Disease relevance of dnqx

• In addition, the effects of a new calcium antagonist, KB-2796, and a glutamate receptor antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX); were evaluated in this model 1 month after ischemia [1].
• This effect was antagonized by the non-NMDA antagonists 6-nitro-7-cyanoquinoxaline-2,3-dione (CNQX) and 6,7-dinitroquinoxaline-2,3-dione (DNQX), suggesting a non-NMDA receptor-mediated action, that may also be involved in excitotoxicity in some neurodegenerative disorders [2].

Psychiatry related information on dnqx

• The injection of 6,7-dinitroquinoxaline-2,3-dione (DNQX) into the SI/LPO inhibited the hypermotility responses to AMPA or kainic acid while having no significant inhibitory effect on N-methyl-D-aspartic acid stimulated locomotor activity [3].

High impact information on dnqx

• The non-NMDA responses were potently blocked by 6,7-dinitroquinoxaline-2,3 dione [4].
• The glutamate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) reduced average unitary EPSP amplitudes; in contrast to the above manipulations, it had no effect on mcv, but significantly altered qcv, which is consistent with its presumed postsynaptic mechanism of action [5].
• Population EPSPs (pEPSPs) mediated by NMDA receptor activation were isolated by application of a solution containing the kainate/quisqualate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione and either low (0.1 mM) Mg2+ or 100 microM bicuculline [6].
• At a high AnTx concentration (25 microM), alpha7 nAChR antagonists (methyllycaconitine, alpha-conotoxin-ImI) and glutamate receptor (GluR) antagonists [kynurenic acid, 6,7-dinitroquinoxaline-2,3-dione (DNQX)] partially inhibited [(3)H]NA release [7].
• Intraventricular (i.c.v.) AMPA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX, 5-10 microg) decreased the commissural evoked potential and the amplitude of the hippocampal EEG, including the theta rhythm [8].

Biological context of dnqx

• Whole cell patch-clamp techniques were used to record spontaneous and miniature inhibitory postsynaptic currents (sIPSCs and mIPSCs) in the presence of 6,7-dinitroquinoxaline-2,3-dione and dl-2-amino-5-phosphonopentanoic acid to block glutamatergic excitatory synaptic transmission [9].
• The elicited mPSCs with rapid kinetics were blocked by 6,7-dinitroquinoxaline-2,3-dione (DNQX), but not by bicuculline (excitatory mPSCs) [10].
• Furthermore, exposure at early stages to 6,7-dinitroquinoxaline-2,3-dione (DNQX), or GYKI 53655, (competitive and non-competitive AMPA receptor antagonists, respectively) strongly reduced cell survival [11].
• In contrast, KA induced complete cell death, which was antagonized by 6,7-dinitroquinoxaline-2,3-dione, quisqualate, (RS)-amino-3-hydroxy-5-methylisoxazole-4-propionic acid and glutamate [12].
• 6,7-dinitroquinoxaline-2,3-dione inhibited maximum KA responses with an IC50 of approximately 1 microM; EtOH (50, 100 mM) did not alter the IC50 for 6,7-dinitroquinoxaline-2,3-dione but did not produce further inhibition of KA-induced currents [13].

Anatomical context of dnqx

• 3. In further studies of the DRN and nucleus accumbens, kainate-induced increases in extracellular 5-HT were blocked by the EAA receptor antagonists, kynurenate and 6,7-dinitroquinoxaline-2,3-dione (DNQX) [14].
• The development of negative image responses is blocked by micropressure ejection of the glutamate antagonist 6,7-dinitroquinoxaline-2,3-dione into the neighborhood of the pyramidal cell apical dendrites [15].
• In the presence of 6,7-dinitroquinoxaline-2,3-dione (20 microM) and bicuculline methiodine (20 microM), NMDA receptor-mediated excitatory postsynaptic currents were isolated from pyramidal cells of the posterior cingulate cortex (PCC) [16].
• The distal release of each amino acid in the substantia nigra was sensitive to the administration of 6,7-dinitroquinoxaline-2,3-dione and tetrodotoxin to the neostriatum [17].
• The occurrence of the radial dendrite swelling was prevented when 6,7-dinitroquinoxaline-2,3-dione (500 microM) was perfused in the cochlea 10 min prior, then concomitantly with AMPA [18].

Associations of dnqx with other chemical compounds

• Perfusion with the NMDA-receptor antagonist 3-[(R)-2-carboxypiperazin-4-yl]-propyl-1-phosphonic acid (1 mM) or the AMPA/kainate-receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) (1 mM) attenuated the increases produced by PDC (4 mM) on [DA], [GABA], and [Tau], and decreases in [DOPAC] and [HVA] [19].
• The NMDA receptor antagonist D(-)-2-amino-7-phosphonoheptanoic acid and the non-NMDA antagonist 6,7-dinitroquinoxaline-2,3-dione brought about small, not statistically significant decreases of adenosine and inosine outflow [20].
• Activations elicited by suprachiasmatic nucleus stimulation, either in the presence or absence of bicuculline, were blocked by the non-N-methyl-D-aspartate and N-methyl-D-aspartate glutamate receptor antagonists 6,7-dinitroquinoxaline-2,3-dione and (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (10/10 cells) [21].
• The NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (AP-5), the non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) or normal saline were intrathecally administered 15 min before an intramuscular or intraplantar injection of turpentine oil [22].
• The short latency components (the P3(2) and N2(2)) are blocked by general excitatory receptor antagonists, including the non-NMDA-receptor blockers 6,7-dinitroquinoxaline-2,3-dione (DNQX) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), but are insensitive to NMDA-receptor antagonists [23].

Gene context of dnqx

• An alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate antagonist, 6,7-dinitroquinoxaline-2,3-dione (100 microM), blocked SRIF-induced DA and Tau release and reduced that of Asp, Glu, and GABA [24].
• Under these conditions, non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) had no effect on the level of tyrosine phosphorylation [25].
• In addition, bicuculline slightly increased the number of calretinin-positive neurons, while 6,7-dinitroquinoxaline-2,3-dione exerted no effect [26].
• Antagonism of monosynaptic excitations in the mouse olfactory cortex slice by 6,7-dinitroquinoxaline-2,3-dione [27].
• In the presence of the excitatory amino acid receptor antagonists 6,7-dinitroquinoxaline-2,3-dione (DNQX) and D,L-2-amino-5-phosphonovalerate (APV), stimulation in stratum radiatum evoked monosynaptic fast, GABAA and late, GABAB receptor-mediated IPSPs and fast and late positive field potentials recorded in s. radiatum [28].

Analytical, diagnostic and therapeutic context of dnqx

• Perfusion with the non-NMDA receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX, 1 mM) alone increased DA synthesis slightly, whereas DNQX + AP-5 (10 mM) increased DA synthesis to levels comparable with those observed with AP-5 alone [29].
• IPSCs were evoked by electrical stimulation of the white matter surrounding the DCN in the presence of non-N-methyl-D-aspartate (non-NMDA) glutamate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (20 microM) [30].
• 3. Microinjection of 6,7-dinitroquinoxaline-2,3-dione (DNQX) (10 nmol/0.2 microliter), an antagonist of the non-N-methyl-D-aspartate (non-NMDA) type of glutamate receptor, into the medial vestibular nucleus blocked the increase of hippocampal ACh release by electrical stimulation to the round window [31].
• The responses are inhibited by prior intrathecal injection of the specific excitatory amino acid subtype receptor antagonist, 2-amino-5-phosphonovaleric acid (AP-5) or 6,7-dinitroquinoxaline-2,3-dione (DNQX), respectively [32].
• We treated prepubertal rats with intraperitoneal injections of NAL, NMDA antagonist dextromethorphan (DMT) and non-NMDA antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX), alone and in combinations among them [33].

References