Alcohol-induced effects on microglia are less well understood. Microglia express PRRs, produce cytokines, and modulate neuroinflammatory reactions in brain injury and neurodegenerative diseases (Block, Zecca et al. 2007). Activated microglia respond to neuronal damage by removing damaged cells via phagocytosis, and chronic activation of microglia contributes to the pathology in a number of neurodegenerative diseases including Parkinson’s disease, Alzheimer’s disease, prion diseases, multiple sclerosis, and HIV-dementia (Dheen, Kaur et al. 2007). In Sprague Dawley rats exposed to 25% (w/v) ethanol via intragastric gavage every 8 hours for 4 days, increased activation and proliferation of microglia as evidenced by morphological changes and BrdU incorporation were observed in the hippocampus (McClain, Morris et al. 2011). Changes persisted at least 30 days after alcohol exposure suggestive of longlasting consequences of ethanol on microglia function (McClain, Morris et al. 2011). There is also evidence that ethanol-induced microglia activation is mediated by signaling through TLR4 (Fernandez-Lizarbe, Pascual et al. 2009).
