(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
Product name(R)-CPP, NMDA antagonist
DescriptionPotent NMDA antagonist
Chemical name(R)-3-(2-Carboxypiperazin-4-yl)propyl-1-phosphonic acid
Storage instructionsStore at Room Temperature. Store under desiccating conditions. The product can be stored for up to 12 months.
Solubility overviewSoluble in water to 100 mM
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.
2D chemical structure image of ab120159, (R)-CPP, NMDA antagonist
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<0.05; **p<0.01; ***p<0.001.
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.
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab120159 has been referenced in 20 publications.
- Balmer TS et al. Incomplete removal of extracellular glutamate controls synaptic transmission and integration at a cerebellar synapse. Elife 10:N/A (2021). PubMed: 33616036
- Babola TA et al. Purinergic Signaling Controls Spontaneous Activity in the Auditory System throughout Early Development. J Neurosci 41:594-612 (2021). PubMed: 33303678
- Guo C et al. Purkinje cell outputs selectively inhibit a subset of unipolar brush cells in the input layer of the cerebellar cortex. Elife 10:N/A (2021). PubMed: 34369877
- Rudolph S et al. Cerebellum-Specific Deletion of the GABAA Receptor d Subunit Leads to Sex-Specific Disruption of Behavior. Cell Rep 33:108338 (2020). PubMed: 33147470
- Khan MM & Regehr WG Loss of Doc2b does not influence transmission at Purkinje cell to deep nuclei synapses under physiological conditions. Elife 9:N/A (2020). PubMed: 32347796