MW 209.14 Da, Purity >99%. Competitive NMDA receptor antagonist (Ki = 35 nM for displacement of CPP binding in rat brain). Potent oral anticonvulsant activity in vivo.
AMPA 1, AMPA-selective glutamate receptor 1, AW490526, EB11, EIEE27, EPND, FESD, GLUH1, GRIA1_HUMAN, GRIN 2A, GRIN 2B, GRIN3A, GRIN3B, GluA1, GluN1, GluN2A, GluN2C, GluN2D, GluR-1, GluR-A, GluR-K1, Glutamate Receptor Ionotropic N Methyl D Aspartate 2B, Glutamate Receptor Ionotropic N Methyl D Aspartate 2C, Glutamate Receptor Ionotropic N Methyl D Aspartate subunit 2B, Glutamate Receptor Ionotropic N methyl D aspartate 3A, Glutamate [NMDA] receptor subunit epsilon-1, Glutamate [NMDA] receptor subunit epsilon-2, Glutamate [NMDA] receptor subunit epsilon-3, Glutamate [NMDA] receptor subunit epsilon-4, Glutamate [NMDA] receptor subunit zeta-1, Glutamate receptor, Glutamate receptor 1, Glutamate receptor ionotropic, Glutamate receptor ionotropic AMPA 1, Glutamate receptor ionotropic N methyl D aspartate 1, Glutamate receptor ionotropic N methyl D aspartate 2A, Glutamate receptor ionotropic N methyl D aspartate 3B, Glutamate receptor ionotropic NMDA2B, Glutamate receptor ionotropic, N-methyl-D aspartate, subunit 1, Glutamate receptor ionotropic, NMDA 2C, Glutamate receptor subunit epsilon 2, Glutamate receptor, ionotropic, N-methyl D-aspartate 2D, Glutamate receptor, ionotropic, NMDA2B (epsilon 2), Grin2c, Grin2d, HBGR1, LKS, MGC133252, MGC142178, MGC142180, MRD6, MRD8, N Methly D Aspartate Receptor Channel Subunit Epsilon 3, N methyl D asparate receptor channel subunit epsilon 2, N methyl D aspartate receptor channel subunit zeta 1, N methyl D aspartate receptor channel, subunit epsilon 1, N methyl D aspartate receptor subunit 2A, N methyl D aspartate receptor subunit 2B, N methyl D aspartate receptor subunit 2C, N methyl d aspartate receptor subunit 2D, N-methyl D-aspartate receptor subtype 2A, N-methyl D-aspartate receptor subtype 2B, N-methyl D-aspartate receptor subtype 2C, N-methyl D-aspartate receptor subtype 2D, N-methyl-D-aspartate receptor, N-methyl-D-aspartate receptor subunit 3, N-methyl-D-aspartate receptor subunit NR1, NMD-R1, NMDA 1, NMDA 2D, NMDA NR2B, NMDA receptor 1, NMDA receptor subtype 2A, NMDA receptor subunit 3A, NMDA receptor subunit 3B, NMDAR, NMDAR2C, NMDAR2D, NMDE1_HUMAN, NMDE2_HUMAN, NMDE3_HUMAN, NMDE4_HUMAN, NMDZ1_HUMAN, NR1, NR2A, NR2B, NR2C, NR2D, NR3, OTTHUMP00000041930, OTTHUMP00000160135, OTTHUMP00000160643, OTTHUMP00000165781, OTTHUMP00000174531, OTTHUMP00000224241, OTTHUMP00000224242, OTTHUMP00000224243, estrogen receptor binding CpG island, glutamate receptor ionotropic NMDA 2D, glutamate receptor ionotropic, NMDA 1, hNR 3, hNR2A
MW 209.14 Da, Purity >99%. Competitive NMDA receptor antagonist (Ki = 35 nM for displacement of CPP binding in rat brain). Potent oral anticonvulsant activity in vivo.
Soluble in water to 100 mM (with warming).
Competitive NMDA receptor antagonist (Ki = 35 nM for displacement of CPP binding in rat brain). Potent oral anticonvulsant activity in vivo.
NMDAR2A NMDAR2B GluN2C NMDAR1 Glutamate Receptor 1 (AMPA subtype) NMDAR3A + 3B and GluN2D are subunits of ionotropic glutamate receptors specifically the N-methyl-D-aspartate (NMDA) receptor and AMPA receptor subtypes. These receptors are integral membrane proteins involved in synaptic transmission and plasticity. NMDA receptors which include these subunits form a tetrameric structure typically composed of two GluN1 and two GluN2 or GluN3 subunits. The mass of each subunit varies but GluN1 has an approximate molecular weight of 120 kDa. These receptors are primarily expressed in the central nervous system within the neuronal synapses modulating excitatory neurotransmission.
These receptor subunits play an important role in synaptic plasticity memory and learning by mediating calcium ion influx in response to glutamate binding. They form part of a complex that includes auxiliary proteins that modulate their function and pharmacology. NMDAR subunits assemble to establish functional NMDA receptors requiring co-agonists such as glycine or D-serine and distinguished by their dependence on membrane depolarization to remove the Mg²⁺ block. Meanwhile AMPA receptors through the GluR1 subunit rapidly mediate excitatory postsynaptic potentials.
NMDARs and associated subunits participate significantly in the long-term potentiation (LTP) and long-term depression (LTD) pathways essential for synaptic strengthening and weakening. These synaptic plasticity pathways heavily involve signaling proteins such as calcium/calmodulin-dependent protein kinase II (CaMKII) and protein kinase C (PKC). Furthermore the interaction with neuronal nitric oxide synthase (nNOS) links NMDAR activity to downstream signaling cascades which can influence synaptic strength and neuronal health.
Aberrations in NMDA receptor function are implicated in neurological conditions such as Alzheimer's disease and schizophrenia. Reduced NMDAR activity is associated with cognitive decline and synaptic dysfunction in Alzheimer's partly due to interactions with amyloid-beta proteins. In schizophrenia altered expression of NMDAR subunits especially NMDA antagonists like MK-801 and DL-AP5 hint at a dysregulated glutamatergic system contributing to symptoms. Addressing these pathways and interactions provides a foundation for developing therapeutic strategies.
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