NMDA (BAT-008102)
* For research use only

NMDA is a specific agonist for NMDA receptor mimicking the action of glutamate, the neurotransmitter which normally acts at that receptor. Unlike glutamate, NMDA only binds to and regulates the NMDA receptor and has no effect on other glutamate receptors.

Category
D-Amino Acids
Catalog number
BAT-008102
CAS number
6384-92-5
Molecular Formula
C5H9NO4
Molecular Weight
147.13
NMDA
IUPAC Name
(2R)-2-(methylamino)butanedioic acid
Synonyms
LC488A; LC 488A; LC-488A
Appearance
White to Off-White Solid
Purity
>98%
Density
1.343 g/cm3
Melting Point
187-192 °C
Boiling Point
258.2ºC at 760 mmHg
Storage
Store at 2-8 °C
Solubility
Soluble in Aqueous Acid, DMSO, Water
InChI
InChI=1S/C5H9NO4/c1-6-3(5(9)10)2-4(7)8/h3,6H,2H2,1H3,(H,7,8)(H,9,10)/t3-/m1/s1
InChI Key
HOKKHZGPKSLGJE-GSVOUGTGSA-N
Canonical SMILES
CNC(CC(=O)O)C(=O)O
1.GluN3A promotes NMDA spiking by enhancing synaptic transmission in Huntington's disease models.
Mahfooz K1, Marco S1, Martínez-Turrillas R1, Raja MK1, Pérez-Otaño I1, Wesseling JF2. Neurobiol Dis. 2016 Apr 9. pii: S0969-9961(16)30074-2. doi: 10.1016/j.nbd.2016.04.001. [Epub ahead of print]
Age-inappropriate expression of juvenile NMDA receptors (NMDARs) containing GluN3A subunits has been linked to synapse loss and death of spiny projection neurons of the striatum (SPNs) in Huntington's disease (HD). Here we show that suppressing GluN3A expression prevents a multivariate synaptic transmission phenotype that precedes morphological signs at early prodromal stages. We start by confirming that afferent fiber stimulation elicits larger synaptic responses mediated by both AMPA receptors and NMDARs in SPNs in the YAC128 mouse model of HD. We then show that the enhancement mediated by both is fully prevented by suppressing GluN3A expression. Strong fiber-stimulation unexpectedly elicited robust NMDAR-mediated electrogenic events (termed "upstates" or "NMDA spikes"), and the effective threshold for induction was more than 2-fold lower in YAC128 SPNs because of the enhanced synaptic transmission. The threshold could be restored to control levels by suppressing GluN3A expression or by applying the weak NMDAR blocker memantine.
2.Lysosomal iron modulates NMDA receptor-mediated excitation via small GTPase, Dexras1.
White RS1, Bhattacharya AK1, Chen Y1, Byrd M1, McMullen MF1, Siegel SJ1, Carlson GC1, Kim SF2. Mol Brain. 2016 Apr 14;9(1):38. doi: 10.1186/s13041-016-0220-8.
BACKGROUND: Activation of NMDA receptors can induce iron movement into neurons by the small GTPase Dexras1 via the divalent metal transporter 1 (DMT1). This pathway under pathological conditions such as NMDA excitotoxicity contributes to metal-catalyzed reactive oxygen species (ROS) generation and neuronal cell death, and yet its physiological role is not well understood.
3.Cocaine-Induced Synaptic Alterations in Thalamus to Nucleus Accumbens Projection.
Neumann PA1, Wang Y2, Yan Y3, Wang Y3, Ishikawa M1, Cui R2, Huang YH3, Sesack SR1,3, Schlüter OM1, Dong Y1,3. Neuropsychopharmacology. 2016 Apr 14. doi: 10.1038/npp.2016.52. [Epub ahead of print]
Exposure to cocaine induces addiction-associated behaviors partially through remodeling neurocircuits in the nucleus accumbens (NAc). The paraventricular nucleus of thalamus (PVT), which projects to the NAc monosynaptically, is activated by cocaine exposure and has been implicated in several cocaine-induced emotional and motivational states. Here, we show that disrupting synaptic transmission of select PVT neurons with tetanus toxin activated via retrograde trans-synaptic transport of cre from NAc efferents decreased cocaine self-administration in rats. This projection underwent complex adaptations after self-administration of cocaine (0.75 mg/kg/infusion; 2 h/d × 5d, 1d overnight training). Specifically, 1d after cocaine self-administration, we observed increased levels of AMPA receptor (AMPAR)-silent glutamatergic synapses in this projection, accompanied by a decreased ratio of AMPAR-to-NMDA receptor (NMDAR)-mediated EPSCs. Furthermore, the decay kinetics of NMDAR EPSCs was significantly prolonged, suggesting insertion of new GluN2B-containing NMDARs to PVT-to-NAc synapses.
4.Variability in the effect of antidepressants upon Wfs1-deficient mice is dependent on the drugs' mechanism of actions.
Reimet R1, Raud S2, Loomets M2, Visnapuu T2, Volke V3, Reimets A2, Plaas M2, Vasar E2. Behav Brain Res. 2016 Apr 11. pii: S0166-4328(16)30212-1. doi: 10.1016/j.bbr.2016.04.011. [Epub ahead of print]
There is significant comorbidity between mood disorders and diabetes. Wolfram syndrome-related to deficient WFS1 gene function-causes diabetes and mood disorders in humans. Mice lacking the Wfs1 gene display impaired emotional behaviour and glucose metabolism. Various antidepressant drugs are used for alleviating the symptoms of mood disorders. For this study the tail suspension test and locomotor activity test were used to compare the effects of different antidepressants upon homozygous Wfs1-deficient, heterozygous Wfs1-deficient and wild-type mice. Mouse glucose metabolism was concurrently studied using the glucose tolerance test. We showed that ketamine(10mg/kg),NMDA antagonist, escitalopram(2.5-10mg/kg), selective serotonin reuptake inhibitor(SSRI), and amitriptyline(10mg/kg), noradrenaline and serotonin reuptake inhibitor, elicited a stronger antidepressant-like effect in homozygous Wfs1-deficient mice compared to wild-type mice. The effect of noradrenaline and serotonin reuptake inhibitor desipramine(10 and 20mg/kg) did not differ between genotypes.
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