ライフサイエンスコーパス: N-methyl-D-aspartic acid

1 hyl-3-oxo-1,2-oxazol-4-yl) propanoic acid or N-methyl-d-aspartic acid.

2 ibition but not loss of excitatory glutamate/N-methyl-d-aspartic acid.

3 NMDA subtype, named for its specific ligand N-methyl-D-aspartic acid.

4 after intrastriatal injection of 5 mumol of N-methyl-D-aspartic acid.

5 d now show potential, e.g. second-generation N-methyl-D-aspartic acid and alpha-amino-3-hydroxy-methy

6 Both oxygen and glucose deprivation and N-methyl-D-aspartic acid exposure led to neuronal death;

7 a-amino-butyric acid receptor modulators and N-methyl-D-aspartic acid glutamate receptor antagonists,

8 N-methyl-D-aspartic acid/glutamate receptor antagonists

9 Calcium influx- and N-methyl-d-aspartic acid-induced processing of EphB2 is

10 eived bilateral injections of the neurotoxin N-Methyl-D-Aspartic acid into the MPOA.

11 influx of calcium mediated through neuronal N-methyl-d -aspartic acid (NMDA) glutamate-gated ion cha

12 cultured hippocampal neurons, treatment with N-methyl-D-aspartic acid (NMDA) (10 muM) for 48 hours re

13 Distribution patterns of N-methyl-D-aspartic acid (NMDA) (NR1 and NR2A/B) and alp

14 propionic acid (AMPA), kainic acid (KA), and N-methyl-D-aspartic acid (NMDA) activated permeation of

15 N-methyl-D-aspartic acid (NMDA) and alpha-amino-3-hydrox

16 ne combined with postnatal administration of N-methyl-D-aspartic acid (NMDA) and determine brain stru

17 we tested the hypothesis that activation of N-methyl-D-aspartic acid (NMDA) and non-NMDA glutamate r

18 henyl-butyl-tert-nitrone (alphaPBN), and the N-methyl-D-aspartic acid (NMDA) antagonist MK801-in mous

19 al disorder-associated pathways and identify N-methyl-d-aspartic acid (NMDA) antagonists as potential

20 eflex excitation and direct iontophoresis of N-methyl-D-aspartic acid (NMDA) but without altering res

21 ince voltage sensitive conductances, such as N-methyl-D-aspartic acid (NMDA) channels can be more eas

22 The N-methyl-D-aspartic acid (NMDA) class of glutamate recep

23 of the PVN by unilateral microinjections of N-methyl-d-aspartic acid (NMDA) elicited increases in HR

24 When we targeted the N-methyl-D-aspartic acid (NMDA) excitatory amino acid re

25 N-methyl-D-aspartic acid (NMDA) excited nociceptive as w

26 ncluding light-induced circadian arrhythmia, N-Methyl-D-aspartic acid (NMDA) excitotoxicity, and Casp

27 Agents that act at the glycine site of the N-methyl-D-aspartic acid (NMDA) glutamatergic receptor h

28 The effects of reverse microdialysis of N-methyl-D-aspartic acid (NMDA) into the lateral hypotha

29 N-methyl-D-aspartic acid (NMDA) or radiofrequency (RF) l

30 ns and presynaptic vesicles was dependent on N-methyl-D-aspartic acid (NMDA) receptor activation duri

31 isorder induced in healthy volunteers by the N-methyl-D-aspartic acid (NMDA) receptor antagonist keta

32 th subanesthetic ketamine, a non-competitive N-methyl-D-aspartic acid (NMDA) receptor antagonist, is

33 t with ketamine, a non-competitive glutamate N-methyl-d-aspartic acid (NMDA) receptor antagonist, is

34 erlying this action of ketamine [a glutamate N-methyl-D-aspartic acid (NMDA) receptor antagonist] hav

35 mice were found to exhibit severe defects in N-methyl-D-aspartic acid (NMDA) receptor function, inclu

36 aptic current increases and TNF-alpha-evoked N-methyl-D-aspartic acid (NMDA) receptor hyperactivity i

37 holine-evoked, currents 3-fold and increased N-methyl-D-aspartic acid (NMDA) receptor open probabilit

38 e assembly of iGluRs into AMPA, kainate, and N-methyl-d-aspartic acid (NMDA) receptor subtypes is reg

39 Agents that antagonize the N-methyl-D-aspartic acid (NMDA) receptor, such as phency

40 We investigated inhibition of the N-methyl-D-aspartic acid (NMDA) receptor-channel complex

41 -methylisoxazole-4-propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptor-mediated synapt

42 identified subunits required for assembly of N-methyl-d-aspartic acid (NMDA) receptors (NMDA-Rs), alp

43 ioning, an effect dependent on activation of N-methyl-D-aspartic acid (NMDA) receptors and ERK, and b

44 nels mediate excitation at central synapses: N-methyl-D-aspartic acid (NMDA) receptors and non-NMDA r

45 Functional N-methyl-d-aspartic acid (NMDA) receptors are formed fro

46 Blockade of N-methyl-D-aspartic acid (NMDA) receptors by intra-CA3 i

47 5 is not directly required for clustering of N-methyl-D-aspartic acid (NMDA) receptors in PSDs early

48 rotrophins is accompanied by the increase of N-Methyl-D-aspartic acid (NMDA) receptors in the hippoca

49 Is glutamate, by acting on N-methyl-D-aspartic acid (NMDA) receptors in the vestibu

50 soxazole-4-propioinc acid (AMPA)/kainate and N-methyl-D-aspartic acid (NMDA) receptors mediate neurot

51 N-methyl-D-aspartic acid (NMDA) receptors play an import

52 ), postsynaptic density protein-95 (PSD-95), N-methyl-d-aspartic acid (NMDA) receptors, and neuronal

53 e of the most common targets and mechanisms: N-methyl-d-aspartic acid (NMDA) receptors, voltage gated

54 epends on Ca(2+) influx through postsynaptic N-methyl-D-aspartic acid (NMDA) receptors.

55 The N-methyl-D-aspartic acid (NMDA) subtype of glutamate rec

56 ment of baseline responding, the excitotoxin N-methyl-D-aspartic acid (NMDA) was bilaterally administ

57 (TTX) to block sodium-dependent spiking; TTX+N-methyl-D-aspartic acid (NMDA)+picrotoxin (PTX) or gamm

58 Specific antagonists of N-methyl-d-aspartic acid (NMDA), alpha-amino-3-hydroxy-5

59 nstrate that the glutamate receptor agonist, N-methyl-D-aspartic acid (NMDA), nitric oxide (NO) and c

60 itreal injections of tetrodotoxin (TTX), TTX+N-methyl-D-aspartic acid (NMDA), TTX+NMDA with the gamma

61 GICs), gamma-aminobutyric acid (GABA(A)) and N-methyl-D-aspartic acid (NMDA), was established using f

62 N-Methyl-d-aspartic acid (NMDA), which mimics the action

63 N-methyl-D-aspartic acid (NMDA)-activated currents were

64 ations in glutamate-mediated transmission at N-methyl-D-aspartic acid (NMDA)-sensitive receptors in h

65 rtex were created by epidural application of N-methyl-D-aspartic acid (NMDA).

66 roinjections of L-glutamate (L-Glu, 5 mM) or N-methyl-D-aspartic acid (NMDA, 1 mM) into different sub

67 amining the expression of GABAergic markers, N-methyl-d-aspartic-acid (NMDA) receptor subunits, and c

68 es where it is recruited into complexes with N-methyl-d-aspartic acid or alpha-amino-3-hydroxy-5-meth

69 asmids were constructed with portions of the N-methyl-d-aspartic acid-R1 (NMDA-R1) receptor subunit d

70 and glutamate-binding GluN2A subunits of the N-methyl D-aspartic acid receptor upon binding agonists

71 In addition to LRP1, we demonstrate that the N-methyl-D-aspartic acid receptor (NMDA-R) is expressed

72 ibited by MK-801, a specific pore blocker of N-Methyl-D-aspartic acid receptor (NMDAR) channels, and

73 Because N-methyl-D-aspartic acid receptor (NMDAR) dysregulation

74 By measuring N-methyl-d-aspartic acid receptor (NMDAR)-driven calcium

75 c owing to their free radical-generating and N-methyl-d-aspartic acid receptor agonist activities.

76 pinal fluid (CSF) levels of the glia-derived N-methyl-D-aspartic acid receptor antagonist kynurenic a

77 ccur when mice were treated with the partial N-methyl-d-aspartic acid receptor antagonist memantine.

78 ast, alpha6beta2* activation did not enhance N-methyl-D-aspartic acid receptor function.

79 The N-methyl-d-aspartic acid receptor hypofunction model of

80 elease in schizophrenia, as predicted by the N-methyl-d-aspartic acid receptor hypofunction model.

81 ow that glutamate-mediated activation of the N-methyl-D-aspartic acid receptor in STEP-deficient neur

82 On the other hand, experiments using N-methyl-d-aspartic acid receptor inhibitors suggested t

83 Moreover, the majority of these larger N-methyl-d-aspartic acid receptor subunit immunoreactive

84 ligomer treatment also significantly reduced N-methyl-d-aspartic acid receptor subunit NR2B phosphoty

85 These events were strongly influenced by N-methyl-D-aspartic acid receptor- and cyclic AMP-depend

86 N-methyl-D-aspartic acid receptor-dependent long term po

87 ent experiment, we found abnormally enhanced N-methyl-d-aspartic acid receptor-dependent long-term de

88 ectly exposed to glucocorticoids, exhibit an N-methyl-d-aspartic acid receptor-independent form of lo

89 l-4-yl)-propanoic acid receptor-mediated and N-methyl-D-aspartic acid receptor-mediated synaptic curr

90 ate and glycine agonist-binding sites of the N-methyl-d-aspartic acid receptor.

91 potentiation of CA2 synapses relies on NMDA (N-methyl-D-aspartic acid) receptor activation, calcium a

92 tory synapses by interacting and trafficking N-methyl-D-aspartic acid receptors (NMDAR) and alpha-ami

93 membrane insertions of new, NR2B-containing N-methyl-D-aspartic acid receptors (NMDARs).

94 We report that activation of N-methyl-D-aspartic acid receptors causes internalizatio

95 ects of odor habituation require functioning N-methyl-d-aspartic acid receptors in the olfactory bulb

96 kainate receptors were also decreased, while N-methyl-D-aspartic acid receptors were not different co

97 s and decreasing glutamatergic excitation at N-methyl-D-aspartic acid receptors, alters both the ampl

98 tes both folate absorption and activation of N-methyl-d-aspartic acid receptors, the authors examined

99 -5-methyl-4-isoxazole-propionate (AMPA), and N-methyl-d-aspartic acid receptors.

100 may also be injured independently via NMDA (N-methyl-D-aspartic acid) receptors located on periphera

101 hyl-3-oxo-1,2-oxazol-4-yl)propanoic acid and N-methyl-D-aspartic acid, respectively).

102 tissue by glutamate-dependent regulation of N-methyl-d-aspartic acid-type channels.