process length. For this analysis, we focused on microglia in the hippocampus, the site of significant peripheral macrophage infiltration (Fig. 2c) and an increase in protein and mRNA expression of proinflammatory cytokines (Fig. 4). Microglial morphology is one indicator of an inflammatory milieu, as these cells change their shape in response to immune activation, and our flow cytometry data suggested that microglia are significantly affected by alcohol and CVC administration (Fig. 5). CVC treatment partially rescued microglial morphology. Compared with alcohol-fed untreated mice, the CVC treatment groups had slightly larger cell bodies but retained the shortened cell process phenotype of alcohol-fed mice. This mixed microglial phenotype, despite the absence of IM infiltration, likely represents the innate response of microglia to alcohol which is characterized by activation and production of proinflammatory cytokines and reactive oxygen species [30–32]. The imaging in Fig. 5 suggests that microglial morphology was altered by chronic alcohol exposure although histologic examination of the complete microglial architecture is technically limited as some microglial processes may be disrupted by the histologic preparation. Additional studies have shown that alcohol consumption may only lead to partial microglia activation [33–35], similar to the findings we present here (Fig. 5a, b). Therefore, we
