Either acute or chronic ethanol exposure is considered as a stressor. The sensitivity of the hippocampus to various stressors is well documented [11–14]. At both immunological and neurological levels, alcohol has deleterious effects on the hippocampus. Studies have shown that chronic alcohol use is associated with morphological changes in the hippocampus, including decreased hippocampal volume [15, 16]. Ethanol exposure also changes CD14 and TLR4 expression; while ethanol decreases neurogenesis in the hippocampus, neurogenesis is increased in TLR4 knockout mice [17]. The inflammatory cascade in the brain induced by alcohol consumption has also been found to increase the duration and magnitude of proinflammatory cytokines and microglial activation, thus increasing susceptibility to chronic illnesses [9]. One such chronic illness linked to Cd14 and neuroinflammation is Alzheimer’s disease, which is heavily implicated with the hippocampus and can be detected in the hippocampal formation at an early stage before further symptoms arise [18, 19]. Perhaps more importantly, our previous studies have shown that gene expression in the hippocampus is particularly sensitive to the effects of acute ethanol (1.8 g/kg) [20, 21]. Others have also
