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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

44 Because NMDA-type glutamate receptors are critical regulators of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 NMDA-type glutamate receptors in dopamine neurons are cr

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

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

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

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

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

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

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

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

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

77 2+) influx through the N-methyl-d-aspartate (NMDA)-type glutamate receptor leads to activation and po

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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