(R)-CPP, NMDA antagonist (ab120159)
Key features and details
- Potent NMDA antagonist
- CAS Number: 126453-07-4
- Soluble in water to 100 mM
- Form / State: Solid
- Source: Synthetic
Overview
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Product name
(R)-CPP, NMDA antagonist -
Description
Potent NMDA antagonist -
Biological description
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CAS Number
126453-07-4 -
Chemical structure
Properties
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Chemical name
(R)-3-(2-Carboxypiperazin-4-yl)propyl-1-phosphonic acid -
Molecular weight
252.20 -
Molecular formula
C8H17N2O5P -
PubChem identifier
6603754 -
Storage instructions
Store at Room Temperature. Store under desiccating conditions. The product can be stored for up to 12 months. -
Solubility overview
Soluble in water to 100 mM -
Handling
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20°C. Generally, these will be useable for up to one month. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please visit our frequently asked questions (FAQ) page for more details.
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SMILES
O=C(O)[C@H]1CN(CCCP(=O)(O)O)CCN1 -
Source
Synthetic
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Research areas
Images
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Functional Studies - (R)-CPP, NMDA antagonist (ab120159) Herman et al PLoS One. 2011;6(11):e26501. doi: 10.1371/journal.pone.0026501. Epub 2011 Nov 1. Fig 3. Reproduced under the Creative Commons license http://creativecommons.org/licenses/by/4.0/
Transporter blockade does not reveal an ambient glutamate concentration gradient between extracellular compartments.
A. Average Ca2+ increase in a spine during a 40 ms voltage step, with iontophoresis of L-aspartate (black), without iontophoresis (red), a second L-aspartate application (gray), L-aspartate in the presence of 100 µM TBOA (blue), and TBOA alone (green).
B. Comparison of spine Ca2+ transients in each condition, normalized to the first response to L-aspartate iontophoresis (n = 5). Error bars indicate SEM. Significance determined by Friedman ANOVA with Conover posthoc test: *p
If the extrasynaptic glutamate concentration is higher than that in the cleft because transporters prevent diffusion of glutamate into the synapse, blocking transporters should result in a large Ca2+ increase in the spine as extrasynaptic glutamate rushes into the cleft and activates synaptic NMDARs. Spines exhibited a Ca2+ increase during a 40 ms depolarization with iontophoresis of the glutamate transporter substrate and NMDAR agonist, L-aspartate (A; black and gray traces), confirming the presence of NMDARs. However, TBOA (100 µM) did not increase the Ca2+ transient in the same spines during the 40 ms depolarization when compared to the control voltage step without L-aspartate iontophoresis (See image compare green and red traces; 20.6±13.62%; p>0.5; n = 5;). TBOA was effective in blocking transporters, however, as the NMDAR-mediated Ca2+ signal evoked by iontophoresis of L-aspartate was increased in the presence of TBOA (See image). This result indicates that glutamate transporters do not normally generate a concentration gradient of ambient glutamate between extrasynaptic and synaptic extracellular compartments.