the distinct stages of alcohol addiction cycle [21, 71]. Mechanistic studies have convincingly shown that excitatory NMDARs in the brain are important sites for EtOH’s actions [72–74]. Concurrently, NMDARs play an important role in learning and memory, and provide a unique role in maintaining and regulating synaptic plasticity [75–77]. Therefore, it appears that EtOH’s actions via the NMDARs could be facilitating the EtOH-induced deficits in synaptic plasticity and learning and memory functions [2, 74, 78, 79]. A number of studies have demonstrated that EtOH alters synaptic plasticity in the dorsal striatum, neocortex and hippocampus [49, 80–84]. The following paragraphs will briefly discuss the effects of EtOH on synaptic plasticity in the dorsal striatum, neocortex and the hippocampus.
