DNQX (FG 9041)
(Synonyms: 二硝基喹酮; FG 9041) 目录号 : GC32755
A non-
Cas No.:2379-57-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
DNQX is a competitive, non-
1.Armstrong, N., and Gouaux, E.Mechanisms for activation and antagonism of an AMPA-sensitive glutamate receptor: Crystal structures of the GluR2 ligand binding coreNeuron28(1)165-181(2000) 2.Honoré, T., Davies, S.N., Drejer, J., et al.Quinoxalinediones: Potent competitive non-NMDA glutamate receptor antagonistsScience241(4866)701-703(1988) 3.Lee, S.H., Govindaiah, G., and Cox, C.L.Selective excitatory actions of DNQX and CNQX in rat thalamic neuronsJ. Neurophysiol.103(4)1728-1734(2010) 4.Muller, D., Joly, M., and Lynch, G.Contributions of quisqualate and NMDA receptors to the induction and expression of LTPScience242(4886)1694-1697(1988)
| Cas No. | 2379-57-9 | SDF | |
| 别名 | 二硝基喹酮; FG 9041 | ||
| Canonical SMILES | O=C1C(NC2=CC([N+]([O-])=O)=C([N+]([O-])=O)C=C2N1)=O | ||
| 分子式 | C8H4N4O6 | 分子量 | 252.14 |
| 溶解度 | DMSO : ≥ 35 mg/mL (138.81 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.9661 mL | 19.8303 mL | 39.6605 mL |
| 5 mM | 0.7932 mL | 3.9661 mL | 7.9321 mL |
| 10 mM | 0.3966 mL | 1.983 mL | 3.9661 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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Selective excitatory actions of DNQX and CNQX in rat thalamic neurons
J Neurophysiol 2010 Apr;103(4):1728-34.PMID:20107128DOI:10.1152/jn.00540.2009.
The thalamic reticular nucleus (TRN) consists of GABA-containing neurons that form reciprocal synaptic connections with thalamic relay nuclei. Excitatory synaptic innervation of TRN neurons arises from glutamatergic afferents from thalamocortical relay neurons and deep layer corticothalamic neurons, and they produce excitation via both N-methyl-D-aspartate (NMDA) and non-NMDA receptors. Quinoxaline derivatives [e.g., 6,7-dinitroquinoxaline-2,3-dione (DNQX), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)] have routinely been used as non-NMDA receptor antagonists over the last two decades. In this study, we examined whether quinoxaline derivatives alter the intrinsic properties of thalamic neurons in light of recent findings indicating that these compounds can alter neuronal excitability in hippocampal and cerebellar neurons via transmembrane AMPA receptor (AMPAR) regulatory proteins (TARPs). Whole cell recordings were obtained from TRN and ventrobasal (VB) thalamic relay neurons in vitro. DNQX and CNQX produced a consistent depolarization in all TRN neurons tested. The depolarization persisted in tetrodotoxin and low Ca²+/high Mg²+ conditions, suggesting a postsynaptic site of action. In contrast, DNQX and CNQX produced little or no change in VB thalamocortical relay neurons. The nonspecific ionotropic glutamate receptor antagonist, kynurenic acid, and the selective AMPAR antagonist, 4-(8-methyl-9H-1,3-dioxolo[4,5-h][2,3]benzodiazepin-5-yl)-benzenamine hydrochloride, blocked the DNQX-mediated depolarizations. Our results indicate that the DNQX- and CNQX-mediated depolarizations are mediated by AMPAR but not kainate receptors in TRN neurons. The AMPAR-positive allosteric modulator, trichloromethiazide, potentiated the DNQX-mediated depolarization in TRN neurons but did not unmask any excitatory actions of DNQX/CNQX in relay neurons. This selective action may not only reveal a differential TARP distribution among thalamic neurons but also may provide insight into distinct characteristics of AMPA receptors of thalamic neurons that could be exploited by future pharmacological development. Furthermore, these data suggest that quinoxaline derivatives could modulate synaptic transmission and alter neuronal excitability.
DNQX-induced toxicity in cultured rat hippocampal neurons: an apparent AMPA receptor-independent effect?
Neurochem Int 2003 Feb;42(3):251-60.PMID:12427479DOI:10.1016/s0197-0186(02)00089-x.
To evaluate the involvement of AMPA receptor activation in neuronal cell death and survival, rat hippocampal neurons in culture were treated with AMPA receptor antagonists. A 46 h treatment with 6,7-dinitroquinoxaline-2,3-dione (DNQX), added 2 h after cell plating, induces a dose-dependent neurotoxicity. Similar effects are also observed in more mature hippocampal neurons (treatment at 14 days in vitro). DNQX toxic effect is neuron-specific since cultured hippocampal glial cells are unaffected. Attempts to characterise the site of action of DNQX suggest that ionotropic glutamate receptors would not be implicated. Indeed, (i) other AMPA receptor antagonists are either ineffective or only moderately efficient in mimicking DNQX effects; (ii) AMPA alone or in the presence of cyclothiazide, as well as, other AMPA receptor agonists, do not reverse DNQX action; (iii) DNQX neurotoxicity is not likely to involve blockade of NMDA receptor glycine site, since this effect is neither mimicked by 7-chlorokynurenate nor reversed by D-serine. Thus, DNQX toxicity in cultured hippocampal neurons is apparently mediated through an ionotropic glutamate receptor-independent way.
Redox properties and prooxidant cytotoxicity of a neuroleptic agent 6,7-dinitrodihydroquinoxaline-2,3-dione (DNQX)
Acta Biochim Pol 2013;60(2):227-31.PMID:23757451doi
In order to characterize the possible mechanism(s) of cytotoxicity of a neuroleptic agent 6,7-dinitrodihydroquinoxaline-2,3-dione (DNQX) we examined the redox properties of DNQX, and its mononitro- (NQX) and denitro- (QX) derivatives. The irreversible electrochemical reduction of the nitro groups of DNQX was characterized by the reduction peak potentials (Ep,7) of -0.43 V and -0.72 V vs. Ag/AgCl at pH 7.0, whereas NQX was reduced at Ep,7 = -0.67 V. The reactivities of DNQX and NQX towards the single-electron transferring enzymes NADPH:cytochrome P-450 reductase and NADPH:adrenodoxin reductase/adrenodoxin complex were similar to those of model nitrobenzenes with the single-electron reduction potential (E¹₇) values of -0.29 V - -0.42 V. DNQX and NQX also acted as substrates for two-electron transferring mammalian NAD(P)H:quinone oxidoreductase (DT-diaphorase). The cytotoxicity of DNQX in bovine leukemia virus-transformed lamb kidney fibroblasts (line FLK) was prevented by antioxidants and an inhibitor of NQO1, dicoumarol, and was enhanced by the prooxidant alkylating agent 1,3-bis(2-chloromethyl)-1-nitrosourea. A comparison with model nitrobenzene compounds shows that the cytotoxicity of DNQX and NQX reasonably agrees with the ease of their electrochemical reduction, and/or their reactivities towards the used enzymatic single-electron reducing systems. Thus, our data imply that the cytotoxicity of DNQX in FLK cells is exerted mainly through oxidative stress.
Effects of the AMPA/kainate receptor antagonist DNQX in the nucleus accumbens on drug-induced conditioned place preference
Brain Res 1993 Jul 23;617(2):267-73.PMID:8402155DOI:10.1016/0006-8993(93)91094-9.
Activation of AMPA/kainate glutamatergic receptors in the nucleus accumbens may be a component of the mechanism of drug induced reward. To test this hypothesis, 6,7-dinitroquinoxaline-2,3-dione (DNQX), an alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA)/kainate glutamatergic receptor anatagonist, was injected into the nucleus accumbens before the administration of amphetamine or morphine during the training phase (acquisition) of a conditioned place preference paradigm. Rats were then tested for place preference in the absence of drugs. In other experiments, DNQX was given before testing for place preference (expression) but not during the training phase. Bilateral injection of DNQX (1 microgram/0.5 microliters/side) inhibited acquisition of place preference to amphetamine (1 mg/kg) but not morphine (10 mg/kg). During acquisition, DNQX marginally attenuated the locomotor stimulation elicited by amphetamine during the first but not subsequent training sessions, while the combination of morphine plus DNQX produced marked akinesia during each training session. When given prior to testing, DNQX inhibited the expression of place preference induced by amphetamine and morphine but did not affect locomotor activity. The results suggest that activation of AMPA/kainate receptors is involved in the primary reward stimulation (acquisition of place preference) of amphetamine but not morphine and in behaviors elicited by memory of primary reward stimulation (expression of place preference) for both drugs. Furthermore, locomotor activity during conditioning is not necessary for acquisition of place preference.
A slight anticonvulsant effect of CNQX and DNQX as measured by homocysteine- and quisqualate-induced seizures
Pharmacol Biochem Behav 1990 May;36(1):177-81.PMID:1971950DOI:10.1016/0091-3057(90)90145-8.
CNQX and DNQX are compounds that have recently been reported to show potent non-NMDA excitatory amino acid receptor antagonist activity. Effects of these compounds on seizures induced by homocysteine thiolactone and quisqualic acid were studied in order to examine the pharmacological properties of these compounds. In a dosage of 1.16 micrograms intracerebroventricularly (ICV), CNQX prolonged the latency to the onset of quisqualate-, but not homocysteine-induced seizures. DNQX was not effective when given either ICV or systemically, although a 3.78 micrograms dose of DNQX given ICV markedly increased the variability in latency to seizure onset, suggesting a combination of pro- and anticonvulsant effects. Higher dosages of both CNQX and DNQX induced seizure-like activity after ICV injection. These data confirm that CNQX has pharmacological effects corresponding to its effects on cellular responses to quisqualate and kainate agonists, but these effects are weak and may limit its usefulness as a pharmacological tool.