Microglia, astrocytes, and neurons all seem to induce neuroimmune-related changes in the brain that may translate to changes in synaptic activity and alcohol behaviors. Typically, astrocytes and microglia are both “activated” in response to an injury or immune insult. A systemic immune challenge increases cytokines in microglia, which precede astrocyte reactivity (Norden et al., 2016). Studies of neuroinflammatory neurodegenerative disorders suggest that early microglial activation produces an inflammatory microenvironment which subsequently interferes with astrocyte and other glial cell function as pathological conditions progress (Sastre et al., 2006). Release of inflammatory factors from activated microglia stimulates a subtype of astrocytes to secrete neurotoxic factors, which has been proposed as a common mechanism for several human neurodegenerative diseases (Liddelow et al., 2017). Indeed, glial activation acts as a precursor to drug-induced neurotoxicity (Chastain and Sarkar, 2014; Friend and Keefe, 2013); however, the time course of activation for different populations of glia and neurons by alcohol and other drugs of abuse is not known. While it is increasingly apparent that chronic alcohol exposure induces neuroimmune pathology in brain, we must determine the key
