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N-Methyl-d-aspartate (NMDA) receptors are widely expressed in the mammalian central nervous system (CNS). Activation of the NMDA receptors depends on the simultaneous binding of two co-agonists: glutamate and either glycine or d-serine. Glutamate binds to the GluN2 subunits, and binding of glycine to the GluN1 subunit results in activation via the opening of the channel pore and subsequently causes the flow of ions through NMDA receptors. Functionally, NMDA receptors mediate excitatory synaptic transmission and plasticity by allowing the flux of calcium ions into neurons. NMDA-dependent synaptic plasticity is essential for many types of learning and memory formation. Dysfunction of NMDA receptors has been implicated in many neurological and psychiatric disorders, including Alzheimer’s disease, Parkinson’s disease, neuropathic pain, stroke, brain trauma, schizophrenia, and depression.

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