TLR4 were also observed in rats exposed to intermittent alcohol using a binge-drinking model [41]. A role for cytokines and NF-κB in innate immune gene expression was reported in rat brain slice cultures given that blockade of the cytokine TNFα or blockade of NF-κB reduced ethanol induction of pro-inflammatory target genes [39]. There is also evidence in humans for involvement of the NF-κB system in prefrontal cortex of alcoholics [42]. Furthermore, ethanol consumption and preference in mice was decreased slightly following administration of caffeic acid phenethyl ester (CAPE), an inhibitor of NF-κB activation, providing behavioral evidence for NF-κB activation mediating alcohol behavior [3].
