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 These were abolished by glutamate receptor antagonists.

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

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

8 inputs were blocked by selective ionotropic glutamate receptor antagonists.

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

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

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

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

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

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

15 aftereffect were blocked by coapplication of glutamate receptor antagonists.

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

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

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

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

20 of gambierol on tau hyperphosphorylation by glutamate receptor antagonists.

21 benzodiazepine class of noncompetitive AMPA glutamate receptor antagonists.

22 ocretin neurons were abolished by ionotropic glutamate receptor antagonists.

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

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

25 5-HT because it was abolished by ionotropic glutamate receptor antagonists.

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

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

28 This can be blocked by ionotropic glutamate receptor antagonists.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 Ionotropic glutamate receptor antagonists are valuable tool compoun

70 Moreover, glutamate receptor antagonists attenuated the increase i

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

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

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

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

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

76 Since ionotropic glutamate receptor antagonists can partially or fully re

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

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

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

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

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

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

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

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

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

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

87 GABA or glutamate receptor antagonists did not block the ethanol

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

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

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

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

92 Glutamate receptor antagonists fully blocked ChAT inhibi

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

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

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

96 Glutamate receptor antagonists had no effect on the ACh-

97 Ionotropic glutamate receptor antagonists had no effect.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 Inclusion of the ionotropic glutamate receptor antagonist kynurenate during preparat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

146 The glutamate receptor antagonist MK801 modulates bone resor

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

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

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

150 0 ms) and was blocked by non-NMDA ionotropic glutamate receptor antagonists NBQX or CNQX.

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

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

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

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

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

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

157 The glutamate receptor antagonists prevented decreases in 5-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 Glutamate receptor antagonists therefore represent, to o

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

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

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

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

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

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

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