinction memory network to help prevent relapse.
“Our long-term goal is to understand how maladaptive alcohol memories are formed, stored, retrieved, and suppressed at the level of specific brain circuits,” Wang said. “We are particularly interested in identifying mechanisms that could selectively weaken relapse-promoting memory circuits or strengthen extinction-related circuits. In the long run, this type of work may help guide new strategies to improve the durability of behavioral therapies and reduce relapse risk.”
The study, “Dual-engram architecture within a single striatal cell type distinctly controls alcohol relapse and extinction,” was authored by Xueyi Xie, Yufei Huang, Ruifeng Chen, Zhenbo Huang, Himanshu Gangal, Ziyi Li, Jiayi Lu, Adelis M. Cruz, Anita Chaiprasert, Emily Yu, Nicholas Hernandez, Valerie Vierkant, Runmin Wang, Xuehua Wang, Rachel J. Smith, and Jun Wang.
URL: https://www.psypost.org/brain-cells-store-competing-memories-that-drive-or-suppress-alcohol-relapse/
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