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Chemical Compound Review

CNQX     7-nitro-2,3-dioxo-1,4- dihydroquinoxaline-6...

Synonyms: Tocris-0190, AC1MWAKF, C127_SIGMA, SureCN1662279, SureCN2460241, ...
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Disease relevance of CNQX


Psychiatry related information on CNQX

  • Additional control experiments indicated that attenuation of cue-induced reinstatement by CNQX, NBQX, L-701,324, and MPEP was not accompanied by significant suppression of spontaneous locomotor activity [6].
  • Intense feeding responses associated with an increased duration of feeding behavior were consistently recorded after injections of MK-801 or CNQX into the medial two-thirds of the tuberculum olfactorium (TO), the ventral aspect of lobus parolfactorium (LPOv), or the ventral pallidum (VP) [7].
  • In the present study, the effects of local injections of MK-801 (6 nmol), CNQX (160 nmol) or vehicle (0.2 microl) into a number of ventral striatopallidal nuclei on feeding, drinking and non-ingestive (sleep, preening) spontaneous behaviors were investigated in free-feeding pigeons (Columba livia) [7].
  • We have previously demonstrated that the posttraining infusion of 6-cyano-7-nitroquinoxaline-2,3-dione, an alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor blocker, into the dorsal hippocampus of rats, causes retrograde amnesia of an inhibitory avoidance training [8].
  • In a lethality test, intracerebroventricular (i.c.v.) pretreatment of MK-801 (1 microg), but not CNQX (0.5 microg), attenuated the time to lethality induced by KA (0.5 microg) administered i.c.v. In the memory test (a passive avoidance test), MK-801, but not CNQX, prevented the memory loss induced by KA (0.1 microg) [9].

High impact information on CNQX

  • AMPA receptor antagonists (CNQX) blocked targeting of Arc mRNA in a small region, and mGluR antagonists (MCPG) did not affect localization [10].
  • The down-regulation of GABAergic inhibition was not affected by antagonism of metabotropic receptors, while it was attenuated by CNQX [11].
  • This neurotoxicity was blocked by CNQX, an antagonist to the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)/kainate receptor but not by two N-methyl-D-aspartate (NMDA) antagonists [12].
  • We show that neither reactive sprouting nor functional recovery of synaptic transmission occur in the presence of the non-N-methyl-D-aspartate (NMDA) receptor antagonist 6-nitro-7-sulfamoylbenzoquinoxaline-2,3-dione (CNQX) [13].
  • Blockade of transmission of visceral nociceptive signals through the rat sacral cord by microdialysis administration of morphine or 6-cyano-7-nitroquinoxaline-2,3-dione shows that postsynaptic DC neurons in the sacral cord transmit visceral nociceptive signals to the gracile nucleus [14].

Chemical compound and disease context of CNQX


Biological context of CNQX


Anatomical context of CNQX


Associations of CNQX with other chemical compounds


Gene context of CNQX


Analytical, diagnostic and therapeutic context of CNQX

  • In 23 of 49 (47%) of the above cells, AMPA antagonist iontophoresis (either CNQX or DNQX) selectively decreased the excitatory response to thalamic stimulation [39].
  • Excitatory synaptic mechanisms associated with burst suppression activity were probed using glutamate receptor antagonists (CNQX and APV), GABA receptor antagonists, and simultaneous whole cell patch clamp and microelectrode EEG recordings [40].
  • Local perfusion of an alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)/kainate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione, blocked the stress-induced increase in dopamine levels, whereas an NMDA receptor antagonist, 2-amino-5-phosphonopentanoic acid, at the dose tested, was not able to alter this response significantly [41].
  • These behavioral responses could be significantly blocked by intrathecal injection of the NMDA receptor antagonists MK-801 and AP-5, the non-NMDA receptor antagonist CNQX or the nitric oxide synthase inhibitor L-NAME [42].
  • AMPA also elicited Ca2+ elevations that were inhibited by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and occurred after treatment with omega-conotoxin MVIIC to block neurotransmitter release [43].


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  23. Mechanism of acute ischemic injury of oligodendroglia in early myelinating white matter: the importance of astrocyte injury and glutamate release. Wilke, S., Thomas, R., Allcock, N., Fern, R. J. Neuropathol. Exp. Neurol. (2004) [Pubmed]
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