ライフサイエンスコーパス: glutamate receptor antagonist

1 IgG-blocking reagents or by CNQX, a non-NMDA glutamate receptor antagonist.

2 ues, is a N-methyl-d-aspartate- (NMDA-) type glutamate receptor antagonist.

3 roke, which were selectively attenuated by a glutamate receptor antagonist.

4 ion of either a D1 dopamine receptor or NMDA glutamate receptor antagonist.

5 5-HT because it was abolished by ionotropic glutamate receptor antagonists.

6 These were abolished by glutamate receptor antagonists.

7 -only synapses was prevented by metabotropic glutamate receptor antagonists.

8 to single spines and blocked by metabotropic glutamate receptor antagonists.

9 inputs were blocked by selective ionotropic glutamate receptor antagonists.

10 ng activity that was abolished by ionotropic glutamate receptor antagonists.

11 pendent and could be specifically blocked by glutamate receptor antagonists.

12 n the ICX using iontophoretic application of glutamate receptor antagonists.

13 ly reduced by this combination of ionotropic glutamate receptor antagonists.

14 llular electrical stimuli in the presence of glutamate receptor antagonists.

15 ulum was stimulated, even in the presence of glutamate receptor antagonists.

16 aftereffect were blocked by coapplication of glutamate receptor antagonists.

17 ctor or insulin-like growth factor I but not glutamate receptor antagonists.

18 c transmission was blocked with bath-applied glutamate receptor antagonists.

19 I but not N-methyl-D-aspartate- or AMPA-type glutamate receptor antagonists.

20 PSPs persisted in the presence of ionotropic glutamate receptor antagonists.

21 s and avoids important off-target effects of glutamate receptor antagonists.

22 s, first detected at E16, were eliminated by glutamate receptor antagonists.

23 of gambierol on tau hyperphosphorylation by glutamate receptor antagonists.

24 benzodiazepine class of noncompetitive AMPA glutamate receptor antagonists.

25 ocretin neurons were abolished by ionotropic glutamate receptor antagonists.

26 d by chronic "chemical deafferentation" with glutamate receptor antagonists.

27 t was insensitive to GABA(B) or metabotropic glutamate receptor antagonists.

28 l seconds and were inhibited by metabotropic glutamate receptor antagonists.

29 cal administration of NMDA and non-NMDA-type glutamate receptor antagonists.

30 This can be blocked by ionotropic glutamate receptor antagonists.

31 that is resistant to high concentrations of glutamate receptor antagonists.

32 s were blocked in the presence of ionotropic glutamate receptor antagonists.

33 Addition of glutamate receptor antagonists (15 microM MK-801 plus 75

34 ctivity study of the broad-acting ionotropic glutamate receptor antagonist 1a.

35 lex EPSCs was markedly reduced by ionotropic glutamate receptor antagonists (2-amino-5-phosphonopenta

36 n of the presynaptic (group II) metabotropic glutamate receptor antagonist 2S-alpha-ethylglutamic aci

37 in the presence of the group II metabotropic glutamate receptor antagonist (2S,1'S, 2'S)-2-methyl-2-(

38 The non-N-methyl-D-aspartate glutamate receptor antagonist 6,7-dinitroquinoxaline-2,3

39 with a glutamate receptor antibody, and the glutamate receptor antagonist 6-cyano-7-nitroquinoxaline

40 and kainate were abolished by the ionotropic glutamate receptor antagonist 6-cyano-7-nitroquinoxaline

41 V), but were eliminated by both the non-NMDA glutamate receptor antagonist 6-cyano-7-nitroquinoxaline

42 ration, or in combination with an ionotropic glutamate receptor antagonist 6-cyano-7-nitroquinoxaline

43 icantly affected by local application of the glutamate receptor antagonists 6-cyano-7-nitroquinoxalin

44 could be blocked by the selective ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxalin

45 re abolished by coinfusion of the ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxalin

46 agonist picrotoxin (50 microM, n = 9) or the glutamate receptor antagonist (6-cyano-7-nitroquinoxalin

47 ons in that bead formation is not blocked by glutamate receptor antagonists, a voltage-gated Na(+) ch

48 used iontophoresis to eject small amounts of glutamate receptor antagonists, aiming to perturb, but n

49 otoxin-MVIIC, and the selective metabotropic glutamate receptor antagonist alpha-methyl-4-carboxyphen

50 slow EPSP was unaffected by the metabotropic glutamate receptor antagonist (+)-alpha-methyl-4-carboxy

51 orticolimbic dopamine system by topiramate-a glutamate receptor antagonist and gamma-aminobutyric aci

52 h concentrations of MK-801 (10-20 microM), a glutamate receptor antagonist and voltage-gated calcium

53 nionic liposomes was comparable with that by glutamate receptor antagonists and a chemical inhibitor

54 were performed in the presence of ionotropic glutamate receptor antagonists and gamma-aminobutyric ac

55 ese hypotheses were tested by microinjecting glutamate receptor antagonists and morphine into the ven

56 pting to interrupt the loop by administering glutamate receptor antagonists and Na(+)-channel blocker

57 red in the presence of AMPA and metabotropic glutamate receptor antagonists and NOS inhibitors.

58 ated by bicuculline methiodide (BMI) but not glutamate receptor antagonists and reverse at the Cl- eq

59 the presence of 4-aminopyridine, ionotropic glutamate receptor antagonists and the GABAA receptor an

60 inence-induced withdrawal, the same doses of glutamate receptor antagonists and the kappa agonist adm

61 In rats, both glutamate receptor antagonists and the kappa agonist mic

62 ffects of both pre- and post-treatment using glutamate receptor antagonists and the sodium channel bl

63 predicted, combined microperfusion of D-AP5 (glutamate receptor antagonist) and muscimol (GABAA recep

64 nl, 10 mM), kynurenic acid (10 nl, 50 mM, a glutamate receptor antagonist), and red dye into the ITR

65 re to non-NMDA (CNQX) and NMDA (CPP, MK-801) glutamate receptor antagonists, and a metabotropic recep

66 These persisted in TTX, ionotropic glutamate receptor antagonists, and low extracellular ca

67 lly calcium-free medium with high magnesium, glutamate receptor antagonists, and sodium and calcium c

68 the presence of kynurenate, a broad spectrum glutamate-receptor antagonist, and elevated amounts of m

69 esidual component was suppressed by the NMDA glutamate receptor antagonist AP-5.

70 Third, infusion of the glutamate receptor antagonists AP-5 and CNQX into the LS

71 inhibitory, were virtually eliminated by the glutamate receptor antagonists AP5 and CNQX, underlining

72 tic standpoint because numerous metabotropic glutamate receptor antagonists are available, many of wh

73 N-Methyl-D-aspartate (NMDA) glutamate receptor antagonists are being developed as th

74 Ionotropic glutamate receptor antagonists are valuable tool compoun

75 Moreover, glutamate receptor antagonists attenuated the increase i

76 s abolished the neurotoxic activity, and (4) glutamate receptor antagonists blocked the neurotoxicity

77 r of calcineurin activity, or MK801, an NMDA glutamate receptor antagonist, blocked BAD dephosphoryla

78 ists in the presence of group I metabotropic glutamate receptor antagonists but is entirely absent fr

79 antly, synchrony was resistant to ionotropic glutamate receptors antagonists but was strongly reduced

80 hyl-4-isoxazolepropionic acid (AMPA)/kainate glutamate receptor antagonists, but not by selective AMP

81 Since ionotropic glutamate receptor antagonists can partially or fully re

82 onobutyric acid (APB), and/or the ionotropic glutamate receptor antagonist cis-2,3 piperidinedicarbox

83 The low-affinity glutamate receptor antagonist cis-2,3-piperidine dicarbo

84 The AMPA/kainate glutamate receptor antagonist CNQX (10-20 microM) regula

85 L were attenuated by the non-NMDA ionotropic glutamate receptor antagonist CNQX; the residual compone

86 the cerebral peduncle in the presence of the glutamate receptor antagonists CNQX (6-cyano-7-nitroquin

87 spontaneous EPSCs were blocked by ionotropic glutamate receptor antagonists CNQX and D-AP5.

88 Application of the ionotropic glutamate receptor antagonists CNQX or DNQX enhanced the

89 The present study used glutamate receptor antagonists (CNQX/APV) or low calcium

90 non-competitive N-methyl-D-aspartate (NMDA) glutamate receptor antagonist, could achieve rapid anti-

91 The glutamate receptor antagonists, D,L-2-amino-5-phosphonov

92 GABA or glutamate receptor antagonists did not block the ethanol

93 direct and indirect DA agonists and with the glutamate receptor antagonist, dizocilpine (MK-801).

94 Pretreatment with the glutamate receptor antagonists (DL-2-amino-5-phosphonova

95 parametric analysis revealed that a group of glutamate receptor antagonists enhances branching and ne

96 vation, stimulation of granule cell axons in glutamate receptor antagonists evoked a greater [K+]o in

97 ers of the SC, in the presence of ionotropic glutamate receptor antagonists, evoked IPSCs that were b

98 Glutamate receptor antagonists fully blocked ChAT inhibi

99 f EPSCs, and application of the low-affinity glutamate receptor antagonist gamma-D-glutamylglycine sh

100 The low-affinity glutamate receptor antagonists gamma-d-glutamylglycine a

101 y-5-methyl-4-isoxazole propionic acid (AMPA) glutamate receptor antagonist GYKI 52466.

102 Glutamate receptor antagonists had no effect on the ACh-

103 Ionotropic glutamate receptor antagonists had no effect.

104 Ketamine, an N-methyl-d-aspartate glutamate receptor antagonist, has demonstrated a rapid-

105 ne, and/or the N-methyl-d-aspartate class of glutamate receptor antagonists have been shown to be eff

106 emia and stroke; however, clinical trials of glutamate receptor antagonists have demonstrated their l

107 ceive skin grafts and that mice treated with glutamate receptor antagonists have improved graft survi

108 Previous studies using glutamate receptor antagonists have revealed that the me

109 effects of ketamine, an N-methyl-D-aspartate glutamate receptor antagonist, have not been fully eluci

110 In the presence of TTX and glutamate receptor antagonists, hypocretin-1-mediated in

111 t received injections of mixed AMPA and NMDA glutamate receptor antagonists in LHb were unresponsive

112 nital reflexes in anesthetized rats and that glutamate receptor antagonists in the MPOA impair copula

113 tic doses, ketamine, an N-methyl-D-aspartate glutamate receptor antagonist, increases glutamate relea

114 hibited by bath application of an ionotropic glutamate receptor antagonist, indicating that the incre

115 cium transients were inhibited by ionotropic glutamate receptor antagonists, indicating that the resp

116 by administration of TTX (2 mum) or specific glutamate receptor antagonists, indicating that they res

117 N-methyl-D-aspartic acid/glutamate receptor antagonists induce psychotomimetic ef

118 ol were used to determine whether a range of glutamate receptor antagonists influenced expression of

119 Similar microinjection of glutamate receptor antagonists into the DMH also suppres

120 e normally induced by injection of GABAA and glutamate receptor antagonists into the IO, suggesting t

121 The lack of effect of microinjecting glutamate receptor antagonists into the vPAG indicates t

122 Injection of kynurenic acid (Kyn, ionotropic glutamate receptor antagonist) into RVLM or the retrotra

123 sion of kynurenate (1.0 mM), a non-selective glutamate receptor antagonist, into the basal forebrain

124 s to normalize behavioral changes induced by glutamate receptor antagonists is abolished in the absen

125 as antidepressants: the N-methyl-D-aspartate glutamate receptor antagonist ketamine and the delta opi

126 e effects of the N-methyl-D-aspartate (NMDA) glutamate receptor antagonist ketamine hydrochloride in

127 banesthetic dose of the N-methyl-D-aspartate glutamate receptor antagonist ketamine produced meaningf

128 The N-methyl-D-aspartate glutamate receptor antagonist ketamine, delivered via an

129 Here, we show that administration of an NMDA glutamate receptor antagonist, ketamine, disrupted the r

130 nteers administered the N-methyl-D-aspartate glutamate receptor antagonist, ketamine.

131 Inclusion of the ionotropic glutamate receptor antagonist kynurenate during preparat

132 H2 )5 [D-Tyr(2) ,Thr(4) ]OVT, the ionotropic glutamate receptor antagonist kynurenate or the GABAA an

133 the time of testing by microinfusion of the glutamate receptor antagonist kynurenate.

134 ndent (1 microM-1 mM) and was blocked by the glutamate receptor antagonist, kynurenate.

135 Bilateral microinjection of the ionotropic glutamate receptor antagonist kynurenic acid (1 nmol) an

136 c acid (D-APV) as well as the broad-spectrum glutamate receptor antagonist kynurenic acid but were re

137 Microinjection of the non-specific glutamate receptor antagonist kynurenic acid or the NMDA

138 ntranucleus accumbens (NAc) infusions of the glutamate receptor antagonist kynurenic acid.

139 the presence of both MCPG and the ionotropic glutamate receptor antagonist kynurenic acid.

140 sponse curve for antinociception whether the glutamate receptor antagonists kynurenic acid or MK-801

141 nase inhibitor; AIDA, a group I metabotropic glutamate receptor antagonist; L733,060, an NK1 tachykin

142 presence of the broad-spectrum metabotropic glutamate receptor antagonist LY341495 and the GABA(B) r

143 administration of the group II metabotropic glutamate receptor antagonist LY341495.

144 The clinical benefits of the glutamate receptor antagonists memantine and ketamine ha

145 r kynurenic acid (a non-selective ionotropic glutamate receptor antagonist) microinjected bilaterally

146 Treatment with the glutamate receptor antagonist MK-801 strongly reduced bi

147 The N-methyl-D-aspartate (NMDA) glutamate receptor antagonist MK-801, when applied local

148 cium, or administration of the specific NMDA glutamate receptor antagonist MK-801.

149 Glutamate receptor antagonists MK-801 (1 or 4 mg/kg) and

150 s not seen in the presence of the ionotropic glutamate receptor antagonists MK-801 and 6-cyano-7-nitr

151 ong with an N-methyl-d-aspartate (NMDA)-type glutamate receptor antagonist, MK-801, and a non-NMDA-ty

152 The glutamate receptor antagonist MK801 modulates bone resor

153 is blocked by the N-methyl-d-aspartate-type glutamate receptor antagonist, MK801.

154 n (0.3 mul/hemisphere) of saline or the AMPA glutamate receptor antagonist NBQX (2,3-dioxo-6-nitro-1,

155 lectrodes, which allowed picoejection of the glutamate receptor antagonists NBQX or AP5 to block eith

156 0 ms) and was blocked by non-NMDA ionotropic glutamate receptor antagonists NBQX or CNQX.

157 In the presence of glutamate receptor antagonists (NBQX, 5 microm and D-APV

158 ptor antagonist, MK-801, and a non-NMDA-type glutamate receptor antagonist, NBQX, resulted in a reduc

159 ehaving rats to study the effect of GABA and glutamate receptor antagonists on opioid-induced changes

160 We further studied the influence of glutamate receptor antagonists on the stimulated express

161 simultaneous iontophoretic application of a glutamate receptor antagonist, or a vasopressin V(1a) an

162 triatal injections of either MK 801, an NMDA glutamate receptor antagonist, or SCH 23390, a D1 dopami

163 The glutamate receptor antagonists prevented decreases in 5-

164 Hence, glutamate receptor antagonists preventing excitotoxicity

165 ptor modulators and N-methyl-D-aspartic acid glutamate receptor antagonists, produce apoptotic neurod

166 In contrast, infusion of glutamate receptor antagonists produced larger decreases

167 Application of P2 and glutamate receptor antagonists (pyridoxal-5'-phosphate-6

168 BAB antagonist baclofen and the metabotropic glutamate receptor antagonist (R,S)-a-cyclopropyl-4-phos

169 roMMP-2 release, whereas non-NMDA ionotropic glutamate receptor antagonists reduced IL-6 production b

170 Application of either AMPA or metabotropic glutamate receptor antagonists reduced the likelihood of

171 y nerve in media containing the metabotropic glutamate receptor antagonist (RS)-alpha-methyl-4-carbox

172 tate granule cells after FPI, and ionotropic glutamate receptor antagonists selectively decreased the

173 and morphological analyses after exposure to glutamate receptor antagonists show that a combination o

174 In contrast, nigral application of either glutamate receptor antagonist significantly attenuated t

175 d macrophages by N-methyl-D-aspartate (NMDA) glutamate receptor antagonists, similar to effects seen

176 ices, synaptic transmission was blocked with glutamate receptor antagonists, sodium and calcium chann

177 also were blocked by local infusion of NMDA glutamate receptor antagonists, suggesting a role for gl

178 n was reduced by ionotropic and metabotropic glutamate receptor antagonists, suggesting an indirect,

179 ntiation is blocked by putative postsynaptic glutamate receptor antagonists, suggesting that a retrog

180 as blocked by tetrodotoxin and by ionotropic glutamate receptor antagonists, suggesting that norepine

181 ost-occlusion administration of memantine, a glutamate receptor antagonist that reduces cognitive dec

182 Ketamine is a glutamate receptor antagonist that was developed over 50

183 gy defined coordinates for microinjection of glutamate receptor antagonists that nearly abolished cou

184 Glutamate receptor antagonists therefore represent, to o

185 cularly those involving N-methyl-D-aspartate glutamate receptor antagonists, to illustrate principles

186 after exposure to glutamate, with or without glutamate receptor antagonists, was measured by calcein-

187 n-EAAT current from the response recorded in glutamate receptor antagonists, we have obtained an esti

188 -dependent, and was selectively sensitive to glutamate receptor antagonists, we suggest that the diff

189 mediating sensorimotor orientation behavior, glutamate receptor antagonists were infused into the lef

190 tal size was prevented by TTX and ionotropic glutamate receptor antagonists, whereas the increase in

191 tified as a competitive AMPA-type ionotropic glutamate receptor antagonist, whilst (S)-3,4-DCPG is a