ArticleAlcohol, clinical & experimental research2025
Repeated cycles of binge-like ethanol consumption and abstinence alter neuropeptide mRNA in prefrontal and insular cortex, amygdala, and lateral hypothalamus of male and female C57BL/6J mice.
Article in Alcohol, clinical & experimental research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Neuropeptide Y1 receptor expressing circuit from the central amygdala to lateral hypothalamus modulates binge-like ethanol consumption in a sex-dependent manner.Alcohol, clinical & experimental research · 2025Article
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Abstract
backgroundBinge drinking is a risky pattern of alcohol (ethanol) consumption associated with a variety of negative outcomes, including the development of alcohol use disorder (AUD). Many neuropeptide systems are thought to become dysregulated in AUD; however, whether repeated cycles of binge-like ethanol consumption and abstinence following binge-like drinking alter neuropeptide mRNA in key brain regions, such as the medial prefrontal cortex (mPFC), insular cortex (IC), amygdala, and lateral hypothalamus (LH), remains unknown.
methodsMale and female mice underwent 0, 3, or 6 cycles of binge-like ethanol consumption using the "Drinking in the Dark" (DID) paradigm. Brain tissue was collected either immediately following the final session of DID or after a 24-h period of abstinence, and quantitative polymerase chain reaction (qPCR) was performed to assess how repeated cycles of binge-like ethanol intake and abstinence alter relative mRNA expression for 22 neuropeptide-related targets.
resultsWe observed that repeated cycles of binge-like ethanol consumption and abstinence altered relative mRNA expression for 11 targets in the mPFC, five targets in the IC, eight targets in the amygdala, and two targets in the LH. Two of these alterations were specific to female mice, while one was specific to male mice.
conclusionsThese data suggest that neuropeptide mRNA is altered by repeated cycles of binge-like ethanol intake and abstinence in a brain region and sex-dependent manner. The current findings provide a useful foundation from which to explore potential targets to decrease binge-like ethanol consumption and prevent the development of AUD.
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