Several studies have examined the effects of alcohol consumption on neuroinflammatory gene expression. Transcript profiling has been carried out using RNA from the whole brain of mice fed alcohol 4 h per day for 4 days [4]; from amygdala (AMY) after 30 days drinking using a 2-bottle choice [21]; from prefrontal cortex (PFC) after chronic (30 day), chronic intermittent (every other day for 29 days) or drinking in the dark (DID, 4 h in the dark for 36 days) [22]; and from PFC, Nucleus Accumbens (NAC), and AMY after 4 weekly cycles of chronic intermittent drinking [23]. In these studies, pathway analysis identified enrichment for many microglial mRNAs and networks, consistent with a role for microglia activation by alcohol. In microglia acutely isolated from prefrontal cortex of mice after alcohol consumption for 60 days in an every-other day drinking paradigm [24], 1010 Alc-DEs were identified in the microglial samples, compared to 2461 in total homogenates. Of the 1010 DEs, 846 were unique to microglia and not detected in the total homogenates. Similar to our findings, the largest differences were less
