ライフサイエンスコーパス: ifenprodil

1 receptors, these events were not affected by ifenprodil.

2 NMDA receptor 2B (NR2B)-selective antagonist ifenprodil.

3 e pharmacology of these agents overlaps with ifenprodil.

4 istically related to the atypical antagonist ifenprodil.

5 permine stimulation or sensitivity to pH and ifenprodil.

6 emantine or an alternative NMDAR antagonist, ifenprodil.

7 0a displayed higher inhibitory activity than ifenprodil.

8 s sensitive to a GluN2B-selective antagonist ifenprodil.

9 ty to the GluN2B-containing NMDAR antagonist ifenprodil.

10 the high-affinity binding sites for zinc and ifenprodil.

11 agonist AP-5 and the NR2B subunit antagonist ifenprodil.

12 s abolished by NR2B-specific NMDA antagonist ifenprodil.

13 rent transients that were blocked by APV and ifenprodil.

14 eceptor in LA using the selective antagonist ifenprodil.

15 Ifenprodil (1) is a potent GluN2B-selective N-methyl-d-a

16 Many of these antagonists, for example ifenprodil (1), incorporate a 4-hydroxy substituent on t

17 tration of NMDA was increased to 200 microm, ifenprodil (10 microm) produced the expected reduction i

18 The NR2B subunit-selective NMDAR antagonist ifenprodil (10 microM) reduced whole-cell NMDA-evoked cu

19 The NR2B-specific NMDA receptor inhibitor ifenprodil (10muM) suppressed EFP in dysplastic slices.

20 (1R,2R)-Configured ifenprodil (1R,2R)-1c exhibited high selectivity for Glu

21 (1R,2R)-Ifenprodil ((1R,2R)-1c) showed the highest affinity towa

22 ng NMDA receptors such as Ro 25-6981 (1) and ifenprodil (2) results in neuroprotective effects.

23 NMDA receptor inhibitors Ro 25-6981 (1) and ifenprodil (2).

24 (30 mum) or GluN2B-containing receptors with ifenprodil (3 mum) prevents CREB shutoff effectively in

25 ting compounds with structural similarity to ifenprodil (5) and 6 (CP101,606) resulted in compound 7

26 for compounds with structural similarity to ifenprodil (5) and haloperidol (7) followed by in vitro

27 Ifenprodil, a GluN2B antagonist, caused modest suppressi

28 Since the discovery of ifenprodil, a range of GluN2B-selective compounds with s

29 Compared to MK-801, ifenprodil, a selective NR2B antagonist, was less effect

30 benzenesulfo namide (TCN-201) or GluN2B with ifenprodil abolished reinstated nicotine seeking.

31 fter Tat infusion and transient rescue after ifenprodil administration (10 mg/kg, i.p.).

32 In this study, we examined how ifenprodil affects the gating reaction of NMDA receptors

33 Ifenprodil also mitigated cue-induced reinstatement of c

34 Ifenprodil also occluded the ethanol effect, suggesting

35 In vitro studies have shown that ifenprodil, an antagonist selective for GluN2B-containin

36 A combination of zinc plus ifenprodil, an inhibitor of NR1/NR2B receptors, produced

37 blocks astrocytic Ca2+ signals in vivo, and ifenprodil, an NMDA receptor antagonist that reduces the

38 ted by a combination of the NMDA antagonists ifenprodil and 5, 7-dichlorokynurenic acid.

39 ubunit mRNAs) and posttranscriptional ([(3)H]ifenprodil and [(3)H]MDL105,519 binding to polyamine and

40 utations also markedly reduced inhibition by ifenprodil and by protons at NR1A/NR2B receptors.

41 ve N-methyl-D-aspartate receptor antagonists ifenprodil and CP-101,606 blocked cocaine-induced habits

42 mine, NMDA NR2B receptor subunit antagonists ifenprodil and CP-101,606, and the glycine(B) partial ag

43 The phenylethanolamines, ifenprodil and CP-101,606, are NMDA receptor antagonists

44 that of the approved GluN2B NMDAR antagonist ifenprodil and excellent safety profiles.

45 (phenylalkyl)amines, structural analogues of ifenprodil and nylidrin, were synthesized and tested for

46 These studies provide evidence that ifenprodil and polyamines interact at discrete sites on

47 801) and by the antagonists of NR2B receptor ifenprodil and R-(R, S)-alpha-(4-hydroxyphenyl)-beta-met

48 Ifenprodil and related phenylethanolamine compounds, whi

49 s prevented by the selective NR2B inhibitors ifenprodil and Ro 25-6981.

50 The sigma ligands, haloperidol, ifenprodil and verapamil inhibited the production of erg

51 rm part of a binding site for polyamines and ifenprodil and/or part of the proton sensor of the NMDA

52 High-affinity NR2B ligands, Ro-25-6981, ifenprodil, and CO101244, showed increasing preblocking

53 s, burst repetition rate did not change with ifenprodil application.

54 NMDA-EPSCs was not significantly changed in ifenprodil at any age tested.

55 found distinct differences in the action of ifenprodil at GluN1/GluN2B in comparison with previous s

56 Systemic injections of ifenprodil before training led to a dose-dependent impai

57 also show a similar interaction between the ifenprodil binding site and the glutamate binding site o

58 led the same molecular interactions with the ifenprodil binding site as the analogous phenols.

59 Docking of the 3-benzazepin-1-ols into the ifenprodil binding site of the crystallized GluN1b/GluN2

60 inetic measurements suggest variation in the ifenprodil binding site of triheteromers compared to Glu

61 Recent structural studies revealed that ifenprodil binds to a unique site at the interface betwe

62 isostere) and beta-aminoalcohol (1R,2R)-11c (ifenprodil bioisostere) exhibited high GluN2B affinity (

63 th lower ifenprodil sensitivity; the reduced ifenprodil block of EPSCs was attributable to synaptic r

64 when relatively few synapses had formed, the ifenprodil block of EPSCs was less than whole-cell curre

65 We used the macroscopic kinetics of ifenprodil block to distinguish between the receptor pop

66 Inhibiting the activity of NR2B subunit with ifenprodil blocked NMDA receptor-induced cGMP synthesis

67 Conversely, NR2B antagonist (ifenprodil) blocked any morphological effect induced by

68 subunit-selective NMDA receptor antagonist, ifenprodil, blocked the high conductance currents sugges

69 NMDA receptor antagonists, D-AP5 and ifenprodil, both blocked LTPs that were induced by HFS o

70 at the same GluN1/GluN2B dimer interface as ifenprodil but adopts a remarkably different binding mod

71 with sensitivity to low micromolar zinc and ifenprodil, but LTP is less dependent on specific NMDAR

72 Drugs such as Ifenprodil, Cerestat and Selfotel, that have failed in c

73 teric modulators of NMDA receptors (TCN-201, ifenprodil, CIQ, and DQP-1105), we provide evidence that

74 common to NR2B-selective antagonists such as ifenprodil, CP 101,606, and Ro 25-6981 are not necessary

75 iheteromers by subunit-selective antagonists ifenprodil, CP-101,606, TCN-201, and extracellular Zn(2+

76 We found that ifenprodil decreased NMDA receptor equilibrium open prob

77 ors, including GluN2B-selective antagonists, ifenprodil, EVT-101 and CP-101-606, which inhibit with s

78 tagonist arcaine or the allosteric modulator ifenprodil had no effect on NMDA-induced changes in moto

79 Ifenprodil had similar effects on EPSCs from N2A KO neur

80 discovered that the anti-hypertensive agent ifenprodil has neuroprotective activity through its effe

81 re sensitive to the NMDA receptor antagonist ifenprodil in the IL-6-treated neurons compared with con

82 At pH 7.9 in cell-attached patches, ifenprodil increased the occupancy of the long-lived shu

83 amatergic synapses and are more sensitive to ifenprodil, indicating an increased contribution of GluN

84 e mature NMDAR-EPSC showed no sensitivity to ifenprodil, indicating lack of NR2B subunits, and no blo

85 hide bond, markedly decreases sensitivity to ifenprodil, indicating that conformational freedom in th

86 Both the ethanol- and ifenprodil-induced depression of NMDAR-mediated EPSPs an

87 earning deficits and that the time course of ifenprodil-induced rescue of spine density correlated wi

88 In contrast, ifenprodil infusion into the IC was effective whether ma

89 Similar to low micromolar zinc, ifenprodil inhibited LTD but not LTP.

90 neurones from rats aged postnatal day (P)7, ifenprodil inhibited NMDA-EPSCs with an estimated IC(50)

91 ) deleted is functional but exhibits reduced ifenprodil inhibition and increased glycine EC(50) with

92 f NR1 splice variants, whereas high affinity ifenprodil inhibition is independent of NR1 isoform expr

93 o localize the high affinity determinants of ifenprodil inhibition on the 2B subunit.

94 due is absolutely required for high affinity ifenprodil inhibition.

95 The mechanism by which ifenprodil inhibits NMDA receptor responses is not fully

96 sensitivity rather than to the appearance of ifenprodil-insensitive (NR1/NR2A) receptors.

97 acids 198 and 356 of NR2B for high affinity ifenprodil interaction.

98 found that infusion of the NMDAr antagonist ifenprodil into the BLA only abolished outcome devaluati

99 mol, or the NMDA receptor (NMDAR) antagonist ifenprodil into the PRh impaired associative formation.

100 Ifenprodil is a well tolerated NMDA receptor inhibitor;

101 Ifenprodil is an allosteric inhibitor of GluN1/GluN2B N-

102 Ifenprodil is an atypical noncompetitive modulator of th

103 The ifenprodil kinetics of whole-cell currents from neurons

104 l freedom in the GluN2B ATD is essential for ifenprodil-mediated allosteric inhibition of NMDA recept

105 ted the hypothesis that Tat-induced loss and ifenprodil-mediated rescue of synaptic spines in vivo wo

106 Intra-amygdala infusions of ifenprodil mirrored these results and, in addition, show

107 8), NR2B-selective (ifenprodil, n = 6; threo-ifenprodil, n = 4; Ro25-6985, n = 13), and NR2C/D-select

108 n = 5; NVP-AAM077, n = 18), NR2B-selective (ifenprodil, n = 6; threo-ifenprodil, n = 4; Ro25-6985, n

109 uncover the potential pH-dependent action of ifenprodil on gating.

110 ese results demonstrate intrinsic effects of ifenprodil on NMDA receptor stationary gating kinetics a

111 Coinfusion of an NMDA receptor antagonist (ifenprodil) or infusion of an AMPA receptor endocytosis

112 endent block by extracellular Mg2+, block by ifenprodil, or stimulation by spermine at NR1/NR2B recep

113 nt with either the NMDA receptor antagonist, ifenprodil, or the AMPA receptor antagonist, NBQX, had n

114 eciprocal effects have been reported between ifenprodil potency and that of extracellular ligands inc

115 Kinetic analyses suggested that ifenprodil prevents the transition of the receptor to an

116 tagonists AP5 and GluN2B-selective inhibitor ifenprodil reduced NMDA-activated currents, but had no e

117 antagonist ifenprodil was complex: 1 microm ifenprodil reduced open probability, while 10 microm red

118 In neurons from wild-type mice, zinc or ifenprodil reduced the EPSC peak, but only zinc caused s

119 At a low pH (pH 7.4), but not pH 7.9, ifenprodil reduces the mean open time of GluN1/GluN2B re

120 und to agonists and an allosteric inhibitor, ifenprodil, represent the allosterically inhibited state

121 or NR1/NR2D receptors do not account for the ifenprodil-resistant component of the NMDA-EPSC.

122 NMDAR-GluN2B receptor inhibitors, ifenprodil, RO 25-6981, and RO 04-5595, inhibit the pote

123 In addition, ifenprodil selectively affected the area of shut time co

124 The GluN2B-selective antagonist, ifenprodil, selectively reduced vagal calcium influx wit

125 t, synaptic receptors included both a highly ifenprodil-sensitive (NR1/NR2B) component as well as a s

126 n contrast, Ras-GRF1 mediates signaling from ifenprodil-sensitive (NR2B-containing) NMDARs to the Rac

127 e of D-aminophosphonovaleric acid (APV)- and ifenprodil-sensitive NMDA receptors, and found that the

128 dil, whereas at P28 only TRHR cells remained ifenprodil-sensitive.

129 deletion accelerated NMDAR decay and reduced ifenprodil sensitivity in the VH, suggesting that GluN3A

130 ttributable to synaptic receptors with lower ifenprodil sensitivity rather than to the appearance of

131 Whole-cell current density and ifenprodil sensitivity were reduced in PSD-95gfp cells,

132 nt as well as a second population with lower ifenprodil sensitivity; the reduced ifenprodil block of

133 , the maximum inhibitory effect of 10 microm ifenprodil significantly decreased.

134 The absolute configuration of ifenprodil stereoisomers was determined by X-ray crystal

135 biological data with configuration, all four ifenprodil stereoisomers were prepared by diastereoselec

136 t, and experiments with the NMDAR antagonist ifenprodil suggested that incorporation of NR2A-containi

137 n was overcome by APV and NVP-AAM077 but not ifenprodil, suggesting that zinc chelation unmasks tonic

138 DA receptors to show that, in the absence of ifenprodil, the bi-lobed structure of GluN2 ATD adopts a

139 y (IC50 of 8.9 nmol) for displacement of [3H]ifenprodil, thus showing improved potency with respect t

140 of modulators such as spermine, protons, and ifenprodil to channel gating.

141 oximately 60 %) in the presence of 10 microM ifenprodil, to leave a residual NMDAR-mediated current t

142 nt crystallographic evidence identified that ifenprodil, unlike zinc, binds at the interface of the G

143 When the GluN2B-selective antagonist ifenprodil was applied, the Mg(2+) sensitivity of the re

144 The effect of the NR2B antagonist ifenprodil was complex: 1 microm ifenprodil reduced open

145 rs by the NR2B subunit-selective antagonist, ifenprodil, was not altered by co-expression of the NR3

146 e partially blocked by the GluN2B antagonist ifenprodil, whereas at P28 only TRHR cells remained ifen

147 ht reduction of the visual response, whereas ifenprodil, which targets NMDA receptors containing the

148 kinetics and provide means to anticipate how ifenprodil will affect receptor responses in defined phy

149 o-administer the GluN2B-selective antagonist ifenprodil with cocaine, blocking the later emergence of

150 These were inhibited by ifenprodil, with an IC50 of 19 nM.