CNQX disodium salt is an antagonist of α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) and kainate receptors, with IC50 values of 0.3 and 1.5 μM, respectively [1]. 

AMPA and kainate receptors, collectively referred to as non-N-methyl-D-aspartate receptors, are distinct receptor complexes, but activated by the same agonists. AMPA and kainate receptors are involved in rapidly desensitizing responses in central nervous system [2]. 

In thalamic reticular nucleus neurons, CNQX (20 μM) depolarized all cells tested in a similar manner as DNQX. With longer CNQX application (5 min vs. 1 min), the depolarization persisted throughout CNQX application. However, in ventrobasal neurons, CNQX (20 μM) produced negligible effects on the membrane potential [3]. 

In Sprague-Dawley rats, pretreatment with CNQX (0.02, 0.1, 0.6, 3 and 15 mg/kg), administered intraperitoneally 15 min before capsaicin, significantly reduced c-fos-labelled cells within trigeminal nucleus caudalis by a maximum of 45%. The number of c-fos-like immunoreactivity cells within lateral reticular, medullary reticular, and solitary tract nuclei was not affected [4]. 

References:

[1]. Honoré T, Davies S N, Drejer J, et al. Quinoxalinediones: Potent competitive non-NMDA glutamate receptor antagonists. Science, 1988, 241(4866): 701-703.

[2]. Bettler B, Mulle C. AMPA and kainate receptors. Neuropharmacology, 1995, 34(2): 123-139.

[3]. Lee S H, Govindaiah G, Cox C L. Selective excitatory actions of DNQX and CNQX in rat thalamic neurons. Journal of Neurophysiology, 2010, 103(4): 1728-1734.

[4]. Mitsikostas D D, Sanchez del Rio M, Waeber C, et al. Non-NMDA glutamate receptors modulate capsaicin induced c-fos expression within trigeminal nucleus caudalis. British Journal of Pharmacology, 1999, 127(3): 623-630.