ArticleThe American journal of pathology2026
Microglia Promote Neurodegeneration and Hyperkatifeia during Withdrawal and Abstinence from Binge Alcohol.
Article in The American journal of pathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Pro-inflammatory microglia drive escalated alcohol consumption during early abstinence.bioRxiv : the preprint server for biology · 2026Article
- Specific inhibition of p38α MAPK dampens neuroinflammation during acute alcohol withdrawal in mouse BV2 microglial cell line and rat organotypic hippocampal slice cultures.Alcohol (Fayetteville, N.Y.) · 2026Article
- INTERFERON-REGULATORY FACTOR 7: A NEUROIMMUNE ROLE FOR VAPOR-INDUCED ESCALATIONS IN ETHANOL SELF-ADMINISTRATION.bioRxiv : the preprint server for biology · 2026Article
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Abstract
Proinflammatory microglial polarization, neuronal death, and hyperkatifeia/negative affect during withdrawal are key features of alcohol use disorder (AUD). However, the role microglia play in the development of AUD-related neuronal and behavioral pathology is unclear. Given the ability of microglia to impact neuronal function, it was hypothesized that proinflammatory microglia promote neuronal death and hyperkatifeia during prolonged abstinence from binge alcohol. Proinflammatory signaling and affective state were assessed in mice either during acute withdrawal (24 hours) or abstinence (>4 weeks) to binge alcohol exposure. Ten days of binge alcohol increased proinflammatory gene signaling 24 hours after ethanol, which lasted weeks into withdrawal. Alcohol reduced brain-derived neurotrophic factor in hyperkatifeia-associated regions (ie, the central amygdala and infralimbic cortex) during acute withdrawal and caused persistent microglial structural changes and loss of microglial brain-derived neurotrophic factor in the bed nucleus of the stria terminalis during abstinence. This was associated with increased anxiety-like behavior and hyperarousal, with persistent enhancement of conditioned fear memory during abstinence. Inhibition of proinflammatory microglia with Gi designer receptors exclusively activated by designer drugs blocked neuronal death and prevented persistent proinflammatory gene induction and hyperkatifeia in female mice. Thus, this identifies a direct role for microglia in the development of AUD-related neuropathology and behavioral dysfunction, implicating microglia as cellular targets for the prevention of AUD phenotypes.
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