ArticleNeuron2026
Dual-engram architecture within a single striatal cell type distinctly controls alcohol relapse and extinction.
Article in Neuron, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Acquisition-Recruited and MOR-Expressing Striatal dMSNs Differentially Regulate Extinction and Cue-Induced Relapse of Alcohol Seeking.Addiction biology · 2026Article
- A diffusion MRI-based structural assessment of the striatal compartments, striosome and matrix, in Obsessive Compulsive Disorder.Research square · 2026Article
- Early-Stage Corticostriatal Hyperactivity Impairs Cognitive Flexibility Alongside Striatal Cholinergic Dysfunction in an Alzheimer's Disease Model.Nature communications · 2026Article
- Extended Amygdala CRF Projections to Striatal Striosomes Potentiate Dopamine Suppression During Fentanyl Withdrawal.bioRxiv : the preprint server for biology · 2026Article
- Subregion-Specific Input Organization of Prefrontal-Projecting Basal Forebrain Cholinergic Neurons and Weakened Striatal-NBM Inhibitory Transmission in 5xFAD mice.bioRxiv : the preprint server for biology · 2026Article
- Extinction Training Suppresses Alcohol Relapse by Inhibiting Acquisition-Recruited Striatal Ensembles and Engaging Striosomal Neurons.bioRxiv : the preprint server for biology · 2026Article
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Abstract
Relapse remains a major obstacle in treating alcohol and drug addiction and is thought to be driven by persistent drug-associated memories formed during use. Extinction training reduces relapse and is proposed to generate a competing memory, yet where and how these opposing memories are stored is unknown. Here, we show that two anatomically and functionally distinct engram ensembles within the same striatal cell type, direct-pathway medium spiny neurons (dMSNs), encode these opposing memories in mice. Operant alcohol learning recruits a broadly distributed dMSN ensemble that encodes relapse-promoting alcohol memories. By contrast, operant extinction recruits a striosome-enriched dMSN ensemble that encodes an extinction memory to suppress relapse. We further demonstrate that relapse-promoting memory is embedded in persistently strengthened corticostriatal synapses engaged during learning and that mimicking this synaptic strengthening is sufficient to drive relapse-like behavior. Together, these findings reveal a dual-engram architecture within dorsostriatal dMSNs governing relapse and extinction.
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