ライフサイエンスコーパス: CNQX

1 CNQX did not affect non-rectifying electrical synapses i

2 CNQX dose-dependently reduced motivation for cocaine in

3 CNQX induced small depolarizing currents in neurons of t

4 CNQX, an AMPA/kainate antagonist (10 nM-10 microM), sign

5 CNQX, APV, bicuculline, CGP35348 (GABAB receptor antagon

6 CNQX, given from E8 to E15 or only from E8 to E10, also

7 CNQX-mediated inhibition was also blocked by pep2-SVKI (

8 tic application of AP-5 (n = 12, P < 0.001), CNQX (n = 13, P < 0.001) or NBQX (n = 11, P < 0.001).

9 there were no significant differences in [3H]CNQX binding between any of the experimental groups and

10 gonist assessed from the displacement of [3H]CNQX.

11 P-5 alone, CNQX alone, or a cocktail of AP-5+CNQX, indicating that joint activation of NMDA plus non-

12 In the presence of GYKI 52466, CNQX, (RS)-CPP and MK-801, residual corticothalamic resp

13 lls responded to glutamate or kainate with a CNQX-sensitive conductance increase.

14 change during contractions before and after CNQX.

15 ses were attenuated similarly by AP-5 alone, CNQX alone, or a cocktail of AP-5+CNQX, indicating that

16 ligand-binding domain showed that, although CNQX induces partial domain closure, this movement is no

17 of NMDA (7-chloro-kynurenic acid) and AMPA (CNQX) receptor blockers, GVS-induced afferent spike acti

18 t gamma-2 is associated with surface AMPARs, CNQX, a partial agonist at AMPARs associated with Type I

19 Co-application of AP-5 and CNQX completely eliminated the Off responses in majority

20 In contrast, application of AP-5 and CNQX often markedly increased baseline sIPSC activity wi

21 MDA and AMPA receptor antagonists MK-801 and CNQX, respectively.

22 iperazine-4-yl)-propyl-1-phosphonic acid and CNQX or by uncaging IP3.

23 Simultaneous microinfusion of both AP5 and CNQX considerably increased the proportion of LC neurons

24 y the glutamate receptor antagonists AP5 and CNQX, underlining the functional importance of glutamate

25 fect alone, but the combination of D-AP7 and CNQX completely abolished the STR.

26 ynaptic transmission is strong, both APV and CNQX decrease dendritic arbor branch length, consistent

27 g both ionotropic receptor subtypes (APV and CNQX).

28 ed by 4-aminophosphonovaleric acid (APV) and CNQX whereas the outward current only was blocked by bic

29 Although TTX, APV, and CNQX treatment had no effect, blockade of GABA(A)Rs with

30 ining: glutamate, NMDA, or KA; glutamate and CNQX, MK-801, or AP-7; ACh, nicotine or muscarine; ACh a

31 Importantly, both MK801 and CNQX blocked Tat-induced death of immature OLs, but only

32 Here we report that NBQX and CNQX elicit feeding in a dose dependent manner and are m

33 and glutamate receptor blockers ([Mg2+]o and CNQX or DNQX plus D-AP-5) and to the inhibition of gluta

34 d the effect was blocked by tetrodotoxin and CNQX.

35 Inclusion of the kainate/AMPA antagonist CNQX (100 microM) or melatonin (100 microM) to the mediu

36 croM) but not by the kainate/AMPA antagonist CNQX (100 microM).

37 ause coadministration of the AMPA antagonist CNQX blocked the rewarding effects of AMPA, and administ

38 A(A) agonist muscimol or the AMPA antagonist CNQX lowered call frequencies emitted at rest and during

39 platelets treated with the AMPAR antagonist CNQX or platelets derived from GluR1 knockout mice are r

40 is blocked both by their general antagonist CNQX and also by the relatively specific AMPA receptor a

41 mpletely blocked by the glutamate antagonist CNQX.

42 The AMPA/KA antagonist CNQX completely blocked glutamine-stimulated AGB labelin

43 , but not by the AMPA and kainate antagonist CNQX.

44 reports, infusion of the non-NMDA antagonist CNQX into the NAC core subregion did not alter PPI, but

45 azole propionate/kainate receptor antagonist CNQX (0, .01, .03, .1 mug/side) were determined.

46 tion of the AMPA/kainate receptor antagonist CNQX (0, 0.03, or 0.3 mug) into either the core or the s

47 e AMPA/kainate glutamate receptor antagonist CNQX (10-20 microM) regularly abolished DR-EPSCs.

48 arbor, whereas the AMPA receptor antagonist CNQX (20 microM) or the sodium channel blocker TTX (1 mi

49 tion of the AMPA/kainate receptor antagonist CNQX attenuated the ability of NAc core GLP-1R activatio

50 nist APV or the non-NMDA receptor antagonist CNQX blocked the prolonged bursts.

51 pal infusion of the AMPA receptor antagonist CNQX impaired retrieval (experiment 3).

52 p), the competitive AMPA receptor antagonist CNQX inhibited transmission at the rectifying electrical

53 stration of AMPA/kainate receptor antagonist CNQX into the fourth ventricle (n=6).

54 ministration of the AMPA receptor antagonist CNQX into the nucleus accumbens.

55 Infusion of the AMPA-receptor antagonist CNQX or dopamine D1-receptor antagonist SCH-23390 into t

56 tion of the AMPA/kainate receptor antagonist CNQX significantly reduced the iCGRP release evoked by e

57 t not of an AMPA/kainate receptor antagonist CNQX, completely inhibited DOM-mediated cGMP production

58 The AMPA/kainate receptor antagonist CNQX, when administered at doses of 200-300 microg/d fro

59 not reduced by the AMPA receptor antagonist CNQX.

60 s blocked by the AMPA/KA receptor antagonist CNQX.

61 agonized by the non-NMDA receptor antagonist CNQX.

62 also by the AMPA/kainate receptor antagonist CNQX.

63 annels or by the AMPA/KA receptor antagonist CNQX.

64 MDA ionotropic glutamate receptor antagonist CNQX; the residual component was suppressed by the NMDA

65 responses, and the AMPA-selective antagonist CNQX attenuated 52%.

66 e, inhibition by the glycine-site antagonist CNQX, and insensitivity to the glutamate-site antagonist

67 cral segments were blocked by the antagonist CNQX.

68 nd structural properties with an antagonist (CNQX), a partial agonist (kainate), and two full agonist

69 ntagonist (APV) or AMPA receptor antagonist (CNQX).

70 with the non-selective AMPA/KAR antagonist, CNQX, suppresses ATPA-elicited feeding, and (3) LH injec

71 petitive and noncompetitive AMPA antagonists CNQX and GYKI 52466, respectively, blocked ED when given

72 ptor antagonists but not by AMPA antagonists CNQX and NBQX.

73 a full agonist, and competitive antagonists CNQX and DNQX acted as a partial agonists.

74 The non-NMDA receptor antagonists CNQX (400 nmol) or DNQX (60 nmol) affected neither the a

75 esence of the glutamate receptor antagonists CNQX (6-cyano-7-nitroquinoxaline-2,3-dione) and AP5 (2-a

76 by ionotropic glutamate receptor antagonists CNQX and D-AP5.

77 The non-NMDA receptor antagonists CNQX and GYKI 52466 reversibly blocked responses to glut

78 he ionotropic glutamate receptor antagonists CNQX or DNQX enhanced the on-centre responses of AII cel

79 In contrast to the antagonists CNQX and DNQX, UBP277 and UBP282 produce complexes with

80 re blocked by non-NMDA receptor antagonists (CNQX or NBQX) and the NMDA receptor antagonist, AP-5.

81 AMPA receptor antagonists (CNQX) blocked targeting of Arc mRNA in a small region, a

82 t study used glutamate receptor antagonists (CNQX/APV) or low calcium to block synaptic transmission,

83 ection of the non-NMDA receptor antagonists, CNQX and NBQX decreased KA-induced MMP-9 activity and pr

84 tected in the presence of tetrodotoxin, AP5, CNQX and bicuculline, supporting an indirect effect.

85 ls in young cultures were insensitive to AP5-CNQX, but were eliminated by bicuculline, indicating tha

86 ceptor antagonists: 100 microM/10 microM AP5/CNQX (1X cultures) and 200 microM/20 microM AP5/CNQX (2X

87 X (1X cultures) and 200 microM/20 microM AP5/CNQX (2X cultures).

88 y suppressed by higher concentrations of AP5/CNQX.

89 APV, CNQX, and bicuculline were included to block fast synapt

90 The bath solution contained APV, CNQX and bicuculline to block ionotropic glutamate and G

91 ome classically defined antagonists, such as CNQX.

92 ar Na+, or the AMPA/kainate receptor blocker CNQX reduced the fluorescence increase by 50%.

93 s, were blocked by the AMPA receptor blocker CNQX, and displayed multiple forms of short-term plastic

94 to D-APV but almost completely abolished by CNQX.

95 slices, the effect of KA was antagonized by CNQX, and persisted after pretreatment with a cocktail o

96 activation in LC neurons was also blocked by CNQX and CBX.

97 ase in synaptic activity that was blocked by CNQX but not by bicuculline.

98 es extracellular Ca2+, and can be blocked by CNQX treatment but not by NMDA, implicating axonal AMPA/

99 ring protocol were almost totally blocked by CNQX.

100 These bursts of IPSCs were eliminated by CNQX and may therefore reflect correlated feedback inhib

101 (HCs) and off-bipolar cells) are mediated by CNQX-sensitive AMPA/KA glutamate receptors.

102 nti-BDNF or TrkB-IgG-blocking reagents or by CNQX, a non-NMDA glutamate receptor antagonist.

103 desensitizing and inhibited significantly by CNQX and hence pertain to activation of the AMPA recepto

104 +]i changes that were virtually unaltered by CNQX.

105 affinity for isolated LBDs without changing CNQX affinity.

106 In contrast, CNQX increased the [H+]i change and decreased the [Na+]i

107 In contrast, CNQX or GYKI 52466 injected into the LH at the onset of

108 nd [3H]-6-cyano-7-nitroquinoxaline-2,3-dion (CNQX) binding were determined following preincubation of

109 agonist 6-cyano-7-nitroquinoxaline-2,3-dion (CNQX) markedly decreased NMDA-induced responses and conv

110 gonist, 6-cyano-7-nitroquinoxaline-2,3-dione CNQX.

111 X) and 6-cyano-7-nitroquinoxaline-2,3 dione (CNQX) induce drinking in rats.

112 nist (6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX) 10 microM, n = 8).

113 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) acted on RGCs to reduce On responses of ganglion c

114 ion of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and (2R)-amino-5-phosphonovaleric acid (AP-5) on t

115 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and 50 microM 2-amino-5-phosphonovaleric acid (APV

116 onists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D(-)-2-amino-5-phosphonopentanoic acid (AP5).

117 onists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and DL-2-amino-5-phosphonopentanoic acid (AP-5; 30

118 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the AMPA receptor antagonist GYKI 53655.

119 gonist 6-cyano-7-nitroquinoxiline-2,3-dione (CNQX) and the Ca(2+)-permeable AMPA receptor channel blo

120 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the gap-junction blockers, carbenoxolone (CBX)

121 ked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and were identified as EPSCs mediated by glutamate

122 uch as 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) are the most commonly used alpha-amino-3-hydroxy-5

123 locker 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) at a concentration of 10 microM did not.

124 QX) or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) at rest.

125 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) blocked KA-evoked changes in [H+]i and [Na+]i, ind

126 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) blocked learned and normal responses equally.

127 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) decreased respiratory rate in a dose dependent man

128 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) eliminated the effects of glutamate and kainate.

129 alt of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) reversibly to block cerebellar cortical AMPA-kaina

130 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) to block ionotropic glutamate-induced currents and

131 X) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) were not altered in any of the tagged receptors.

132 icroM 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX)) to the washout solution did not affect the post-g

133 52466, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), (RS)-CPP and (5R, 10S)-(+)-5-methyl-10,11-dihydro

134 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a partial agonist at TARP-associated AMPARs, enha

135 ked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an AMPA receptor antagonist.

136 nce of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an AMPA receptor antagonist.

137 onist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and a slow EPSP was sensitive to the NMDA recepto

138 ) and 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX), respectively.

139 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), whereas this drug had no effect on FGM.

140 fast, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)-sensitive, monosynaptic EPSP followed by long-dura

141 locker 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX).

142 onist 6-cyano-7-nitroquionoxaline-2,3-dione (CNQX).

143 ked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX).

144 V) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX).

145 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) abolished field population spiking and

146 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 200 microm) to block light-evoked activity of inne

147 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 25 or 50 microM) also significantly reduced evoked

148 roM), 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX, 30 microM) and tetrodotoxin (TTX, 1 microM).

149 onist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 4 nmol) or the selective AMPAR antagonist, GYKI 52

150 ked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 5 microM).

151 tering 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, an AMPA-receptor antagonist) into the rostral (RVL

152 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 0.01 mM).

153 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 1 microM) reduced both the evoked current and the

154 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) and by the NMDA receptor antagonist 2-a

155 onists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) and D,L-2-amino-5-phosphonovalerate (AP

156 agonist 6-cyano-7-nitroqinoxaline-2,3-dione (CNQX; 10 microM) in Ringer solution containing physiolog

157 ion of 6-cyano-7-nitroquinoxaline-2-3-dione (CNQX; 10 microM), suggesting the activity was all mediat

158 tors, 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX; 10 microM).

159 gonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 20-50 microM) had no effect.

160 ist beta-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 5 microM) eliminated the evoked EPSP.

161 onists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; n = 8, P < 0.05) or 1,2,3,4-tetrahydro-6-nitro-2,

162 6-cyano-7-nitroquinoxaline-2,3(1H,4H)-dione (CNQX, 0.2 mM) or cis-2,3-piperidinedicarboxylic acid (PD

163 odiazocine-10-carboxylic acid methyl ester], CNQX, APV, and TTX, and was inhibited in the presence of

164 In a second experiment, CNQX disrupted the stability of rat hippocampal place ce

165 Following CNQX perfusion into the CVLM, the levels of extracellula

166 us trapping in various conditions, including CNQX, a competitive antagonist; kainate, a weak partial

167 KA, CNQX (6-cyano-7-nitroquinoxaline-2,3,-dione), NBQX (2,3-

168 fected by DL-AP5, but it is blocked by Mg2+, CNQX and DNQX, suggesting a non-NMDA channel.

169 and non-NMDA receptor antagonists (20 microM CNQX and 100 microM APV), confirming that glutamate is t

170 icroM DL-APV), non-NMDA receptors (20 microM CNQX), or blocking both ionotropic receptor subtypes (AP

171 r antagonists (40-100 microM D-APV+20 microM CNQX, or 5 mM kynurenic acid) plus the GABA(A)-receptor

172 rotoxin (PiTX) but were blocked by 25 microM CNQX/50 microM APV.

173 ynurenic acid, 100 microm AP-5, or 50 microm CNQX) from a micropipette adjacent to the recording elec

174 by pretreatment with 30 muM AP-5 and 10 muM CNQX, indicating the involvement of both NMDA and non-NM

175 However, when applied during Idelay neither CNQX nor Na+-free solution had any effect on Idelay.

176 In many neurons CNQX also eliminated mEPSCs; however, in a number of cas

177 6-Cyano-2,3-dihydroxy-7-niroquiinoxaline (CNQX)-sensitive excitatory postsynaptic currents were re

178 of tetrodotoxin, 6-cyano-7-nitroquinoxaline (CNQX) and 2-amino-5-phosphonopentanoic acid (AP-5).

179 es also indicated that exposure to non-NMDA (CNQX) and NMDA (CPP, MK-801) glutamate receptor antagoni

180 on of NMDA [AP-5 (100 microM)] and non-NMDA [CNQX (10 microM)] receptor antagonists or by tetrodotoxi

181 en-5,10-imine maleate (MK-801)] or non-NMDA [CNQX or 4-(8-methyl-9H-1,3-dioxolo[4,5-h][2,3]benzodazep

182 n, neither picrotoxin (50 microM, n = 5) nor CNQX (10 microM, n = 5) had any effect on the frequency

183 Application of CNQX (10 microm) reduced peak power amplitude and integr

184 gic IPSCs were blocked by the application of CNQX, AP-5 and bicuculline.

185 lover from climbing fibers or application of CNQX, evoked GABA release was reduced; in stargazer mice

186 n of the Ca2+ increase by the combination of CNQX and lidocaine.

187 However, during ETX the concentration of CNQX or AP5 needed to block these EPSPs was elevated sig

188 Analysis of the effects of CNQX or NBQX on spontaneous embryonic motility at E10 sh

189 icit feeding, we tested whether injection of CNQX, another AMPA/KA receptor antagonist, also stimulat

190 Microdialysis of CNQX (1.0 microM) for 30 min into the RVLM attenuated th

191 Microdialysis of CNQX into the CVLM (n=8) potentiated the contraction-evo

192 e disinhibition persisted in the presence of CNQX and d-AP-5.

193 tion intensity was raised in the presence of CNQX/APV, a second alkalinization arose, presumably due

194 A crystal structure of CNQX bound to the TARP-less AMPA receptor ligand-binding

195 of either an excitatory amino acid (AP-5 or CNQX) and a nicotinic cholinergic (DHbetaE or mecamylami

196 MK-801 or CNQX also prevented death induced by either hypoxia or i

197 Infusion of either AMPH or CNQX into the NAC shell subregion reduced PPI independen

198 d responses (81%), compared to either AP5 or CNQX alone (approximately 50% each).

199 C could be evoked in the presence of DNQX or CNQX.

200 enzo [a,d] cyclohepten-5,10-imine maleate or CNQX.

201 Melatonin or CNQX protects against this effect by scavenging free rad

202 ropic glutamate receptor antagonists NBQX or CNQX.

203 6), an antagonist for the NMDA receptor, or CNQX (10 mM, 2 microliters, I.C.V.; n = 5), an antagonis

204 After P9, CNQX continued to block the prolonged bursts, but APV me

205 6-cyano-2,3-dihydroxy-7-nitro-quinoxaline (CNQX), and its analog CGP78608, bind to NR3A S1S2 with l

206 -7-nitroquinoxaline-2,3-dione disodium salt [CNQX]), and (b) changes in motor function expressed foll

207 The PPI-disruptive effects of intra-shell CNQX infusion were not blocked by haloperidol.

208 5,212-2 (100 nM) inhibited stereoselectively CNQX-sensitive excitatory postsynaptic currents (EPSCs)

209 which are AMPA receptor auxiliary subunits, CNQX acts as a partial agonist.

210 oteolysis protection experiments reveal that CNQX and CGP78608 bind to and stabilize domain 1 of NR3A

211 Additionally, the CNQX-sensitivity did not increase for either sEPSCs or o

212 Furthermore, the CNQX/d-AP-5-resistant response was blocked by l-AP-4, me

213 ) increases PKA and PKC activity only if the CNQX-sensitive field-EPSP (f-EPSP) is also potentiated.

214 60 min depending on the concentration of the CNQX infusion and its location within HVI.

215 nternal dynamics are minimal compared to the CNQX-bound form of the protein (which makes minimal cont

216 This CNQX-mediated inhibition of the electrical synapse was b

217 This was true even though CNQX eliminated driven postsynaptic potentials.

218 At -60 mV, EPSCs were wholly due to CNQX-sensitive, non-NMDA glutamate receptors; at depolar

219 a proportion of the mEPSCs were resistant to CNQX suggesting that in these instances different mediat

220 ing and non-homing pigeons were sensitive to CNQX indicating that glutamate may be a neurotransmitter

221 When added together, CNQX and lidocaine inhibited the fluorescence increase m

222 d by antagonists of excitatory transmission, CNQX (40 microM) or D-AP5 (50 microM).

223 trodotoxin, and both sEPSCs and emEPSCs were CNQX-sensitive.

224 tion, a form of synaptic plasticity, whereas CNQX impaired fast excitatory transmission, at perforant

225 ked using GYKI or Joro spider toxin, whereas CNQX was ineffective.

226 ty was prohibited by NAc AMPAR blockade with CNQX during cocaine reexposure and mimicked by intra-NAc

227 After pharmacological blockade with CNQX, TTX still reduced b-wave amplitudes in cone-isolat

228 f CGP78608 increases 1000-fold compared with CNQX.

229 Treatment either with CNQX or the more highly selective NBQX from E8 to E10, b

230 chaemia was prevented by pre-incubation with CNQX, MK-801 or tetrodotoxin.

231 uced current response at receptor level with CNQX or at ionic level with Na+-free solution eliminated

232 pression of glutamate neurotransmission with CNQX or kynurenate, or glycine neurotransmission with st

233 rk pharmacologically with CNQX alone or with CNQX, AP-5, strychnine, bicuculline, and carbenoxolone.

234 e respiratory network pharmacologically with CNQX alone or with CNQX, AP-5, strychnine, bicuculline,

235 c transmission in the rat postsubiculum with CNQX, or NMDA receptor-dependent plasticity with d-AP5.

236 g) that was blocked by LH pretreatment with CNQX, but was unaffected by pretreatment with the AMPAR