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(RS)-MCPG

(RS)-MCPG

Catalog No. BCC6610
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10mg $153.00 Ship Within 7 Days
50mg $644.00 Ship Within 7 Days
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Quality Control of (RS)-MCPG

Chemical structure

(RS)-MCPG

Biological Activity of (RS)-MCPG

Non-selective group I/group II metabotropic glutamate receptor antagonist. (S)-isomer and sodium salt also available.

(RS)-MCPG Dilution Calculator

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(RS)-MCPG Molarity Calculator

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Chemical Properties of (RS)-MCPG

Cas No. 146669-29-6 SDF Download SDF
Chemical Name (RS)-α-Methyl-4-carboxyphenylglycine
SMILES C[C@]([NH3+])(C([O-])=O)c1ccc(cc1)C([O-])=O
Standard InChIKey DNCAZYRLRMTVSF-SNVBAGLBSA-M
Standard InChI InChI=1S/C10H11NO4/c1-10(11,9(14)15)7-4-2-6(3-5-7)8(12)13/h2-5H,11H2,1H3,(H,12,13)(H,14,15)/p-1/t10-/m1/s1
Formula C10H11NO4 M.Wt 209.2
Solubility Soluble to 100 mM in 1.1eq. NaOH
Storage Store at RT
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

Preparing Stock Solutions of (RS)-MCPG

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.7801 mL 23.9006 mL 47.8011 mL 95.6023 mL 119.5029 mL
5 mM 0.956 mL 4.7801 mL 9.5602 mL 19.1205 mL 23.9006 mL
10 mM 0.478 mL 2.3901 mL 4.7801 mL 9.5602 mL 11.9503 mL
50 mM 0.0956 mL 0.478 mL 0.956 mL 1.912 mL 2.3901 mL
100 mM 0.0478 mL 0.239 mL 0.478 mL 0.956 mL 1.195 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

References on (RS)-MCPG

The metabotropic glutamate receptor antagonist (RS)-MCPG produces hyperlocomotion in amphetamine pre-exposed rats.[Pubmed: 9680243]


It is known that, over a wide range of doses, the selective metabotropic glutamate receptor (mGluR) agonist, 1-aminocyclopentane-trans-1,3-dicarboxylic acid [(1S,3R)-ACPD], increases locomotion whereas the selective mGluR antagonist, (RS)-alpha-methyl-4-carboxyphenylglycine (MCPG) [(RS)-MCPG], is without effect when microinjected into the nucleus accumbens (NAcc) of drug-naive rats. The present experiments determined whether these responses are altered by pre-exposing rats to a regimen of systemic amphetamine (AMPH) injections known to produce locomotor sensitization. Rats in different groups were administered four injections of saline or AMPH (1.0 mg/kg, i.p.), one injection every third day. Two weeks after the last injection, rats were challenged with microinjections of either saline, (RS)-MCPG (2.5 nmole/side) or (1S,3R)-ACPD (0.5 nmole/side) into the NAcc. While (1S,3R)-ACPD increased locomotor activity when injected into the NAcc, no significant difference between saline and AMPH pre-exposed rats was observed. However, and interestingly, (RS)-MCPG which had no effect on locomotor activity when given to saline pre-exposed rats induced significantly higher locomotor activity in AMPH compared to saline pre-exposed rats. These results indicate that glutamatergic neurotransmission mediated by mGluRs in the NAcc is altered by repeated systemic injections of AMPH. Such changes may ultimately position the mGluR to contribute to the expression of sensitization by AMPH as well as other psychomotor stimulant drugs.

Agonist action of (RS)-alpha-methyl-4-carboxyphenylglycine (MCPG) in the amygdala.[Pubmed: 7632895]


Glutamatergic excitatory postsynaptic potentials (EPSPs) in the basolateral amygdala (BLA) are reduced in amplitude following agonist activation of presynaptic metabotropic glutamate receptors (mGluR). In this study, the effect of a presumed mGluR antagonist, (RS)-alpha-methyl-4-carboxyphenylglycine (MCPG), was investigated on the EPSP recorded intracellularly in BLA neurons. Superfusion of MCPG (500 microM) significantly reduced the amplitude of evoked EPSPs. In the presence of MCPG, postsynaptic responses to alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA, 1 microM) were unaltered while responses to N-methyl-D-aspartate (NMDA, 3-5 microM) were potentiated. These data suggest that the MCPG-induced reduction of EPSP amplitude is due to a mGluR agonist action at a presynaptic mGluR 'autoreceptor'.

(RS)-alpha-methyl-4-carboxyphenylglycine (MCPG) does not block theta burst-induced long-term potentiation in area CA1 of rat hippocampal slices.[Pubmed: 8041499]


We have used the selective metabotropic glutamate receptor antagonist (RS)-alpha-methyl-4-carboxyphenylglycine (MCPG) to investigate in the CA1 hippocampal subregion in vitro whether coactivation of N-methyl-D-aspartate (NMDA) and metabotropic glutamate receptors is necessary for the induction of long-term potentiation (LTP) when LTP is induced by theta burst stimulation (TBS). When MCPG (500 microM) was bath applied 14-30 min prior to a triple high-frequency tetanization (100 Hz, 1 s) and washed out immediately afterwards the potentiation of the extracellularly recorded field potentials decayed gradually to baseline (P < 0.05) over 2-3 h. However, when MCPG was applied in the same manner before a triple TBS (10 bursts at 5 Hz, 100 Hz within the bursts) the resulting potentiation remained stable for at least 4 h. MCPG had no effect on baseline synaptic transmission or post-tetanic potentiation. These results demonstrate a clear difference in the mechanisms underlying these two different forms of LTP.

Kewords:

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