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| Preferred IUPAC name 6,7-Dinitro-1,4-dihydroquinoxaline-2,3-dione | |
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| Properties | |
| C8H4N4O6 | |
| Molar mass | 252.142 g·mol−1 |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
DNQX (6,7-dinitroquinoxaline-2,3-dione) is a competitive antagonist atAMPA andkainatereceptors, twoionotropic glutamate receptor (iGluR) subfamilies.[1] It is used in a variety ofmolecular biology subfields, notablyneurophysiology, to assist researchers in determining the properties of various types ofion channels and their potential applications in medicine.
DNQX (anAMPAreceptor antagonist) displays significant effects on neurons. When applied to rathippocampus neurons in culture, it produces a dose-dependentneurotoxicity which intriguingly seems to operate through a mechanism independent ofionotropic glutamate receptors. This effect is specific to neurons and does not impact the surroundingglial cells.[2]
In the context ofamphetamine-induced behavioral sensitization in mice, DNQX demonstrates the capacity to block both the onset and the manifestation of this sensitization. Rather than impacting the overallamphetamine activity, DNQX specifically intervenes in the sensitization process. This phenomenon might be attributed to the activation of excitatory amino acid receptors which subsequently provoke an increaseddopamine release in thestriatum. Therefore, DNQX's actions appear to be both potent and specific hinting at complex mechanisms beyond traditionalionotropic glutamate receptor pathways.[3]
An activation of both AMPA/kainate and dopaminergic receptors in thenucleus accumbens may be crucial for the reward response triggered bypsychostimulant drugs.Dopaminergicantagonists often do not prevent the acquisition of a conditioned place preference forcocaine, a common measure of drug reward. In experiments where DNQX, anAMPA receptorantagonist, was injected into the nucleus accumbens prior to systemic cocaine administration, it diminished the acquisition of this place preference, highlightingAMPA receptors' role in this process. Conversely, thedopaminergicantagonistfluphenazine did not alter cocaine-induced place preference, possibly due to adaptations following repeated drug exposure. Both DNQX andfluphenazine blocked the expression of conditioned place preference in rats previously trained with cocaine alone, indicating the involvement of both AMPA anddopaminergicreceptors in the expression of cocaine-induced place preference.[4]
