Figure 1. CNQX disodium salt inhibition of evoked and spontaneous EPSCs mediated in mouse cortical neurons
The AMPA receptor antagonist CNQX disodium salt is commonly used at concentrations of 10 µM to inhibit the actions of glutamate acting on AMPARS. CNQX disodium from Hello Bio reduces both spontaneous and evoked EPSCs in cortical neurons at concentrations of 1 µM with full AMPA receptor blockade at 10 µM. For assay protocol, see #Protocol 1 in Application Notes below.
Figure 2. Percentage inhibiton of glutamate (30 µM) stimulated increase of Ca2+ fluorescence in HEK293 cells expressing GluK2
See Alt et al., 2004 for methodology and protocol
CNQX disodium salt: Scientist Approved
CNQX disodium salt - vial
Figure 1. CNQX disodium salt inhibition of evoked and spontaneous EPSCs mediated in mouse cortical neurons
The AMPA receptor antagonist CNQX disodium salt is commonly used at concentrations of 10 µM to inhibit the actions of glutamate acting on AMPARS. CNQX disodium from Hello Bio reduces both spontaneous and evoked EPSCs in cortical neurons at concentrations of 1 µM with full AMPA receptor blockade at 10 µM. For assay protocol, see #Protocol 1 in Application Notes below.
Figure 2. Percentage inhibiton of glutamate (30 µM) stimulated increase of Ca2+ fluorescence in HEK293 cells expressing GluK2
See Alt et al., 2004 for methodology and protocol
CNQX disodium salt: Scientist Approved
CNQX disodium salt - vial
Biological Data
Biological description
CNQX disodium salt is a water soluble, potent and competitive AMPA and kainate receptor antagonist. CNQX also antagonizes NMDA receptors at the glycine site.
CNQX increases GABAA receptor spontaneous postsynaptic currents (sPSCs) and also shows neuroprotective actions.
The AMPA receptor antagonist CNQX disodium salt is commonly used at concentrations of 10 μM to inhibit the actions of glutamate acting on AMPARs.
CNQX disodium salt from Hello Bio reduces both spontaneous and evoked EPSCs in cortical neurons at concentrations of 1 μM with full AMPA receptor blockade at 10 μM (see Fig 1 above).
#Protocol 1: Evoked and spontaneous excitatory post synaptic currents (EPSCs)
Whole cell voltage clamp recordings were obtained from layer V neurons of the mouse prelimbic cortex brain slice.
EPSCs were evoked via a stimulating electrode placed in layers II/III delivering a single square (150 μs) pulse every 10 sec at an intensity that gave a reliable EPSC.
Neurons were held at -70 to -60 mV (the reversal potential of GABA currents). EPSCs were continuously stimulated and recorded in response to 5 min applications of varying concentrations of CNQX disodium salt until complete receptor inhibition.
Spontaneous EPSCs were recorded before and after addition of CNQX disodium salt by holding the neuron at -70 mV and recording for 10 sec.
Recordings for EPSCs were made in the absence of GABAA-R antagonists.
Solubility & Handling
Storage instructions
Room temperature (desiccate)
Solubility overview
Soluble in water (20mM)
Handling
Hydroscopic solid, contact with air may cause material to change colour and become sticky. Product performance should not be affected but we recommend storing the material in a sealed jar.
Important
This product is for RESEARCH USE ONLY and is not intended for therapeutic or diagnostic use. Not for human or veterinary use.
References are publications that support the biological activity of the product
The calpain inhibitor MDL-28170 and the AMPA/KA receptor antagonist CNQX inhibit neurofilament degradation and enhance neuronal survival in kainic acid-treated hippocampal slice cultures.
Lopez-Picon FR et al (2006) Eur J Neurosci 23(10) : 2686-94.
6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX) increases GABAA receptor-mediated spontaneous postsynaptic currents in the dentate granule cells of rat hippocampal slices.
Hashimoto Y et al (2004) Neurosci Lett 358(1) : 33-6.
6,7-Dinitro-quinoxaline-2,3-dion and 6-nitro,7-cyano-quinoxaline-2,3-dion antagonise responses to NMDA in the rat spinal cord via an action at the strychnine-insensitive glycine receptor.
Birch PJ et al (1988) Eur J Pharmacol 156(1) : 177-80.