DNQX - CAS 2379-57-9
Category: Inhibitor
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Molecular Formula:
C8H4N4O6
Molecular Weight:
252.14
COA:
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Targets:
NMDA Receptor
Description:
DNQX is a selective non-NMDA receptor antagonist and could probably be useful in the treatment of Alzheimer's disease.
Purity:
≥98% by HPLC
Appearance:
Yellow Solid
Synonyms:
6,7-Dinitroquinoxaline-2,3-dione
MSDS:
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InChIKey:
RWVIMCIPOAXUDG-UHFFFAOYSA-N
InChI:
InChI=1S/C8H4N4O6/c13-7-8(14)10-4-2-6(12(17)18)5(11(15)16)1-3(4)9-7/h1-2H,(H,9,13)(H,10,14)
Canonical SMILES:
C1=C2C(=CC(=C1[N+](=O)[O-])[N+](=O)[O-])NC(=O)C(=O)N2
1.Mechanism for the acute effects of organophosphate pesticides on the adult 5-HT system.
Judge SJ;Savy CY;Campbell M;Dodds R;Gomes LK;Laws G;Watson A;Blain PG;Morris CM;Gartside SE Chem Biol Interact. 2016 Feb 5;245:82-9. doi: 10.1016/j.cbi.2015.12.014. Epub 2015 Dec 22.
The neurotransmitter serotonin (5-HT) is involved in mood disorder aetiology and it has been reported that (organophosphate) OP exposure affects 5-HT turnover. The aim of this study was to elucidate the mechanism underlying OP effects on the adult 5-HT system. First, acute in vivo administration of the OP diazinon (0, 1.3, 13 or 39 mg/kg i.p.) to male Hooded Lister rats inhibited the activity of the cholinergic enzyme acetylcholinesterase in blood and in the hippocampus, dorsal raphe nucleus (DRN), striatum and prefrontal cortex. Diazinon-induced cholinesterase inhibition was greatest in the DRN, the brain's major source of 5-HT neurones. Second, acute in vivo diazinon exposure (0 or 39 mg/kg i.p.) increased the basal firing rate of DRN neurones measured ex vivo in brain slices. The excitatory responses of DRN neurones to α1-adrenoceptor or AMPA/kainate receptor activation were not affected by in vivo diazinon exposure but the inhibitory response to 5-HT was attenuated, indicating 5-HT1A autoreceptor down-regulation. Finally, direct application of the diazinon metabolite diazinon oxon to naive rat brain slices increased the firing rate of DRN 5-HT neurones, as did chlorpyrifos-oxon, indicating the effect was not unique to diazinon.
2.AMPA/kainate receptor-mediated up-regulation of GABAA receptor delta subunit mRNA expression in cultured rat cerebellar granule cells is dependent on NMDA receptor activation.
Salonen V;Kallinen S;Lopez-Picon FR;Korpi ER;Holopainen IE;Uusi-Oukari M Brain Res. 2006 May 4;1087(1):33-40. Epub 2006 Apr 13.
We have studied the effects of AMPA/kainate receptor agonists on GABA(A) receptor subunit mRNA expression in vitro in cultured rat cerebellar granule cells (CGCs). Kainate (KA) (100 microM) and high K(+) (25 mM) dramatically up-regulated delta subunit mRNA expression to 500-700% of that in control cells grown in low K(+) (5 mM). KA or high K(+) had no effect on the expression of the other major GABA(A) receptor subunits alpha1, alpha6, beta2, beta3 or gamma2. Up-regulation of delta mRNA was also detected with the AMPA receptor-selective agonist CPW-399 and to a lesser extent with the KA receptor-selective agonist ATPA. AMPA/kainate receptor-selective antagonist DNQX completely inhibited KA-, CPW-399- and ATPA-induced delta mRNA up-regulation indicating that the effects were mediated via AMPA and KA receptor activation. NMDA receptor-selective antagonist MK-801 inhibited 76% of the KA- and 57% of the CPW-399-induced delta up-regulation suggesting that KA and CPW-399 treatments may induce glutamate release resulting in NMDA receptor activation, and subsequently to delta mRNA up-regulation. In CGCs, delta subunit is a component of extrasynaptic alpha6betadelta receptors that mediate tonic inhibition.
3.[Relation between GLu-R and the protective effect of hypothermia on oxygen and glucose deprivation injury in hippocampal slice or rat].
Liu SL;Wang ZP;Zeng YM;Jiang S;Wang SQ Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2005 May;21(2):127-32.
AIM: ;To investigate the relation between Glu-R and the protective effect of hypothermia on oxygen and glucose deprivation (OGD) injury in hippocampal slices of rat.;METHODS: ;(1) We had established OGD injury model in rat hippocampal slices. The changes of orthodromic population spike(OPS) during OGD and after administration of hypothermia (32 degrees C, 25 degrees C) were observed. (2) We had established Glu excitatory toxicity injury model in rat hippocampal slices. The changes of OPS after exposure to Glu and the effect of hypothermia (32 degrees C, 25 degrees C) against the Glu excitatory toxicity injury were observed. The non-NMDA receptor-mediated excitatory postsynaptic potentials (EPSP) in the CA1 area were recorded via adding the GABA-R specific agonists bicuculline (BMI) and NMDAR agonists D-(-)-2-Amino-5-phosphonopentanoic Acid (AP5) in normal artificial cerebrospinal fluid (nACSF), the NMDA receptor-mediated EPSP were recorded via adding the BMI and non-NMDA-R agonists 6,7-Dinitroquinoxaline-2, 3(1H,4H)-dione(CNQX) in nACSF. The variety of the changes of OPS during OGD14min in nACSF groups and added BMI compounded AP5 or BMI compounded CNQX ACSF groups were observed after administration of 25 degrees C hypothermia 28 min.
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CAS 2379-57-9 DNQX

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