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 induction of LTP [111]. Furthermore, it is possible that blood ethanol levels achieved during chronic alcohol experience might significantly influence the effect of EtOH on synaptic plasticity [116, 119]. Lastly, given that LTD is also evident with activation of NMDARs, it is interesting to note that EtOH enhances the induction of NMDA receptor-dependent LTD in the CA1 region of the hippocampus [120]. Taken together, results from studies in the hippocampus have demonstrated that EtOH exposure (both acute and in vivo conditions) dysregulates glutamatergic transmission, and that this effect of EtOH may produce impairments in hippocampal dependent learning and memory functions in alcohol dependent subjects.
