ライフサイエンスコーパス: NMDA

1 NMDA receptors (NMDARs) are a subtype of postsynaptic io

2 NMDA receptors (NMDARs) are Ca(2+)-permeant, ligand-gate

3 NMDA receptors (NMDARs) are ion channels activated by th

4 NMDA receptors (NMDARs) are ionotropic glutamate recepto

5 NMDA receptors (NMDARs) contribute to several neuropatho

6 NMDA receptors are also implicated in psychiatric and ne

7 NMDA receptors are ligand-gated ion channels that underl

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

9 hanges in metabotropic glutamate receptor 1, NMDA receptor 2A, alpha-amino-3-hydroxy-5-methyl-4-isoxa

10 , whereas metabotropic glutamate receptor 5, NMDA receptor 2B, GluR2, and GABAARalpha2 levels were no

11 lization of postsynaptic density protein 95, NMDA receptor, and tropomyosin receptor kinase B.

12 Aberrant NMDA receptor (NMDAR) activity contributes to several ne

13 encing CYLD in hippocampal neurons abolishes NMDA-induced chemical long-term depression.

14 e of this association because pHFD abolishes NMDA-LTD, a function that is restored by RELN overexpres

15 ABSTRACT: NMDA receptor independent long-term potentiation (LTP) i

16 ed for assembly of N-methyl-d-aspartic acid (NMDA) receptors (NMDA-Rs), alpha-amino-3-hydroxy-5-methy

17 t are distantly related to glycine-activated NMDA receptors and that bind glycine with unusually high

18 d Ca(2+) channels and synaptically activated NMDA receptors.

19 neurogenic state in vitro and in vivo after NMDA (N-methyl-d-aspartate) damage in young mice.

20 to its unique pharmacological profile among NMDA receptor subtypes (GluN1/2A-D), in which DCS is a s

21 presence of glutamate receptors (i.e. AMPA, NMDA, and kainate receptors) at the synapse.

22 nding site densities for glutamatergic AMPA, NMDA and kainate, GABAergic GABAA , muscarinic M1 , M2 a

23 ting pre- and post-synaptic receptors (AMPA, NMDA, GABA-A, mGluR2/3 receptors and Nav, Cav voltage-ga

24 cNIC decreased baseline AMPA/NMDA ratio, arising from increased NMDA currents enriche

25 receptor properties, we found that the AMPA/NMDA ratio increased at cortical and amygdaloid inputs b

26 rop and the tone change were prevented by an NMDA receptor antagonist.

27 Induction of classical LTP involves an NMDA-receptor- and calcium-dependent increase in functio

28 We previously reported that memantine, an NMDA receptor antagonist, enhanced two biomarkers of ear

29 DA receptor (NMDAR) dysfunction, we analyzed NMDA-dependent synaptic plasticity in hippocampal slices

30 is associated with caspase-3 activation and NMDA receptor-dependent excitotoxicity.

31 n part by increases of synaptic activity and NMDA-receptor-dependent calcium spikes in apical tuft de

32 s are not accompanied by changes in AMPA and NMDA receptor properties at cortical, amygdaloid, and hi

33 hough we observed no alterations of AMPA and NMDA receptor properties, we found that the AMPA/NMDA ra

34 and subunits of l-type calcium channels and NMDA receptors, and increases CaMKIIalpha turnover in in

35 rrents that are insensitive to glutamate and NMDA; these currents remain poorly characterised and the

36 gi cell oscillations, on-beam inhibition and NMDA receptors causing first winner keeps winning of gra

37 ogenetic analysis reveals AMPA, kainate, and NMDA receptor families in insect genomes, suggesting con

38 ene expression revealed AMPA-, Kainate-, and NMDA-type subunits are expressed in zebrafish hair cells

39 dentified ionotropic glutamate receptors and NMDA-Rs, specifically, as potentially important cell sig

40 Opioid, serotonin and NMDA mechanisms acting in rostral ventromedial medulla p

41 s, dynamic unblocking of silent synapses and NMDA-receptor-dependent AP firing.

42 ceptor agonist, a 5-HT7 receptor antagonist, NMDA receptor antagonists, a TREK-1 receptor antagonist,

43 activation of eNMDARs by exogenously applied NMDA inhibited IA in MNCs obtained from sham, but not in

44 Activation of eNMDARs by exogenously applied NMDA inhibited IA in sham rats, but this effect was larg

45 FICANCE STATEMENT Memantine and ketamine are NMDA receptor (NMDAR) channel-blocking drugs with diverg

46 healthy subjects (HS), N-methyl-D-aspartate (NMDA) antagonists like memantine and ketamine increase P

47 mpound that acts as an N-methyl-D-aspartate (NMDA) modulator with glycine-like partial agonist proper

48 opionic acid (AMPA) to N-methyl-D-aspartate (NMDA) ratios, and matrix metalloproteinase activity.

49 plasticity, especially N-methyl-d-aspartate (NMDA) receptor (NMDAR)-dependent long-term potentiation

50 ccessfully to quantify N-methyl-d-aspartate (NMDA) receptor binding in humans.

51 with modulators at the N-methyl-d-aspartate (NMDA) receptor GluN2B N-terminal domain (NTD) aims for t

52 rst time, we show that N-methyl-d-aspartate (NMDA) receptor-dependent Ca(2+) transients are instructi

53 Evoked, N-methyl-D-aspartate (NMDA) receptor-mediated currents were recorded at baseli

54 on (Ca2+) flux through N-methyl-D-aspartate (NMDA) receptors activates Ca2+/calmodulin signal transdu

55 ssion of glutamatergic N-methyl-D-aspartate (NMDA) receptors and decreased expression of alpha-amino-

56 N-methyl-d-aspartate (NMDA) receptors are glutamate- and glycine-gated channel

57 N-Methyl-D-aspartate (NMDA) receptors are glutamate-gated excitatory channels

58 N-methyl-d-aspartate (NMDA) receptors are ligand-gated, cation-selective chann

59 ation of extrasynaptic N-methyl-d-aspartate (NMDA) receptors causes neurodegeneration and cell death.

60 find that ablation of N-methyl-D-aspartate (NMDA) receptors during postnatal development leads to ep

61 ve antagonists against N-methyl-D-aspartate (NMDA) receptors have played critical roles throughout th

62 by overstimulation of N-methyl-D-aspartate (NMDA) receptors, is a mechanism that causes secondary da

63 encing learning is the N-methyl-D-aspartate (NMDA) subtype 2B glutamate receptor (NR2B).

64 amate receptors of the N-methyl-d-aspartate (NMDA) subtype and resulted in removal of glucose transpo

65 s, kainic acid (KA) or N-methyl-D-aspartate (NMDA), contributed to significant, progressive hair cell

66 h the glutamate analog N-methyl-d-aspartate (NMDA), which is excito-toxic and induces RGC death.

67 N-methyl-d-aspartate (NMDA)-type ionotropic glutamate receptors mediate excita

68 ctively inhibit butyrylcholinesterase, block NMDA receptors containing NR2B subunits while maintainin

69 Finally, blocking NMDA, but not GABA, receptors causes ATM levels to rise

70 Furthermore, the same mutant also blocks NMDA-stimulated miRNA-mediated gene silencing.

71 c family kinases (SFKs) are involved in both NMDA-mediated activation of TrkB- and TrkB-mediated tyro

72 f Cacna1c exon 7, and also exclusion of both NMDA receptor gene Grin1 exon 4, and Enah exon 12, all c

73 cation in mitral cells, which was blocked by NMDA and mGluR1 receptor antagonists, converting mitral

74 eurodevelopmental disorders characterized by NMDA receptor-hypofunction.Proper brain function depends

75 Strengthening of synaptic connections by NMDA (N-methyl-d-aspartate) receptor-dependent long-term

76 t not NAD(+) reduces brain damage induced by NMDA injection.

77 chanism whereby elevated [Ca(2+)] induced by NMDA receptor activation modulates Ago2 and miRNA activi

78 cilitating extinction, which are mediated by NMDA receptors (NMDArs).

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

80 nterference with lipid signaling pathways by NMDA receptor inhibition is a novel and promising strate

81 I motoneurons are mediated predominantly by NMDA receptors and to a lesser extent by AMPA receptors,

82 beta/gamma power is significantly reduced by NMDA receptor blockade, a treatment that paradoxically e

83 Gamma oscillations and their regulation by NMDA receptors can be studied via their evoked power (ga

84 cortical network phenotype that is veiled by NMDA-mediated neurotransmission.

85 this study shows that chronic stress causes NMDA-receptor-dependent and subregion-specific cell deat

86 es provide the first view of the most common NMDA receptor assembly and show how incorporation of two

87 peripherally restricted, potent, competitive NMDA receptor antagonist 1l by a structure-activity stud

88 the design of subunit-selective competitive NMDA receptor antagonists by identifying a cavity for li

89 ase in GluA1 may be dependent on concomitant NMDA receptor (NMDAR) activation during self-administrat

90 annels that synergize with GluN2A-containing NMDA receptors to drive t-LTP at extended timing.

91 ole of AICD in controlling GluN2B-containing NMDA receptors (NMDARs) at immature excitatory synapses,

92 T tracer for imaging GluN1/GluN2B-containing NMDA receptors and used it to investigate in rats the do

93 al selectivity of AICP for GluN2C-containing NMDA receptors is more pronounced compared with DCS, sug

94 ints to an essential role of NR2A-containing NMDA receptors in CSD propagation in vitro; however, whe

95 me empirical data to understand how cortical NMDA transmission deficit may lead to opposite modulatio

96 nd that provision of extracellular NR delays NMDA-induced axonal degeneration (AxD) much more strongl

97 roximately 1 ms and mildly voltage-dependent NMDA receptor EPSCs of approximately 0.6 nS that decay i

98 R stimulation requires IP3Rs and can depress NMDA-evoked currents with modest intracellular Ca(2+) bu

99 -d-aspartate-dependent long-term depression (NMDA-LTD) at prefrontal excitatory synapses as a synapti

100 MPARs, are necessary and sufficient to drive NMDA receptor-dependent LTP and LTD, respectively.

101 in the trafficking of AMPA receptors during NMDA-receptor-dependent LTP at mature hippocampal synaps

102 rowing body of evidence supports an elevated NMDA receptor (NMDAR)-mediated glutamate excitatory func

103 The endogenous NMDA receptor (NMDAR) agonist D-aspartate occurs transie

104 Reduced levels of the endogenous NMDA receptor co-agonist d-serine were accompanied by in

105 n by the psychiatric risk gene TCF4 enhances NMDA receptor-dependent early network oscillations.

106 trical and optogenetic stimulation can evoke NMDA-mediated synaptic responses.

107 dulation of both intrinsic firing and evoked NMDA currents in pyramidal cells, whereas D2 receptor fu

108 potentiation without affecting basal-evoked NMDA currents, indicating that NMDAR-GluN2B receptors ar

109 ther the magnitude of the exogenously evoked NMDA current nor the expression of NMDAR subunits were a

110 ns to DNA damaging agents or the excitotoxin NMDA elicited similar results suggesting that IL-34 indu

111 te bath application activating extrasynaptic NMDA receptors.

112 A functional coupling between extrasynaptic NMDA receptors (eNMDARs) and the A-type K(+) current (IA

113 a functional coupling between extrasynaptic NMDA receptors (eNMDARs) and the A-type K(+) current (IA

114 e increased death signaling by extrasynaptic NMDA receptors caused by elevated extracellular glutamat

115 mbat the pathological triad of extrasynaptic NMDA receptor signaling that is common to many neurodege

116 neurogliaform cells remains normal following NMDA receptor-ablation.

117 SK3beta promotes neuronal survival following NMDA-induced injury.

118 ions as a neurotransmitter and coagonist for NMDA receptors and is involved in mediating synaptic pla

119 selective positive allosteric modulators for NMDA receptors.

120 ers, such as schizophrenia, that result from NMDA receptor-hypofunction have been mainly attributed t

121 himeric subunits that combined segments from NMDA and kainate receptors, subtypes with distinct pharm

122 bited and agonist-bound form of a functional NMDA receptor; however, other key functional states (par

123 ed ligand-binding domain of the GluN1-GluN2A NMDA receptor in complex with the GluN1 agonist glycine

124 (11)C-Me-NB1 enables imaging of GluN1/GluN2B NMDA receptor cross talk.

125 GluN1/GluN2B NMDA receptors are fully occupied at neuroprotective dos

126 circulating autoantibodies against glutamate NMDA receptor (NMDAR-Ab) in about 20% of psychotic patie

127 Although glutamate NMDA receptor (NMDAR)-mediated excitatory drive in the h

128 d with increased expression of glutamatergic NMDA receptors in phrenic motoneurons.

129 renic motoneuron expression of glutamatergic NMDA receptors is associated with spontaneous recovery a

130 TATEMENT We recorded neuronal glutamatergic (NMDA and AMPA) responses in prefrontal cortex (PFC) neur

131 ty and found that they exhibited hippocampal NMDA receptor hyperfunction, which likely drives the enh

132 These results indicate that alterations in NMDA-dependent glutamatergic transmission in Tg(CJD) mic

133 arvalbumin interneurons causes a decrease in NMDA-receptor-mediated postsynaptic currents and an incr

134 ngineered interlobe disulfide cross-links in NMDA receptors and found that the cross-linking produced

135 vior, and novel object recognition memory in NMDA receptor hypofunctioning NR1-knockdown mice, and we

136 mation deficits and associated reductions in NMDA receptor-mediated hippocampal synaptic plasticity.

137 ature on structure-function relationships in NMDA receptors, and will guide in-depth studies on the a

138 Regulatory roles of D-serine in NMDA receptor-mediated synaptic plasticity have been rep

139 that both psychostimulants acutely increase NMDA receptor (NMDAR)-mediated synaptic currents and dec

140 line AMPA/NMDA ratio, arising from increased NMDA currents enriched in the NR2B subunit with a concom

141 o work in the VTA, this was due to increased NMDA receptor function with no change in AMPA receptor f

142 mouse models that may be linked to increased NMDA receptor function.

143 metabolism and suggest that AbetaO-induced, NMDA receptor-mediated AMPK inhibition may play a key ro

144 totoxic injury in vitro, without influencing NMDA-induced intracellular calcium responses.

145 oxic neurodegeneration in MoCD and introduce NMDA-R antagonists as potential therapeutics for this fa

146 the mechanism for this upregulation involves NMDA receptor activity during cocaine use.

147 fficacy and safety of adjunctive lanicemine (NMDA channel blocker) in the treatment of major depressi

148 ogliaform cells are characterized by a large NMDA receptor-mediated component.

149 and functionally 'silent', expressing mainly NMDA receptors.

150 -100 microM glutamate or with 0.5-1.0 microM NMDA robustly activated Akt and ERK1/2.

151 Most NMDA receptors comprise two glycine-binding GluN1 and tw

152 Phrenic motoneuron NMDA NR1 subunit mRNA expression was approximately fourf

153 le food via downstream communication to mPFC NMDA receptors.

154 tor, approximately 1 nS, approximately 1 ms; NMDA receptor, approximately 0.6 nS, approximately 7 ms)

155 AR expression and/or function, since neither NMDA current magnitude or reversal potential, nor the le

156 se while ATR levels respond to GABA, but not NMDA, receptor blockade.

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

158 There are currently numerous NMDA receptor antagonists containing a variety of chemic

159 Post-ischemic activation of NMDA receptors (NMDARs) has been linked to NMDAR subunit

160 s phenomena, such as increased activation of NMDA receptors in pain-modulating areas.

161 e rat cerebral cortex, through activation of NMDA receptors.

162 emichannel activity reduced the amplitude of NMDA EPSCs in mouse layer 5 prefrontal cortex pyramidal

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

164 dues in PICK1 results in a complete block of NMDA-induced PICK1-Ago2 disassociation in cortical neuro

165 Pharmacological blockade of NMDA-R, calcium influx, or calpain activity abolished SS

166 ynapses, and loss of compartmentalization of NMDA receptor-mediated calcium influx.

167 ere is a shift in the subunit composition of NMDA receptors (NMDARs) resulting in a dramatic accelera

168 ffinity associated with a strong decrease of NMDA-evoked currents.

169 Genetic deletion of NMDA receptors on dopamine or striatal neurons or optoge

170 complex interfered with surface delivery of NMDA receptors to both extrasynaptic and synaptic membra

171 g and demonstrate by probing the dynamics of NMDA receptor ion channel and kinetics of glycine bindin

172 trial for FXTAS, we examined the effects of NMDA antagonist memantine on attention and working memor

173 ctrophysiological reversal of the effects of NMDA antagonists in rodents.

174 or the rapid-onset antidepressant effects of NMDA receptor inhibition and for the use of electrophysi

175 uations that shows a prominent expression of NMDA receptors (NMDARs) and nitric oxide synthase (NOS)

176 e-NB1 is suitable for the in vivo imaging of NMDA GluN1/GluN2B receptors and the assessment of recept

177 citatory transmission that is independent of NMDA receptors but requires co-activation of Ca(2+) -per

178 +) sources thus converge on the induction of NMDA receptor independent synaptic plasticity.

179 During the induction of NMDA-receptor-dependent LTP, Ca(2+) influx stimulates re

180 roglial network resulted in an inhibition of NMDA EPSC potentiation that was rescued by adding extrac

181 els and support the further investigation of NMDA receptor antagonists as a possible PTHS treatment.

182 To assess the potential involvement of NMDA receptor (NMDAR) dysfunction, we analyzed NMDA-depe

183 reveals that exposure to sublethal levels of NMDA does not alter phosphorylation of Akt, S6, and GSK3

184 LTP of NMDA and AMPA EPSCs after high-frequency stimulation was

185 -selective positive allosteric modulators of NMDA receptor function have therapeutically relevant eff

186 -selective positive allosteric modulators of NMDA receptors.

187 ion because Crispr/Cas9-mediated mutation of NMDA receptors rescued TCF4-dependent morphological phen

188 This activity requires the participation of NMDA receptors and is entirely driven by bottom-up spont

189 nd TrkB-mediated tyrosine phosphorylation of NMDA receptors.

190 ed neither accumulation at nor protection of NMDA-treated RGCs.

191 We show that reconstitution of NMDA-gated current in Xenopus oocytes, or C. elegans mus

192 This reduction of NMDA EPSCs was rescued by addition of D-serine in the ex

193 roglial network resulted in the reduction of NMDA EPSCs, which was rescued by adding extracellular D-

194 alance between relief and reestablishment of NMDA receptor Mg(2+) block.

195 to investigate the functional regulation of NMDA receptors (NMDARs).

196 obliterated ATP-mediated down-regulation of NMDA receptors.

197 lutamate concentrations or relocalization of NMDA receptors to extrasynaptic sites.

198 Here we investigated the role of NMDA receptors on mGluR-dependent long-term depression (

199 in, and involved SK-dependent suppression of NMDA receptor activation.

200 B subunit with a concomitant upregulation of NMDA-only, silent synapses.

201 Several sources of Ca(2+) thus converge on NMDA receptor independent LTP induction in O/A interneur

202 CA1 pathway, distinct forms of LTP depend on NMDA receptors (nmdaLTP) or L-type voltage-gated calcium

203 tramolecular potentiating role of glycans on NMDA receptors.

204 lcohol-exposed rats, and this was reliant on NMDA glycine site availability.

205 Here, we designed a set of optocontrollable NMDA receptors by directly incorporating single photoswi

206 eceptor, TrkB, ERK/MAP kinase activation, or NMDA receptors blocks this attenuating effect, indicatin

207 When glutamate or NMDA was injected directly into crush-injured rat sciati

208 Finally, hair cells exposed to KA or NMDA appear to undergo apoptotic cell death.

209 f afferent and efferent innervation-to KA or NMDA.

210 stration of either a D1 dopamine receptor or NMDA glutamate receptor antagonist.

211 Other NMDA open channel blockers ketamine and memantine showed

212 e, and comparisons with stimulants and other NMDA antagonists.

213 al activity and increases AMPA-mediated over NMDA-mediated excitatory synaptic currents.

214 Ketamine, a pan-NMDA receptor channel blocker, and CP-101,606, an NR2B-s

215 KEY POINTS: NMDA receptor (NMDAR)-mediated Ca(2+) signalling plays a

216 tage-gated Ca(2+) channels, not postsynaptic NMDA receptors (NMDARs), and does not require glutamate

217 piking activity, and depends on postsynaptic NMDA receptors and GSK3beta activity.

218 such as PYD-106, that selectively potentiate NMDA receptors that contain the GluN2C subunit have stru

219 he ability of PDE2A inhibitors to potentiate NMDA signaling and their further development for clinica

220 Presynaptic NMDA receptors (preNMDARs) control synaptic release, but

221 t that MC-GC synapses undergo a presynaptic, NMDA-receptor-independent form of long-term potentiation

222 or STAT blocked LTD induction and prevented NMDA-induced AMPA (alpha-amino-3-hydroxy-5-methyl-4-isox

223 increased amplitude of NMDAR-EPSCs and puff NMDA currents in labeled PVN neurons in SHRs but had no

224 sal amplitude of evoked NMDAR-EPSCs and puff NMDA currents in retrogradely labeled PVN neurons were s

225 NMDAR-mediated EPSCs and puff NMDA-elicited currents were recorded in spinally project

226 GLYX-13 is a putative NMDA receptor modulator with glycine-site partial agonis

227 that the N-methyl-D-aspartic acid receptor (NMDA-R) is expressed by macrophages and essential for an

228 it acts as an N-methyl D-aspartate receptor (NMDA-R) agonist, leading to calcium influx and downstrea

229 f N-methyl-d-aspartic acid (NMDA) receptors (NMDA-Rs), alpha-amino-3-hydroxy-5-methyl-4-isoxazoleprop

230 fferences in agonist efficacy at recombinant NMDA receptor subtypes.

231 GluN2B antagonism reduced NMDA receptor-mediated currents more efficaciously in ce

232 I and MMN in psychotic disorders, as reduced NMDA activity is implicated in the pathogenesis of these

233 luN2B-selective inhibitor ifenprodil reduced NMDA-activated currents, but had no effect on the mechan

234 ased spine density, concomitant with reduced NMDA-evoked currents and impaired NMDAR-dependent insert

235 However, regenerative NMDA conductances can be activated with stronger stimula

236 Here we report a physiologically relevant NMDA-receptor-independent mechanism that drives increase

237 Both st-LTP and st-LTD required NMDA receptors, but st-LTP also required reinforcing sig

238 nriched at the site of stimulation, required NMDA receptor activity, and localized preferentially at

239 TA-CA1 LTD requires NMDA receptor activation and is independent of PI3K or E

240 hese approaches, we estimate that CaM senses NMDA receptor Ca(2+) influx at approximately 9 nm from t

241 or direction computations, in which "silent" NMDA receptors play critical roles.

242 d-cycloserine (DCS), which is a glycine site NMDA receptor agonist, can enhance extinction of conditi

243 ead to efficient temporal summation of small NMDA currents, dynamic unblocking of silent synapses and

244 Knockdown of STN NMDA receptors, which also suppresses proliferation of G

245 n of the STN and increased activation of STN NMDA receptors.

246 ngages calmodulin (CaM) to reduce subsequent NMDA receptor activity in a process known as Ca(2+)-depe

247 esults is hampered by the lack of a suitable NMDA PET tracer for assessing the receptor occupancy of

248 r-561 phosphorylation is induced by synaptic NMDA receptor activation, and the SH3-GK domains exhibit

249 ng signaling effector in the common synaptic NMDA-R-CaMKII-SynGap-Ras-BRaf-MEK-ERK transduction casca

250 (i) reduced GluN1 subunit levels in synaptic NMDA receptors and related currents, and (ii) impaired r

251 The subunit composition of synaptic NMDA receptors (NMDAR), such as the relative content of

252 paradoxically express low levels of synaptic NMDA receptors.

253 of the dorsal SCN via specific pre-synaptic NMDA receptor assemblies containing NR2C subunits.

254 Thus, pharmacotherapy targeting NMDA receptors may inadvertently produce substantial adv

255 Electrophysiological recordings show that NMDA-induced injury causes a significant decrease in spo

256 The NMDA-R and Toll-like receptor-4 were not required for pr

257 rinergic receptor antagonist RB2, blocks the NMDA-induced Kir activation.

258 Finally, the NMDA-R antagonist memantine was protective against the m

259 long-term alcohol exposure and highlight the NMDA receptor coagonist site as a potential therapeutic

260 ionotropic glutamate receptors (iGluRs), the NMDA and kainate receptors, mediate a majority of excita

261 ne-like partial agonist properties; like the NMDA receptor antagonist ketamine GLYX-13 produces rapid

262 diating the tPA response in macrophages, the NMDA-R provides a pathway by which the fibrinolysis syst

263 To decrypt the mechanism of the NMDA receptor activation, structural modeling is essenti

264 iotransmitter, D-serine, a co-agonist of the NMDA receptor at the glycine-binding site, can be releas

265 ptors as well as the PCP binding site of the NMDA receptor.

266 alizing the magnitude and time course of the NMDA-DeltaCa(2+) responses between the two experimental

267 zocilpine and by silencing expression of the NMDA-R NR1 subunit.

268 se, the enzyme responsible for producing the NMDA co-agonist d-serine.

269 t vasodilation in nearby capillaries via the NMDA receptors-neuronal nitric oxide synthase signaling

270 Uniquely within the NMDA receptor family, GluN1/GluN3 receptors produce glyc

271 This NMDA receptor-signaling is prerequisite for developmenta

272 and synaptic K63-polyUb levels and, through NMDA receptors, drives rapid, CYLD-mediated PSD-95 deubi

273 with little contribution from entry through NMDA receptors or voltage-gated sodium channels.

274 ocalized [Na(+)]i increases mediated through NMDA receptors.SIGNIFICANCE STATEMENT Dendritic spines,

275 y was through AMPA receptors and not through NMDA receptors or through voltage-gated sodium channels

276 Thus, NMDA-induced excitotoxicity involves a mechanism that re

277 ater, dendritic spine morphology and AMPA to NMDA ratios were restored as animals became motivated to

278 tic remodeling in the hippocampus leading to NMDA receptor-dependent memory formation and synaptic pl

279 unctional evidence for CaM preassociation to NMDA receptors in living cells.

280 uch as GSK3beta, FOXO1, and mTORC1, prior to NMDA-induced injury.

281 ction (dpi) show that these cells respond to NMDA application with tonic currents, and that both elec

282 ining AMPA receptors (AMPARs) in response to NMDA receptor (NMDAR) stimulation causes a reduction in

283 re shed by metalloproteinases in response to NMDA receptor activation.

284 after cocaine, but no change in the AMPA-to-NMDA ratio.

285 PPN-innervated synapses reducing the AMPA-to-NMDA receptor-mediated current ratio.

286 Ketamine and the two NMDA NR2B NAMs produced selective impairments in memory

287 Memantine and ketamine are clinically useful NMDA receptor (NMDAR) open channel blockers that inhibit

288 emical induction of long-term depression via NMDA receptor activation causes the dissociation of Ago2

289 starbursts via AMPA receptors and DSGCs via NMDA receptors.

290 In the classical view, NMDA receptors (NMDARs) are stably expressed at the post

291 ts were eliminated in nrap-1 mutants, as was NMDA-dependent behavior.

292 Whereas NMDA receptors gate channels with slow kinetics, respons

293 ing synaptic potentiation in oriens, whereas NMDA and adenosine receptors counteracted unpaired strat

294 osure in stationary mice or in mice in which NMDA receptors were partially blocked did not significan

295 AMPA and kainate receptors, along with NMDA receptors, represent different subtypes of glutamat

296 ortical oscillatory dynamics associated with NMDA receptor dysfunction in SZ patients.

297 akpoint cluster region (BCR) associates with NMDA receptors (NMDARs) along with Tiam1 and that this p

298 While interference with NMDA receptor function blocks AMPA receptor upregulation

299 P2X receptors, co-localized with NMDA receptors in the excitatory synapses, can be activa

300 ta/gamma power is significantly reduced with NMDA receptor blockade, revealing a latent cortical netw