There is a burgeoning literature on microglia in alcohol use disorders (see Table II). In adolescent Sprague–Dawley rats, binge-like alcohol intake stimulates hippocampal microglial activation for up to 30 days after last consumption, suggesting that circumscribed exposure over a relatively brief neurodevelopmental window has long-lasting consequences (McClain et al. 2011). Ten days of intragastric ethanol administration to C57BL6/J mice also activates microglia, as detected by increasing nicotinamide adenine dinucleotide phosphate oxidase expression and increased reactive oxygen species production (Qin et al. 2012). In addition to stimulating neuroinflammatory cascades, in hypothalamic mixed cultures, ethanol’s apoptotic effects are mediated by microglia (Boyadjieva et al. 2010). Microglial activation is also critical in treatment response: minocycline, a tetracycline antibiotic and microglial inhibitor, decreases drinking in C57BL/6J mice (Agrawal et al. 2011). In a rodent model of drinking cessation, microgliosis preceded neurogenesis and volumetric recovery (Nixon et al. 2008).
