that NMDARs are the source of calcium that supports this form of LTP [16]. Additional mechanistic studies have demonstrated that both GluN2A and GluN2B subunits of NMDARs play a significant role in induction of hippocampal LTP [57–59]. More notable is that GluN2A subunits selectively play a role in induction of hippocampal LTP without affecting induction of LTD [59]. Therefore, in the hippocampus it is clear that NMDAR subunits are critical factors that determine the polarity of synaptic plasticity. Additional studies indicate that low-frequency stimulation induced LTD in the hippocampus also requires NMDAR activation [17, 60]. In addition, mechanistic studies have revealed a role for GluN2A and GluN2B subunits in induction of hippocampal LTD, indicating that the two distinct forms of plasticity in the hippocampus share a common molecular mechanism [61, 62]. Lastly, there are reports of NMDAR independent mechanisms for induction of LTP and LTD in the hippocampus, indicating that other neurotransmitter systems are involved in these phenomena [53, 60]. Taken together, hippocampal LTP has been widely studied since it is believed that the mechanisms involved in its induction, expression, and maintenance are fundamental to learning and memory, including those that may contribute to relapse to alcohol seeking behaviors [6,
