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1 cine agonist-binding sites of the N-methyl-d-aspartic acid receptor.
2 -isoxazole-propionate (AMPA), and N-methyl-d-aspartic acid receptors.
3 n of CA2 synapses relies on NMDA (N-methyl-D-aspartic acid) receptor activation, calcium and calcium/
4 their free radical-generating and N-methyl-d-aspartic acid receptor agonist activities.
5 asing glutamatergic excitation at N-methyl-D-aspartic acid receptors, alters both the amplitude and f
6 vents were strongly influenced by N-methyl-D-aspartic acid receptor- and cyclic AMP-dependent signali
7  (CSF) levels of the glia-derived N-methyl-D-aspartic acid receptor antagonist kynurenic acid (KYNA)
8 ice were treated with the partial N-methyl-d-aspartic acid receptor antagonist memantine.
9      We report that activation of N-methyl-D-aspartic acid receptors causes internalization and degra
10                                   N-methyl-D-aspartic acid receptor-dependent long term potentiation
11 ent, we found abnormally enhanced N-methyl-d-aspartic acid receptor-dependent long-term depression in
12 beta2* activation did not enhance N-methyl-D-aspartic acid receptor function.
13                               The N-methyl-d-aspartic acid receptor hypofunction model of schizophren
14 chizophrenia, as predicted by the N-methyl-d-aspartic acid receptor hypofunction model.
15 tamate-mediated activation of the N-methyl-D-aspartic acid receptor in STEP-deficient neurons leads t
16 r habituation require functioning N-methyl-d-aspartic acid receptors in the olfactory bulb.
17 ed to glucocorticoids, exhibit an N-methyl-d-aspartic acid receptor-independent form of long-term pot
18 the other hand, experiments using N-methyl-d-aspartic acid receptor inhibitors suggested that these r
19 e injured independently via NMDA (N-methyl-D-aspartic acid) receptors located on peripheral oligodend
20 panoic acid receptor-mediated and N-methyl-D-aspartic acid receptor-mediated synaptic currents in lam
21  to LRP1, we demonstrate that the N-methyl-D-aspartic acid receptor (NMDA-R) is expressed by macropha
22 K-801, a specific pore blocker of N-Methyl-D-aspartic acid receptor (NMDAR) channels, and this occurr
23                           Because N-methyl-D-aspartic acid receptor (NMDAR) dysregulation has been st
24                      By measuring N-methyl-d-aspartic acid receptor (NMDAR)-driven calcium responses
25 es by interacting and trafficking N-methyl-D-aspartic acid receptors (NMDAR) and alpha-amino-3-hydrox
26 nsertions of new, NR2B-containing N-methyl-D-aspartic acid receptors (NMDARs).
27 ver, the majority of these larger N-methyl-d-aspartic acid receptor subunit immunoreactive spots was
28 atment also significantly reduced N-methyl-d-aspartic acid receptor subunit NR2B phosphotyrosine labe
29 late absorption and activation of N-methyl-d-aspartic acid receptors, the authors examined relationsh
30 te-binding GluN2A subunits of the N-methyl D-aspartic acid receptor upon binding agonists of varying
31 eptors were also decreased, while N-methyl-D-aspartic acid receptors were not different compared with