ライフサイエンスコーパス: D-aspartic acid

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

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

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

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

5 w potential, e.g. second-generation N-methyl-D-aspartic acid and alpha-amino-3-hydroxy-methyl-4-isoxa

6 tide and the ones containing a d-serine or a D-aspartic acid are observed.

7 substrates, namely L-glutamic acid (L-Glu), D-aspartic acid (D-Asp), and succinic acid (Suc).

8 oxygen and glucose deprivation and N-methyl-D-aspartic acid exposure led to neuronal death; however,

9 utyric acid receptor modulators and N-methyl-D-aspartic acid glutamate receptor antagonists, produce

10 N-methyl-D-aspartic acid/glutamate receptor antagonists induce ps

11 tify the presence of D-serine, D-alanine, or D-aspartic acid in eight biologically relevant peptides.

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

13 ateral injections of the neurotoxin N-Methyl-D-Aspartic acid into the MPOA.

14 D-aspartic acid is abundant in the developing brain.

15 f calcium mediated through neuronal N-methyl-d -aspartic acid (NMDA) glutamate-gated ion channels.

16 hippocampal neurons, treatment with N-methyl-D-aspartic acid (NMDA) (10 muM) for 48 hours reduced the

17 Distribution patterns of N-methyl-D-aspartic acid (NMDA) (NR1 and NR2A/B) and alpha-amino-

18 acid (AMPA), kainic acid (KA), and N-methyl-D-aspartic acid (NMDA) activated permeation of AGB into

19 N-methyl-D-aspartic acid (NMDA) and alpha-amino-3-hydroxyl-5-meth

20 ed with postnatal administration of N-methyl-D-aspartic acid (NMDA) and determine brain structures in

21 d the hypothesis that activation of N-methyl-D-aspartic acid (NMDA) and non-NMDA glutamate receptors

22 itation and direct iontophoresis of N-methyl-D-aspartic acid (NMDA) but without altering responses of

23 age sensitive conductances, such as N-methyl-D-aspartic acid (NMDA) channels can be more easily activ

24 The N-methyl-D-aspartic acid (NMDA) class of glutamate receptors has

25 VN by unilateral microinjections of N-methyl-d-aspartic acid (NMDA) elicited increases in HR which we

26 When we targeted the N-methyl-D-aspartic acid (NMDA) excitatory amino acid receptor wi

27 N-methyl-D-aspartic acid (NMDA) excited nociceptive as well as no

28 that act at the glycine site of the N-methyl-D-aspartic acid (NMDA) glutamatergic receptor have been

29 effects of reverse microdialysis of N-methyl-D-aspartic acid (NMDA) into the lateral hypothalamus (LH

30 N-methyl-D-aspartic acid (NMDA) or radiofrequency (RF) lesions we

31 esynaptic vesicles was dependent on N-methyl-D-aspartic acid (NMDA) receptor activation during LTP.

32 nduced in healthy volunteers by the N-methyl-D-aspartic acid (NMDA) receptor antagonist ketamine rese

33 tamine, a non-competitive glutamate N-methyl-d-aspartic acid (NMDA) receptor antagonist, is known to

34 sthetic ketamine, a non-competitive N-methyl-D-aspartic acid (NMDA) receptor antagonist, is widely ut

35 his action of ketamine [a glutamate N-methyl-D-aspartic acid (NMDA) receptor antagonist] have not bee

36 found to exhibit severe defects in N-methyl-D-aspartic acid (NMDA) receptor function, including decr

37 rent increases and TNF-alpha-evoked N-methyl-D-aspartic acid (NMDA) receptor hyperactivity in spinal

38 oked, currents 3-fold and increased N-methyl-D-aspartic acid (NMDA) receptor open probability.

39 y of iGluRs into AMPA, kainate, and N-methyl-d-aspartic acid (NMDA) receptor subtypes is regulated by

40 Agents that antagonize the N-methyl-D-aspartic acid (NMDA) receptor, such as phencyclidine a

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

42 oxazole-4-propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptor-mediated synaptic respon

43 d subunits required for assembly of N-methyl-d-aspartic acid (NMDA) receptors (NMDA-Rs), alpha-amino-

44 n effect dependent on activation of N-methyl-D-aspartic acid (NMDA) receptors and ERK, and blocked us

45 ate excitation at central synapses: N-methyl-D-aspartic acid (NMDA) receptors and non-NMDA receptors.

46 Functional N-methyl-d-aspartic acid (NMDA) receptors are formed from the ass

47 Blockade of N-methyl-D-aspartic acid (NMDA) receptors by intra-CA3 infusion o

48 directly required for clustering of N-methyl-D-aspartic acid (NMDA) receptors in PSDs early in develo

49 s is accompanied by the increase of N-Methyl-D-aspartic acid (NMDA) receptors in the hippocampus foll

50 Is glutamate, by acting on N-methyl-D-aspartic acid (NMDA) receptors in the vestibular subnu

51 4-propioinc acid (AMPA)/kainate and N-methyl-D-aspartic acid (NMDA) receptors mediate neurotransmissi

52 N-methyl-D-aspartic acid (NMDA) receptors play an important role

53 naptic density protein-95 (PSD-95), N-methyl-d-aspartic acid (NMDA) receptors, and neuronal nitric ox

54 most common targets and mechanisms: N-methyl-d-aspartic acid (NMDA) receptors, voltage gated calcium

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

56 The N-methyl-D-aspartic acid (NMDA) subtype of glutamate receptor may

57 aseline responding, the excitotoxin N-methyl-D-aspartic acid (NMDA) was bilaterally administered into

58 block sodium-dependent spiking; TTX+N-methyl-D-aspartic acid (NMDA)+picrotoxin (PTX) or gamma-aminobu

59 Specific antagonists of N-methyl-d-aspartic acid (NMDA), alpha-amino-3-hydroxy-5-methyl-4

60 hat the glutamate receptor agonist, N-methyl-D-aspartic acid (NMDA), nitric oxide (NO) and cGMP each

61 jections of tetrodotoxin (TTX), TTX+N-methyl-D-aspartic acid (NMDA), TTX+NMDA with the gamma-aminobut

62 mma-aminobutyric acid (GABA(A)) and N-methyl-D-aspartic acid (NMDA), was established using frontal af

63 N-Methyl-d-aspartic acid (NMDA), which mimics the action of the e

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

65 glutamate-mediated transmission at N-methyl-D-aspartic acid (NMDA)-sensitive receptors in hippocampu

66 created by epidural application of N-methyl-D-aspartic acid (NMDA).

67 ons of L-glutamate (L-Glu, 5 mM) or N-methyl-D-aspartic acid (NMDA, 1 mM) into different subregions o

68 he expression of GABAergic markers, N-methyl-d-aspartic-acid (NMDA) receptor subunits, and cerebellum

69 it is recruited into complexes with N-methyl-d-aspartic acid or alpha-amino-3-hydroxy-5-methyl-isoxaz

70 re constructed with portions of the N-methyl-d-aspartic acid-R1 (NMDA-R1) receptor subunit downstream

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

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

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

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

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

76 id (CSF) levels of the glia-derived N-methyl-D-aspartic acid receptor antagonist kynurenic acid (KYNA

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

78 a6beta2* activation did not enhance N-methyl-D-aspartic acid receptor function.

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

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

81 n the other hand, experiments using N-methyl-d-aspartic acid receptor inhibitors suggested that these

82 eover, the majority of these larger N-methyl-d-aspartic acid receptor subunit immunoreactive spots wa

83 reatment also significantly reduced N-methyl-d-aspartic acid receptor subunit NR2B phosphotyrosine la

84 mate-binding GluN2A subunits of the N-methyl D-aspartic acid receptor upon binding agonists of varyin

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

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

87 iment, we found abnormally enhanced N-methyl-d-aspartic acid receptor-dependent long-term depression

88 osed to glucocorticoids, exhibit an N-methyl-d-aspartic acid receptor-independent form of long-term p

89 ropanoic acid receptor-mediated and N-methyl-D-aspartic acid receptor-mediated synaptic currents in l

90 ion of CA2 synapses relies on NMDA (N-methyl-D-aspartic acid) receptor activation, calcium and calciu

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

92 We report that activation of N-methyl-D-aspartic acid receptors causes internalization and deg

93 dor habituation require functioning N-methyl-d-aspartic acid receptors in the olfactory bulb.

94 eceptors were also decreased, while N-methyl-D-aspartic acid receptors were not different compared wi

95 reasing glutamatergic excitation at N-methyl-D-aspartic acid receptors, alters both the amplitude and

96 folate absorption and activation of N-methyl-d-aspartic acid receptors, the authors examined relation

97 -4-isoxazole-propionate (AMPA), and N-methyl-d-aspartic acid receptors.

98 be injured independently via NMDA (N-methyl-D-aspartic acid) receptors located on peripheral oligode

99 y glutamate-dependent regulation of N-methyl-d-aspartic acid-type channels.

100 The rate of [(3)H]-d-aspartic acid uptake in WM tissue was also decreased a