CNQX is an effective competitive antagonist of AMPA/kainate receptors, with IC50 values of 0.3µM and 1.5µM, respectively[1]. CNQX is a non-NMDA receptor antagonist[2].
In vitro, CNQX (1µM) reduces the frequency of light-induced peak potentials in retinal ganglion cells by 28%±22% and also induces voltage- and magnesium-dependent delayed spike firing[2]. CNQX (0-100 mM; 20-24 h) exhibits dose-dependent toxicity in mixed mouse cortical cells, with neuronal damage effects[3]. CNQX (20 µM) reversibly depolarizes the membrane potential of TRN neurons, inducing smaller depolarizations in thalamic relay neurons in VB[4].
In vivo, CNQX (0.5 µg; i.c.v.) can block hippocampal CA3 pyramidal cell death induced by kainic acid in ICR mice, partially attenuate the increase of p-ERK and the decrease of p-CREB, and inhibit the expression of phosphorylated ERK protein[5]. Bilateral infusion of CNQX (0.5 or 1.25µg) into the amygdala or dorsal hippocampus of rats can block the expression of startle reflex[6].
References:
[1]TAGE HONORÉ, STEVE N. DAVIES, JØRGEN DREJER, et al. Quinoxalinediones: Potent Competitive Non-NMDA Glutamate Receptor Antagonists[J]. SCIENCE.1988(241):701-703.
[2] Jeffrey S. Diamond, David R. Copenhagen. The contribution of NMDA and Non-NMDA receptors to the light-evoked input-output characteristics of retinal ganglion cells[J]. Cell Press. October, 1993:725-738.
[3]Uliasz T F , Hewett S J . A microtiter trypan blue absorbance assay for the quantitative determination of excitotoxic neuronal injury in cell culture[J]. Journal of Neuroscience Methods, 2000, 100(1-2):157-163.
[4]Sang Hun Lee,G. Govindaiah,and Charles L. Cox. Selective Excitatory Actions of DNQX and CNQX in Rat Thalamic Neurons[J].Journal of Neurophysiology, 2010(4):103.
[5]Lee J K , Choi S S , Lee H K ,et al.Effects of MK-801 and CNQX on various neurotoxic responses induced by kainic acid in mice.[J]. Molecules & Cells, 2002, 14(3):339-347.
[6]Kim M, Campeau S, Falls W A, et al. Infusion of the non-NMDA receptor antagonist CNQX into the amygdala blocks the expression of fear-potentiated startle. Behav Neural Biol, 1993, 59(1): 5-8.
CNQX是一种有效的竞争性AMPA /海藻酸酯受体(AMPA/kainate receptor)拮抗剂,IC50 分别为0.3µM和1.5µM[1]。CNQX 是一种非NMDA受体拮抗剂[2]。
在体外,CNQX(1µM)使视网膜神经节细胞的光诱发峰电位频率降低了28%±22%,还引起了电压和镁依赖性的延迟尖峰发作[2]。CNQX(0-100 mM; 20-24 h)对混合小鼠皮质细胞产生剂量依赖性的毒性,具有神经元损伤作用[3]。CNQX(20 µM)以可逆方式使TRN神经元的膜电位去极化,在VB中继神经元中诱发的去极化较小[4]。
在体内,CNQX (0.5 µg; i.c.v.)能阻断红藻氨酸诱导的ICR小鼠海马CA3区锥体细胞死亡,部分减弱p-ERK升高和p-CREB降低,抑制磷酸化ERK蛋白表达[5]。CNQX(0.5或1.25µg)双侧输注到大鼠杏仁核或背侧海马体中,可以阻断惊吓反射的表达[6]。