et al., 2017). These mice also exhibit differences in the effect of ethanol exposure on synaptic protein levels in the hippocampus compared with non-transgenic littermate controls (Gruol et al., 2014). In hippocampal slices, astrocyte-specific increases in CCL2 or the inflammatory cytokine IL-6 confer resistance to the depressive effect of acute ethanol on LTP (Bray et al., 2013; Hernandez et al., 2016). Furthermore, astrocyte-specific CCL2 overexpression alters hippocampal synaptic function associated with ethanol withdrawal (Bray et al., 2018). To summarize, recent work using transgenic mice over-expressing specific inflammatory genes in astrocytes suggests potential roles for astrocytic cytokine release in modulating alcohol effects on synaptic plasticity and behavior. Preclinical studies of astrocyte-specific manipulation and alcohol behaviors are shown in Table 6.
