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 the high-affinity binding sites for zinc and ifenprodil.

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

8 s abolished by NR2B-specific NMDA antagonist ifenprodil.

9 rent transients that were blocked by APV and ifenprodil.

10 eceptor in LA using the selective antagonist ifenprodil.

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

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

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

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

15 (30 mum) or GluN2B-containing receptors with ifenprodil (3 mum) prevents CREB shutoff effectively in

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

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

18 Ifenprodil, a GluN2B antagonist, caused modest suppressi

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

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

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

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

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

24 Ifenprodil also mitigated cue-induced reinstatement of c

25 Ifenprodil also occluded the ethanol effect, suggesting

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

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

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

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

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

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

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

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

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

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

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

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

38 Ifenprodil and related phenylethanolamine compounds, whi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 We found that ifenprodil decreased NMDA receptor equilibrium open prob

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

65 Ifenprodil had similar effects on EPSCs from N2A KO neur

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 due is absolutely required for high affinity ifenprodil inhibition.

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

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

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

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

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

86 Ifenprodil is a well tolerated NMDA receptor inhibitor;

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

88 Ifenprodil is an atypical noncompetitive modulator of th

89 The ifenprodil kinetics of whole-cell currents from neurons

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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