ライフサイエンスコーパス: NMDA receptor

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

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

3 starbursts via AMPA receptors and DSGCs via NMDA receptors.

4 paradoxically express low levels of synaptic NMDA receptors.

5 selective positive allosteric modulators for NMDA receptors.

6 te bath application activating extrasynaptic NMDA receptors.

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

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

9 onse and microglia do not express functional NMDA receptors.

10 (LTD) forms that relay on the activation of NMDA receptors.

11 lex mediating the constitutive exocytosis of NMDA receptors.

12 ic calcium levels throughout their action on NMDA receptors.

13 ion in ATD regulates the channel activity in NMDA receptors.

14 t are highly selective for GluN2A-containing NMDA receptors.

15 nd TrkB-mediated tyrosine phosphorylation of NMDA receptors.

16 obic box differed between mammalian AMPA and NMDA receptors.

17 tramolecular potentiating role of glycans on NMDA receptors.

18 le food via downstream communication to mPFC NMDA receptors.

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

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

21 -selective positive allosteric modulators of NMDA receptors.

22 ating Ca(2+)-permeable N-methyl-D-aspartate (NMDA) receptors.

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

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

25 neurogliaform cells remains normal following NMDA receptor-ablation.

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

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

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

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

30 l synapse pruning was slowed by reduction of NMDA receptor activation or expression and by reduction

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

32 LTPGABA is induced by postsynaptic NMDA receptor activation, leading to calcium increase an

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

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

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

36 sion in response to calcium influx caused by NMDA receptor activation.

37 terval between spikes, N-methyl-D-aspartate (NMDA) receptor activation, and Calcium/calmodulin-depend

38 Neuronal NMDA receptor activity controls glial motility through i

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

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

41 Localization required NMDA receptor activity, a dynamic actin cytoskeleton, an

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

43 ndrites in the tadpole optic tectum requires NMDA receptor activity.

44 ic modulators can upregulate or downregulate NMDA receptor activity.

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

46 gands for the detection of changes in active NMDA receptor and GABA-A receptor in the injured brain.

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

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

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

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

51 chanism as Dyn A peptides were shown to bind NMDA receptors and potentiate their glutamate-evoked cur

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

53 dependent postsynaptic mechanisms, involving NMDA receptors and T-type Ca(2+)channels that allow nonl

54 These mechanisms, involving NMDA receptors and T-type Ca(2+)channels, require tempor

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

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

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

58 spike cycle, likely involving recruitment of NMDA receptors and voltage-gated conductances.

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

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

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

62 s upregulated, leading to over-activation of NMDA receptors, and the reserve pool of glutamatergic sy

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

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

65 STN activity was rescued by NMDA receptor antagonism or the break down of hydrogen p

66 The phenotype appears to be influenced by NMDA receptor antagonism, consistent with a critical rol

67 ial oxidant stress, which was ameliorated by NMDA receptor antagonism.

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

69 rectifier (Kir)2.1, which was blocked by the NMDA receptor antagonist D-AP5.

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

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

72 The NMDA receptor antagonist-induced alteration in neuronal

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

74 ted in healthy volunteers under ketamine, an NMDA receptor antagonist.

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

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

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

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

79 r animal models with neonatal application of NMDA receptor antagonists.

80 depressant activity of N-methyl-D-aspartate (NMDA) receptor antagonists and negative allosteric modul

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

82 NMDA receptors are also implicated in psychiatric and ne

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

84 AMPA and NMDA receptors are glutamate-gated ion channels that med

85 NMDA receptors are ionotropic glutamate receptors that f

86 NMDA receptors are ligand-gated ion channels that underl

87 NMDA receptors are tetrameric ligand-gated ion channels.

88 N-methyl-d-aspartate (NMDA) receptors are expressed throughout the kidney, and

89 N-methyl-D-aspartate (NMDA) receptors are glutamate- and glycine-gated channel

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

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

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

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

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

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

96 of temporal-dependent plasticity mediated by NMDA receptors at thalamocortical synapses in acute PFC

97 A spikes pharmacologically while maintaining NMDA receptors available to initiate synaptic plasticity

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

99 ive cognition 4 months after pharmacological NMDA receptor blockade already were affected by disrupte

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

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

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

103 mimicking axonal activity, and shortened by NMDA receptor blockers.

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

105 Recent crystal structures of GluN1-GluN2B NMDA receptors bound to agonists and an allosteric inhib

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

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

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

109 in the adult brain do not express functional NMDA receptors by recording from microglia cultured from

110 e strong expression of N-methyl-D-aspartate (NMDA) receptors by its cells, are consistent with theore

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

112 h required the activation of NR2B-containing NMDA receptors, Ca(2+) influx, and calpain activation.

113 dings provide strong evidence that targeting NMDA receptors can be a safe and effective treatment for

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

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

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

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

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

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

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

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

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

123 he continual presence of glutamate, AMPA and NMDA receptors containing the GluN2A or GluN2B subunit e

124 tive characteristic of N-methyl-D-aspartate (NMDA) receptors containing a GluN2A subunit is that thei

125 is paradox, we found that both drugs induced NMDA receptor-containing, AMPA receptor-silent excitator

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

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

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

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

130 neuronal Ca(2+) and nitric oxide (NO) in an NMDA receptor-dependent manner.

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

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

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

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

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

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

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

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

139 Blocking NMDA receptors during later stages of circuit developmen

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

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

142 ntagonist of glutamate/N-methyl-D-aspartate (NMDA) receptors, elicits antidepressant actions in hours

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

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

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

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

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

148 While interference with NMDA receptor function blocks AMPA receptor upregulation

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

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

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

152 Whereas NMDA receptors gate channels with slow kinetics, respons

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

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

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

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

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

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

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

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

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

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

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

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

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

166 tly visualized individual exocytic events of NMDA receptors in rat hippocampal neurons by total inter

167 processing, and illustrate a novel role for NMDA receptors in retinal processing.

168 t mechanisms that are regulated by different NMDA receptors in STN.

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

170 Impairment of purinergic modulation of NMDA receptors in the PSD-95 mutants dramatically decrea

171 d that hypofunction of N-methyl-d-aspartate (NMDA) receptors in brain networks supporting perception

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

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

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

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

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

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

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

179 k provides mechanistic insight to allosteric NMDA receptor inhibition, thereby facilitating the devel

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

181 er, how the ATD and LBD move to activate the NMDA receptor ion channel remains unclear.

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

183 The involvement of neuronal NMDA receptors is crucial because NMDA mimics that respo

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

185 The physiology of N-methyl-d-aspartate (NMDA) receptors is fundamental to brain development and

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

187 ed guanylate kinase) scaffolding proteins or NMDA receptors, it is necessary for the recruitment of A

188 nockout mice display a transient speeding of NMDA receptor kinetics during the critical period for TC

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

190 ntaneous and evoked glutamate release driven NMDA receptor mediated Ca2+ transients often occur at th

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

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

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

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

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

196 hancement of long-term potentiation (LTP) of NMDA receptor-mediated glutamatergic transmission in the

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

198 STN neurons exhibited prolonged NMDA receptor-mediated synaptic currents, caused by a de

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

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

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

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

203 how that the stimulation of oligodendroglial NMDA receptors mobilizes glucose transporter GLUT1, lead

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

205 acilitating the development of novel classes NMDA receptor modulators as therapeutic agents.

206 hen myelinated optic nerves from conditional NMDA receptor mutants are challenged with transient oxyg

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

208 n knowledge concerning the role of glutamate NMDA receptors (NMDA-Rs) in the striatum, understanding

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

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

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

212 NMDA receptor (NMDAR) activation in prefrontal cortex (P

213 urons in prefrontal cortex (PFC) mediated by NMDA receptor (NMDAR) activation.

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

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

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

217 Application of MK801 to block neuronal NMDA receptor (NMDAR) currents confirmed a significant r

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

219 Despite strong evidence for NMDA receptor (NMDAR) hypofunction as an underlying fact

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

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

222 eracting with C-kinase 1 (PICK1) to regulate NMDA receptor (NMDAR)-induced AMPAR endocytosis and cere

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

224 accompanied by a decreased ratio of AMPAR-to-NMDA receptor (NMDAR)-mediated EPSCs.

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

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

227 Long-term potentiation (LTP) of NMDA receptor (NMDAR)-mediated glutamatergic transmissio

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

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

230 ivation of D1-dopamine receptors, as well as NMDA receptors (NMDAR) and their calcium-dependent downs

231 e of other ion channels/receptors, including NMDA receptors (NMDAR), in mGluR-LTD.

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

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

234 The magnitude of [Ca2+] increase caused by NMDA-receptor (NMDAR) and voltage-gated Ca2+ -channel (V

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

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

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

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

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

240 NMDA receptors (NMDARs) are ionotropic glutamate recepto

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

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

243 NMDA receptors (NMDARs) contribute to several neuropatho

244 first biochemical purification of endogenous NMDA receptors (NMDARs) directly from adult mouse brain.

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

246 PSD-95), a key scaffold protein that anchors NMDA receptors (NMDARs) in PSD via GluN2-type receptor s

247 Although antagonism of cell-surface NMDA receptors (NMDARs) may trigger ketamine's psychoact

248 Ionotropic activation of NMDA receptors (NMDARs) requires agonist glutamate and c

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

250 matergic synapses in the CNS is regulated by NMDA receptors (NMDARs) that gradually change from a Glu

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

252 To enhance physiological function of NMDA receptors (NMDARs), we identified positive alloster

253 postsynaptic sites bearing GluN2B-containing NMDA receptors (NMDARs), which mature into low-Pr, GluN2

254 ere it associates with the GluN2A subunit of NMDA receptors (NMDARs).

255 regulates surface and synaptic expression of NMDA receptors (NMDARs).

256 postsynaptic spikes to activate postsynaptic NMDA receptors (NMDARs).

257 form of plasticity requires coactivation of NMDA receptors (NMDARs).

258 3 pyramidal cells requires the activation of NMDA receptors (NMDARs).

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

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

261 ease in MA and spinal phosphorylation of the NMDA receptor NR1 subunit expression on day 7 after surg

262 P amplification by T-type Ca(2+)channels and NMDA receptors occurs when synaptic inputs are either cl

263 lease glutamate and oligodendrocytes express NMDA receptors of unknown function.

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

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

266 mpound action potential and/or Memantine, an NMDA receptor open channel blocker, would reduce noise-i

267 xide, whereas LTDGABA depends on presynaptic NMDA receptor opening.

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

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

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

271 Therefore, neuromuscular NMDA receptors play previously unsuspected roles in neur

272 requirements for allosteric potentiation of NMDA receptor pores by pregnenolone sulfate, 24(S)-hydro

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

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

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

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

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

278 tanding where and how these compounds act on NMDA receptors should aid in designing better therapeuti

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

280 This NMDA receptor-signaling is prerequisite for developmenta

281 is likely because of a switch from opioid to NMDA- receptor signalling, while for wt Dyn A, this swit

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

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

284 se and rapidly reversible optical control of NMDA receptor subtypes, LiGluNs should help unravel the

285 fferences in agonist efficacy at recombinant NMDA receptor subtypes.

286 erlies the mechanism of KIF17 binding to the NMDA receptor subunit 2B (NR2B).

287 receptor expression and a decrease in GluN2B NMDA receptor subunits.

288 in mediating the constitutive exocytosis of NMDA receptors, suggesting that this SNARE complex is in

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

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

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

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

293 cryomicroscopy and electrophysiology to rat NMDA receptors to show that, in the absence of ifenprodi

294 ld help unravel the contribution of specific NMDA receptors to synaptic transmission, integration and

295 continuous presence of saturating agonists, NMDA receptors undergo stationary gating, in which the c

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

297 hat decrease signaling through neuromuscular NMDA receptors, whereas application of exogenous NMDA at

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

299 NMDA receptors, which regulate synaptic strength and are

300 Distinct complements of AMPA and NMDA receptors within different interneuron subpopulatio