Apart from anticholinesterases, memantine, a low-affinity NMDA receptor (NMDAR) antagonist, is the only currently approved treatment for clinical dementia of the Alzheimer type.Here we examined if subtype-preferring NMDA receptor antagonists could preferentially protect against the inhibition of NMDA receptor-dependent plasticity of excitatory synaptic transmission by Aβ in the hippocampus by electrophysiology methods in vitro.Antagonists selective for NMDA receptors containing NR2B but not NR2A subunits prevented Aβ-mediated inhibition of plasticity and showed dose-dependent.