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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.Like Aβ, pretreatment with a high dose of NR2B antagonist ifenprodil (1 μM) and Ro 25-6981 (200 nM) completely inhibited LTP.Further experiments indicated that a lower dose of ifenprodil (400 nM) could partially block LTP (131±7%) and reverse Aβ inhibition on LTP (139±6%).However, Ro 25-6981 (50 nM) didnt block LTP (143±10%) but did prevent Aβ inhibition on LTP (132±8 %).