The hippocampus is involved in long and short-term spatial memory and declarative memory, and acute and chronic alcohol exposure causes deficits in these functions dependent on the hippocampus [66, 101–105]. These deficits correlate with altered microstructure of the grey matter, disruption of glial homeostasis and dysregulated neuroplasticity in the hippocampus [79, 106–109]. EtOH (acute and in vivo) inhibits LTP in the hippocampus, and mechanistic studies show that NMDARs are involved [80, 110–116]. Further evaluation indicates that the dose of EtOH (acute studies) and protocols used for LTP induction may influence how EtOH affects LTP in the hippocampus [113, 114]. For example, whereas acute EtOH treatment causes disruption of LTP, chronic in vivo alcohol experience, in some cases, enhances NMDAR activity and induces LTP in CA1 region of the hippocampus. This differential effect on LTP is hypothesized to be influenced by the differential expression of GABARs and NMDARs with alcohol experience [111, 117, 118]. It is also possible that chronic alcohol consumption reduces GABAergic transmission which in turn provides enough depolarization to activate NMDARs during or after tetanus thus leading to
