ArticleNeuropharmacology2025
Abstinence and extinction drive opposing changes in striatal activity and dopamine signaling during alcohol relapse.
Article in Neuropharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Acquisition-Recruited and MOR-Expressing Striatal dMSNs Differentially Regulate Extinction and Cue-Induced Relapse of Alcohol Seeking.Addiction biology · 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
- Dual-engram architecture within a single striatal cell type distinctly controls alcohol relapse and extinction.Neuron · 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
- Nauclea officinalis extract rescues working memory deficits in adolescent maternal immune activation offspring by restoring cholinergic signaling.Frontiers in cell and developmental biology · 2026Article
- Prehabilitation Reimagined as Policy: A Multidimensional Framework to Reduce Pain, Opioid Use, and Surgical Risk.International journal of spine surgery · 2025Article
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Abstract
Relapse remains a major challenge in the treatment of alcohol use disorder, driven in part by persistent neuroadaptations. However, how different post-alcohol experiences, such as passive withdrawal (abstinence) versus active extinction training, differentially shape the neural circuits and synaptic mechanisms that influence relapse vulnerability remains unclear. Here, we show that these experiences have opposing effects on dorsomedial striatal (DMS) direct-pathway medium spiny neurons (dMSNs) and dopamine dynamics during cue-induced reinstatement of alcohol seeking. Using in vivo fiber photometry in D1-Cre rats, we found that abstinence increased both dopamine release and dMSN calcium activity during reinstatement, whereas extinction training reduced dopamine release and prevented abstinence-related elevation in dMSN activity. Given that dopamine regulates corticostriatal plasticity onto dMSNs, and that such plasticity plays a critical role in alcohol-seeking behavior, these opposing dopamine signals suggest experience-dependent changes in medial prefrontal cortex (mPFC)-to-dMSN synaptic strength that may contribute to relapse vulnerability. To test this, we used pathway-specific optogenetic plasticity protocols and found that inducing long-term depression (LTD) after abstinence attenuated reinstatement, whereas inducing long-term potentiation (LTP) after extinction reinstated alcohol seeking. These findings suggest that dopamine-dependent corticostriatal plasticity bidirectionally mediates relapse and is shaped by prior alcohol-related experience, identifying it as a potential target for relapse prevention.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.