ArticleAddiction biology2026
Acquisition-Recruited and MOR-Expressing Striatal dMSNs Differentially Regulate Extinction and Cue-Induced Relapse of Alcohol Seeking.
Article in Addiction biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Relapse to alcohol use is frequently triggered by re-exposure to alcohol-associated cues, and extinction-based interventions can reduce this vulnerability. However, the striatal cellular mechanisms through which extinction alters later alcohol seeking remain unclear. Using a mouse model of operant alcohol self-administration, we examined two distinct direct-pathway medium spiny neuron (dMSN) populations in the dorsomedial striatum. Extinction reduced cue-induced alcohol seeking and decreased the probability that acquisition-recruited dMSNs were reactivated during relapse testing. Chemogenetically maintaining activity in acquisition-recruited dMSNs during extinction slowed the reduction in alcohol-seeking and enhanced subsequent relapse. In contrast, increasing activity in μ-opioid receptor (MOR)-expressing dMSNs, a striosome-enriched population, accelerated the reduction in responding and decreased later relapse without altering inactive-lever responding or locomotor activity. These findings indicate that extinction is associated with reduced re-engagement of acquisition-related dMSN ensembles, whereas enhancing activity in a MOR-defined, striosome-enriched output population can facilitate extinction-related behavioural change. Together, the results identify two complementary striatal processes that regulate alcohol extinction and relapse.
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