The traditional signaling induced by NMDA-Rs is triggered by the Ca2+ ions that pass through the NMDA-R channel. However, preliminary data indicate that blockers at the NR2B subunit, but not the NR1 subunit or the channel of the NMDA receptor, prevent the synaptic effects of the NMDA receptor. These findings suggest that Abeta employs novel, non-ion flux NMDA-R signaling mechanisms to produce synaptic depression. These results may open up a new group of potential therapeutic targets for treatment of Alzheimer’s disease.
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