Alcohol is widely used and abused and produces profound deficits in learning and memory [64–67]. Alcohol abuse and eventual dependence is a chronic relapsing disorder characterized by compulsive alcohol-drinking and alcohol-seeking behaviors [21, 68, 69]. The National Survey on Drug Use and Health estimated that 22.6 million Americans of age 12 or older, or 9.2% of the population, can be considered to have AUD, indicating that AUDs continue to be major economic, social and public health issue [70]. The precise molecular mechanisms by which EtOH produces its effects within central nervous system are only now beginning to be understood [2]. One way to better understand EtOH’s effect on learning and memory is to study its acute and chronic effects on synaptic plasticity in different brain structures, including the hippocampus, neocortex and dorsomedial striatum, as these regions play critical roles in 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
