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 the glutamate receptor antagonists AP-5 and CNQX into the LS prevented the V1aR antagonist-induced d

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

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

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

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

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

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

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

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

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

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

31 entation shift between the glycine-bound and CNQX-bound structures.

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

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

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

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

36 d the effect was blocked by tetrodotoxin and CNQX.

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

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

39 Injection of the AMPA antagonist CNQX blocked the rescue of the behavioral phenotype by R

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

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

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

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

44 mpletely blocked by the glutamate antagonist CNQX.

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

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

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

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

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

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

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

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

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

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

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

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

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

58 Consistently, AMPA receptor antagonist CNQX or calcineurin inhibitor FK506 abolished the S-SCAM

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

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

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

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

63 ministration of the AMPA receptor antagonist CNQX, while auditory nerve responses are completely abol

64 not reduced by the AMPA receptor antagonist CNQX.

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

66 agonized by the non-NMDA receptor antagonist CNQX.

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

68 also by the AMPA/kainate receptor antagonist CNQX.

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

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

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

72 cral segments were blocked by the antagonist CNQX.

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

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

75 s of GluN1-3A NMDARs bound to an antagonist, CNQX, and an agonist, glycine.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 y suppressed by higher concentrations of AP5/CNQX.

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

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

97 ome classically defined antagonists, such as CNQX.

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

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

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

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

102 bserved in DH neurons, which were blocked by CNQX and AP5.

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

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

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

106 ring protocol were almost totally blocked by CNQX.

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

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

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

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

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

112 affinity for isolated LBDs without changing CNQX affinity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 52466, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), (RS)-CPP and (5R, 10S)-(+)-5-methyl-10,11-dihydro

141 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a partial agonist at TARP-associated AMPARs, enha

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 6-cyano-7-nitroquinoxaline-2,3(1H,4H)-dione (CNQX, 0.2 mM) or cis-2,3-piperidinedicarboxylic acid (PD

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 6-Cyano-2,3-dihydroxy-7-niroquiinoxaline (CNQX)-sensitive excitatory postsynaptic currents were re

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

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

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

188 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

209 ropic glutamate receptor antagonists NBQX or CNQX.

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

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

212 6-cyano-2,3-dihydroxy-7-nitro-quinoxaline (CNQX), and its analog CGP78608, bind to NR3A S1S2 with l

213 onists of AMPA and NMDA glutamate receptors, CNQX and AP5, inhibited [Ca(2+)](i) transients in DH neu

214 -7-nitroquinoxaline-2,3-dione disodium salt [CNQX]), and (b) changes in motor function expressed foll

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

216 5,212-2 (100 nM) inhibited stereoselectively CNQX-sensitive excitatory postsynaptic currents (EPSCs)

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

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

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

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

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

222 60 min depending on the concentration of the CNQX infusion and its location within HVI.

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

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

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

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

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

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

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

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

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

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

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

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

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

236 f CGP78608 increases 1000-fold compared with CNQX.

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

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

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

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

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

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

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

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