ライフサイエンスコーパス: NMDA-type glutamate receptor

1 , and CGS 19755, a competitive antagonist of NMDA-type glutamate receptor.

2 of the signaling complex associated with the NMDA-type glutamate receptor.

3 s peptide can drive loss of surface AMPA and NMDA type glutamate receptors.

4 within this pathway primarily use AMPA- and NMDA-type glutamate receptors.

5 hB induces a direct interaction of EphB with NMDA-type glutamate receptors.

6 phosphorylation state of the NR1 subunit of NMDA-type glutamate receptors.

7 esic properties consistent with an action at NMDA-type glutamate receptors.

8 plasticity and neurotoxicity associated with NMDA-type glutamate receptors.

9 D-serine action requires binding to neuronal NMDA-type glutamate receptors.

10 voltage-dependence and kinetics of VGCCs and NMDA-type glutamate receptors.

11 ties indicating the involvement of AMPA- and NMDA-type glutamate receptors.

12 d how visual processing depends on AMPA- and NMDA-type glutamate receptors.

13 an uncompetitive/fast off-rate antagonist of NMDA-type glutamate receptors.

14 itment of Tiam1 to EphB complexes containing NMDA-type glutamate receptors.

15 nity to probe the mechanism of activation of NMDA-type glutamate receptors.

16 by intra-vmPFC blockade of AMPA-type but not NMDA-type glutamate receptors.

17 rt from stimulation of N-methyl-d-aspartate (NMDA)-type glutamate receptors.

18 mined the impact of Shank3 deficiency on the NMDA-type glutamate receptor, a key player in cognition

19 to be dephosphorylated by activation of the NMDA-type glutamate receptor, a key player in synaptic p

20 ented by synapses with N-methyl-D-aspartate (NMDA)-type glutamate receptors, accounts for the experim

21 ters of PSD-95 and subunits of AMPA-type and NMDA-type glutamate receptors accumulate in spines of mu

22 NMDA-type glutamate receptors act as voltage- and ligand

23 elimination through a process that requires NMDA-type glutamate receptor activation.

24 Here, we show that Reelin can regulate NMDA-type glutamate receptor activity through a mechanis

25 n insensitive state of the fear memory where NMDA-type glutamate receptor agonist and antagonist drug

26 conditional fear does not depend acutely on NMDA-type glutamate receptors, although other evidence h

27 ionic acid (AMPA)- and N-methyl-D-aspartate (NMDA)-type glutamate receptors (AMPARs and NMDARs, respe

28 Postsynaptic AMPA- and NMDA-type glutamate receptors (AMPARs, NMDARs) are commo

29 on regulated interactions with AMPA-type and NMDA-type glutamate receptors (AMPARs/NMDARs).

30 ium influx through the N-methyl-d-aspartate (NMDA)-type glutamate receptor and activation of calcium/

31 x through postsynaptic N-methyl-D-aspartate (NMDA)-type glutamate receptors and subsequent activation

32 dence of sensory information, recruitment of NMDA-type glutamate receptors and inhibitory feedback.

33 the mature CNS by regulating trafficking of NMDA-type glutamate receptors and intrinsic properties o

34 we show that nucleus accumbens core (NAcore) NMDA-type glutamate receptors and medial prefrontal (mPF

35 Despite these similarities, inhibitors of NMDA-type glutamate receptors and protein phosphatase 2B

36 tiation that is induced by the activation of NMDA-type glutamate receptors and that requires both glu

37 at is regulated by a combination of AMPA and NMDA-type glutamate receptors and the mitogen-activated

38 tor Tat, activation of N-methyl-D-aspartate (NMDA)-type glutamate receptors, and subsequent rapid ris

39 : the PSD-95 family, the NR2B subunit of the NMDA-type glutamate receptor, and densin-180.

40 xcitatory, driven by activation of AMPA- and NMDA-type glutamate receptors, and can undergo NMDA-rece

41 ton in localizing GABAA receptors, AMPA- and NMDA-type glutamate receptors, and potential anchoring p

42 he early dynamics of regulation of CaMKII by NMDA-type glutamate receptors, and produces a change in

43 n of KCl along with an N-methyl-d-aspartate (NMDA)-type glutamate receptor antagonist, MK-801, and a

44 c acid residues, is a N-methyl-d-aspartate- (NMDA-) type glutamate receptor antagonist.

45 amate receptor antagonist, MK-801, and a non-NMDA-type glutamate receptor antagonist, NBQX, resulted

46 llowing local administration of NMDA and non-NMDA-type glutamate receptor antagonists.

47 nd on dendritic spines and contain AMPA- and NMDA-type glutamate receptors apposed to presynaptic spe

48 N-methyl-D-aspartate (NMDA) type glutamate receptors are constituted of one ob

49 dependent protein kinase II (CaMKII) and the NMDA-type glutamate receptor are key regulators of synap

50 Synaptic NMDA-type glutamate receptors are anchored to the second

51 Because NMDA-type glutamate receptors are critical regulators of

52 NMDA-type glutamate receptors are heterotetrameric compl

53 NMDA-type glutamate receptors are ligand-gated ion chann

54 ntal synaptic currents mediated by AMPA- and NMDA-type glutamate receptors, as well as the abundance

55 ventral spinal neurons cluster AMPA- but not NMDA-type glutamate receptors at excitatory synapses on

56 KII T-site (and thereby also interfered with NMDA-type glutamate receptor binding to the T-site).

57 This effect can be mimicked by blockade of NMDA-type glutamate receptors but not voltage-gated calc

58 ugh both voltage-dependent Ca2+ channels and NMDA-type glutamate receptors, but the relative contribu

59 pendent of the cell-autonomous regulation of NMDA-type glutamate receptors by absolute levels of NL1.

60 Modulation of NMDA-type glutamate receptors by extracellular Zn(2+) ma

61 In this study, we examined the regulation of NMDA-type glutamate receptors by the PFC dopamine D4 rec

62 In neurons, Ca(2+) influx through NMDA-type glutamate receptors causes postsynaptic cluste

63 kinase signaling has been implicated in both NMDA-type glutamate receptor clustering and dendritic sp

64 teins are clustered together with PSD-95 and NMDA type glutamate receptors, consistent with a postsyn

65 es the activation of ionotropic postsynaptic NMDA-type glutamate receptors containing GluN2B subunits

66 The NR2B subunit of N-methyl-d-aspartate (NMDA)-type glutamate receptor, densin-180, and alpha-act

67 Within the hippocampus, mAChRs promote NMDA-type glutamate receptor-dependent forms of long-ter

68 affects currents from N-methyl-D-aspartate (NMDA) type glutamate receptors depending upon their subu

69 ase CaMKIIalpha to the GluN2B subunit of the NMDA-type glutamate receptor disrupts both LTP and activ

70 rons is competitively regulated by their own NMDA-type glutamate receptor during a short, critical pe

71 ber and/or function of N-methyl-D-aspartate (NMDA)-type glutamate receptors, effects that may sensiti

72 no acid stimulation of N-methyl-D-aspartate (NMDA)-type glutamate receptors, excessive Ca2+ influx, a

73 Synaptic vesicle proteins, AMPA- and NMDA-type glutamate receptors, GABAA receptors, and the

74 ive stimulation of the N-methyl-d-aspartate (NMDA)-type glutamate receptor has been implicated in the

75 altered by agonists of N-methyl-D-aspartate (NMDA) type glutamate receptors in this region.

76 The N-methyl-D-aspartate (NMDA)-type glutamate receptors in the shell region of th

77 is differentially regulated by activation of NMDA-type glutamate receptors in cultured neurons.

78 NMDA-type glutamate receptors in dopamine neurons are cr

79 rments may be related to hypersensitivity of NMDA-type glutamate receptors in Mg(2+)-deficient mice.

80 ins transduce calcium signals emanating from NMDA-type glutamate receptors in the CA1 region of the h

81 We find that in mice, NMDA-type glutamate receptors in the hypothalamus are th

82 initiated by pulses of Ca2+ flowing through NMDA-type glutamate receptors into postsynaptic spines.

83 lowing Ca2+ influx via N-methyl-D-aspartate (NMDA)-type glutamate receptors is essential for hippocam

84 cessive stimulation of N-methyl-D-aspartate (NMDA)-type glutamate receptors is thought to be responsi

85 Calcium influx through NMDA-type glutamate receptors is efficiently coupled to

86 ported the idea that the synaptic density of NMDA-type glutamate receptors is fairly static, modulate

87 postsynaptic density in association with the NMDA-type glutamate receptor, Kalirin-7, and Rac1.

88 ustained activation of N-methyl-d-aspartate (NMDA) -type glutamate receptors leads to excitotoxic neu

89 2+) influx through the N-methyl-d-aspartate (NMDA)-type glutamate receptor leads to activation and po

90 l of food intake by endogenous glutamate and NMDA-type glutamate receptors located in the caudomedial

91 These results suggest that the NMDA-type glutamate receptors may be involved in dehydra

92 AMPA- and NMDA-type glutamate receptors mediate distinct postsynap

93 pocampus requires calcium influx through the NMDA-type glutamate receptor (NMDA-R) to activate CaMKII

94 is early developmental time period, synaptic NMDA-type glutamate receptors (NMDA-Rs) contain primaril

95 Ca(2+) influx through the NMDA-type glutamate receptor (NMDAR) and the ensuing act

96 ynapses are synapses whose activation evokes NMDA-type glutamate receptor (NMDAR) but not AMPA-type g

97 The NMDA-type glutamate receptor (NMDAR) is essential for sy

98 -dependent protein kinase II (CaMKII) to the NMDA-type glutamate receptor (NMDAR) subunit GluN2B.

99 dendritic spines depend on activation of the NMDA-type glutamate receptor (NMDAR), which leads to inf

100 ginning at 1 month of age, RAS-GRF1 mediates NMDA-type glutamate receptor (NMDAR)-induction of long t

101 f crossmodal synaptic responses, mediated by NMDA-type glutamate receptor (NMDARs) activation, form t

102 D that was dependent on the co-activation of NMDA-type glutamate receptors (NMDARs) and metabotropic

103 eta-mediated spine loss required activity of NMDA-type glutamate receptors (NMDARs) and occurred thro

104 on (LTP)] require both Ca(2+) influx through NMDA-type glutamate receptors (NMDARs) and the kinase Ca

105 NMDA-type glutamate receptors (NMDARs) are currently reg

106 NMDA-type glutamate receptors (NMDARs) are widely recogn

107 erance), partly because of the activation of NMDA-type glutamate receptors (NMDARs) at the central te

108 NMDA-type glutamate receptors (NMDARs) contribute to man

109 opamine transmission, we tested mice lacking NMDA-type glutamate receptors (NMDARs) exclusively in do

110 terfere with synaptic functions by depleting NMDA-type glutamate receptors (NMDARs) from the neuronal

111 NMDA-type glutamate receptors (NMDARs) guide the activit

112 NMDA-type glutamate receptors (NMDARs) have been propose

113 accepted to depend on Ca(2+) influx through NMDA-type glutamate receptors (NMDARs) in conjunction wi

114 HCI regulates synaptic responses mediated by NMDA-type glutamate receptors (NMDARs) in the mammalian

115 d memory, Ca(2+) influx through postsynaptic NMDA-type glutamate receptors (NMDARs) initiates signali

116 Although inhibition of NMDA-type glutamate receptors (NMDARs) is one mechanism

117 c cleft and possibly stimulate extrasynaptic NMDA-type glutamate receptors (NMDARs) on ganglion cells

118 NMDA-type glutamate receptors (NMDARs) play a central ro

119 NMDA-type glutamate receptors (NMDARs) play a critical r

120 Synaptic NMDA-type glutamate receptors (NMDARs) play important ro

121 Calcium signalling through NMDA-type glutamate receptors (NMDARs) plays a key role

122 Hyperactivation of NMDA-type glutamate receptors (NMDARs) results in excito

123 ve of rats was strengthened by activation of NMDA-type glutamate receptors (NMDARs), which were found

124 w protein synthesis and is often mediated by NMDA-type glutamate receptors (NMDARs).

125 r LTD) after distinct stimuli of hippocampal NMDA-type glutamate receptors (NMDARs).

126 ecific changes in the subunit composition of NMDA-type glutamate receptors (NMDARs).

127 tion via a process mediated by activation of NMDA-type glutamate receptors (NMDARs).

128 result primarily from Ca(2+) influx through NMDA-type glutamate receptors (NMDARs).

129 ed in the neuroscience literature concerning NMDA-type glutamate receptors (NMDARs).

130 in part via effects on N-methyl-D-aspartate (NMDA)-type glutamate receptors (NR).

131 potent, capable of clustering both AMPA- and NMDA-type glutamate receptors on hippocampal interneuron

132 other spinal neurons, cluster both AMPA- and NMDA-type glutamate receptors on the dendritic shafts of

133 riggered, for example, by Ca2+ entry through NMDA-type glutamate receptors--only recently has attenti

134 H]AMPA with no apparent effect on binding to NMDA-type glutamate receptors or to high affinity kainat

135 ted synaptic transmission without changes in NMDA-type glutamate receptor- or in GABAA receptor-media

136 NMDA-type glutamate receptors play a critical role in th

137 Ca2+ influx through N-methyl-D-aspartate (NMDA)-type glutamate receptors plays a pivotal role in s

138 Ca2+ influx through N-methyl-D-aspartate- (NMDA-) type glutamate receptors plays a critical role in

139 Blocking extrasynaptic NMDA-type glutamate receptors prevented amyloid-beta (Ab

140 Contribution of NMDA-type glutamate receptors prolonged postsynaptic eve

141 ith Arc-dependent changes in the function of NMDA-type glutamate receptors, rather than changes in AM

142 cium entry through the N-methyl-d-aspartate (NMDA)-type glutamate receptor regulate synaptic developm

143 These results suggest that NMDA, and not non-NMDA, type glutamate receptors regulate lactate-induced

144 s) in NTS neurons mediated by both AMPA- and NMDA-type glutamate receptors (-Rs).

145 impaired for autonomy (T286A) or binding to NMDA-type glutamate receptor subunit 2B (GluN2B; formerl

146 -dependent protein kinase II (CaMKII) to the NMDA-type glutamate receptor subunit GluN2B is an import

147 l CaMKII roles, in particular binding to the NMDA-type glutamate receptor subunit GluN2B(9-14).

148 or striatal deletion of Grin2b (encoding the NMDA-type glutamate receptor subunit GluN2B) or DS-restr

149 orylation at T286 (pT286) and binding to the NMDA-type glutamate receptor subunit GluN2B.

150 calcium influx through N-methyl-D-aspartate (NMDA)-type glutamate receptors, suggesting that there is

151 nergic interneurons activates both AMPA- and NMDA-type glutamate receptors, suggesting a unique role

152 lance between excitation and inhibition, and NMDA-type glutamate receptors that are involved in the m

153 Triheteromeric NMDA-type glutamate receptors that contain two GluN1 and

154 )-dependent regulation of Ca2+ entry through NMDA-type glutamate receptors that was inhibited by D2Rs

155 The targeting of AMPA- and NMDA-type glutamate receptors to synapses in the central

156 a2+ influx through the N-methyl-d-aspartate (NMDA)-type glutamate receptor triggers activation and po

157 which is known to bind with and regulate the NMDA-type glutamate receptors, was elevated.

158 ole in the function of N-methyl-D-aspartate (NMDA)-type glutamate receptors, which are centrally invo

159 in Alzheimer's disease by impairing neuronal NMDA-type glutamate receptors, whose function is regulat