ArticleNature communications2026
Identification and validation of central amygdala FGFR1 as a therapeutic target for alcohol use disorder using single-nucleus sequencing in rats.
Article in Nature communications, 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
A significant minority of alcohol users develop alcohol addiction, characterized by continued use despite negative consequences, referred to as compulsive-like. We previously showed that vulnerability to compulsive-like alcohol use can be modeled in rats using punished alcohol self-administration and in male rats is mediated by PKCδ+ neurons in the central nucleus of the amygdala (CeA). Here, we used cell-type-specific transcriptomics to identify molecular mechanisms underlying individual differences in this behavior. Transcriptional changes were restricted to a limited number of CeA neuronal populations, including PKCδ+ neurons, where weighted Gene Co-expression Network Analysis identified an upregulated co-expression module in punishment-resistant rats with FGFR1 as a druggable upstream regulator. Selective silencing of FgfR1 in PKCδ+ neurons normalized elevated PKCδ+ expression, and reduced punishment-resistant alcohol self-administration. This effect was recapitulated by systemic administration of the FgfR1-antagonist PD173074. These findings identify distinct CeA circuits that promote addiction vulnerability, and position FGFR1 as potential therapeutic targets.
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