ライフサイエンスコーパス: D-aspartic acid

1 d a decrease in quorum sensing molecules was D-aspartic acid.

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

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

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

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

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

7 d quorum sensing response in the presence of D-aspartic acid and the absence of its L- counterpart at

8 phobic amino acid (optimally phenylalanine), D aspartic acid, and n is the number of repeats of these

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

25 yl-tert-nitrone (alphaPBN), and the N-methyl-D-aspartic acid (NMDA) antagonist MK801-in mouse and rat

26 er-associated pathways and identify N-methyl-d-aspartic acid (NMDA) antagonists as potential treatmen

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

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

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

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

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

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

33 light-induced circadian arrhythmia, N-Methyl-D-aspartic acid (NMDA) excitotoxicity, and Caspase-3-med

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 4-propioinc acid (AMPA)/kainate and N-methyl-D-aspartic acid (NMDA) receptors mediate neurotransmissi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 lutamate-mediated activation of the N-methyl-D-aspartic acid receptor in STEP-deficient neurons leads

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

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

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

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

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

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

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

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

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

97 lycine agonist-binding sites of the N-methyl-d-aspartic acid receptor.

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

99 pses by interacting and trafficking N-methyl-D-aspartic acid receptors (NMDAR) and alpha-amino-3-hydr

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

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

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

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

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

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

106 -4-isoxazole-propionate (AMPA), and N-methyl-d-aspartic acid receptors.

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

108 lutamic acid residues, or changing the l- to d-aspartic acid residue on MitoFlag abolishes the traffi

109 -1,2-oxazol-4-yl)propanoic acid and N-methyl-D-aspartic acid, respectively).

110 cting transactivators with E [glutamic acid]/D [aspartic acid]-rich-carboxylterminal domain4) is indu

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

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