ArticleAlcohol (Fayetteville, N.Y.)2023
Astrocyte expression in the extended amygdala of C57BL/6J mice is sex-dependently affected by chronic intermittent and binge-like ethanol exposure.
Article in Alcohol (Fayetteville, N.Y.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- MAO-B status in alcohol use disorder: a [Molecular psychiatry · 2026Article
- Astrocytes and Alcohol Throughout the Lifespan.Biological psychiatry · 2026Review
- Alcohol dependence-induced astrocyte immune activation in the nucleus accumbens.Neurobiology of disease · 2025Article
- Astrocyte alterations and dysfunction in alcohol use disorder: A comprehensive scoping review of clinical postmortem and preclinical evidence.Progress in neuro-psychopharmacology & biological psychiatry · 2025Article
- Central amygdala neuroimmune signaling in alcohol use disorder.Addiction neuroscience · 2025Article
- Role of glial cells in neurotoxicological effects of alcohol.Advances in neurotoxicology · 2025Article
- Astrocyte Reactivity and Neurodegeneration in the Female Rat Brain Following Alcohol Dependence.Neuroscience · 2023Article
- Sex-dependent factors of alcohol and neuroimmune mechanisms.Neurobiology of stress · 2023Article
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Excessive ethanol drinking is a major problem within the United States, causing alterations in brain plasticity and neurocognitive function. Astrocytes are glial cells that regulate neurosynaptic plasticity, modulate neurochemicals, and monitor other homeostatic roles. Astrocytes have been found to play a part in modulating excessive ethanol consumption. The basolateral amygdala (BLA), central amygdala (CeA), and bed nucleus of the stria terminalis (BNST) are brain regions that process stress, anxiety, and reward; they are also implicated in modulating ethanol intake. Little is understood, however, about how astrocyte expression in each region is modulated by chronic and binge-like ethanol drinking patterns. In the present report, we utilized two separate animal models of excessive drinking: chronic intermittent ethanol (CIE) and "Drinking-in-the-dark" (DID). Following these paradigms, animal brains were processed through immunohistochemistry (IHC) and stained for glial fibrillary acidic protein (GFAP). Collected data illustrated a sex-dependent relationship between ethanol intake and GFAP immunoreactivity (IR) in the BLA and BNST, but not in the CeA. Specifically, CIE and DID ethanol drinking resulted in blunted GFAP-IR (specifically via GFAP-positive cell count) in the BLA and BNST, particularly in males. These findings may implicate sex-dependent ethanol-induced changes in BLA and BNST astrocytes, providing a potential therapeutic target for anxiety and stress disorders.
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