regulation of inflammation, participation in phagocytosis (19), and engagement in specialized brain-specific functions through interactions with neurons, such as the modulation of neurotransmission and synaptic pruning (20, 21). Exposure to ethanol triggers microglia activation, leading to morphological changes and heightened immune responses in rodent models (22–26). Microglial depletion has been shown to mitigate alcohol dependence–associated behaviors, impair synaptic function, and reverse expression changes in alcohol-dependent inflammatory-related genes in mice (27). It has also been suggested that microglia-mediated synaptic pruning may constitute the underlying mechanism behind synapse loss and memory impairment induced by prolonged alcohol consumption (28).
