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Merck
CN

454575

N-Methyl-D-aspartic Acid hydrate

>95% (TLC), solid, excitatory amino acid neurotransmitter, Calbiochem®

Synonym(s):

N-Methyl-D-aspartic Acid, Hydrate, NMDA

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About This Item

Empirical Formula (Hill Notation):
C5H9NO4 · xH2O
CAS Number:
Molecular Weight:
147.13 (anhydrous basis)
UNSPSC Code:
12352209
NACRES:
NA.77
MDL number:
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Product Name

N-Methyl-D-aspartic Acid, Hydrate, Excitatory amino acid neurotransmitter.

SMILES string

N([C@H](CC(=O)O)C(=O)[O-])C

InChI

1S/C5H9NO4/c1-6-3(5(9)10)2-4(7)8/h3,6H,2H2,1H3,(H,7,8)(H,9,10)/p-1/t3-/m1/s1

InChI key

HOKKHZGPKSLGJE-GSVOUGTGSA-M

description

Merck USA index - 14, 6662

assay

>95% (TLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze

color

white

solubility

water: 1 mg/mL

shipped in

ambient

storage temp.

10-30°C

Quality Level

Biochem/physiol Actions

Cell permeable: no
Primary Target
Glutamate receptor that regulates Ca2+ channels
Product does not compete with ATP.
Reversible: no

Disclaimer

Toxicity: Standard Handling (A)

General description

An excitatory amino acid neurotransmitter. Selective agonist of the glutamate receptor that regulates Ca2+ channels. Important in long-term potentiation, ischemia, and epilepsy. NMDA receptors are involved in the "fine tuning" of synaptic connections in the developing brain. Chronic treatment with NMDA produces structural changes in synaptic morphology. Over-excitation of NMDA receptors causes neuronal degeneration and cell death.
Excitatory amino acid neurotransmitter. Selective agonist of the glutamate receptor that regulates Ca2+ channels. Important in long-term potentiation, ischemia, and epilepsy. NMDA receptors are involved in the "fine tuning" of synaptic connections in the developing brain. Chronic treatment with NMDA produces structural changes in synaptic morphology. Over-excitation of NMDA receptors causes neuronal degeneration and cell death.

Other Notes

Mattson, M.P., et al. 1993. J. Neurosci. 13, 4575.
Yen, L-H., et al. 1993. J. Neurosci. 13, 4949.
Swann, J.W., et al. 1992. Epilepsy Res. Suppl. 9, 115.

Preparation Note

Following reconstitution, store in the refrigerator (4°C). Stock solutions are stable for several days at 4°C.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Xinzheng Guo et al.
STAR protocols, 2(4), 100932-100932 (2021-11-23)
The degeneration of retinal ganglion cells (RGCs) leads to irreversible vision loss in a variety of pathological states. Here, we describe a protocol to evaluate the role of a gene in protecting mouse RGCs when they sustain injuries from excitotoxicity

Related Content

Glutamate is an excitatory neurotransmitter found in the synaptic vesicles of glutamatergic synapses. The post-synaptic neurons in these synapses contain ionotropic and metabotropic glutamate receptors. Glutamate binds to AMPA (α-amino-3-hydroxy-5- methylisoxazole-4-propionic acid) subtype glutamate receptors, leading to sodium influx into the post-synaptic cell and resulting in neuronal excitability and synaptic transmission. The NMDA (N-methyl-d-aspartate) subtype glutamate receptors, on the other hand, regulate synaptic plasticity, and can influence learning and memory. The metabotropic g-protein coupled mGluRs modulate downstream calcium signaling pathways and indirectly influence the synapse’s excitability. The synaptic architecture includes intracellular scaffolding proteins (PSD-95, GRIP), intercellular cell adhesion molecules (NCAMs, N-Cadherins), and a variety of signaling proteins (CaMKII/PKA, PP1/PP2B). Processes critical for synaptic transmission and plasticity are influenced by these molecules and their interactions. When the function of these molecules is disrupted, it leads to synaptic dysfunction and degeneration, and can contribute to dementia as seen in Alzheimer’s disease.

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