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].[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.
