ライフサイエンスコーパス: NMDA receptor

1 e-NB1 binding to the human GluN2B-containing NMDA receptor.

2 ligand for imaging the GluN2B subunit of the NMDA receptor.

3 he two agonists glutamate and glycine in the NMDA receptor.

4 ons in the neonatal cortex via high-affinity NMDA receptors.

5 the actions of therapeutic agents targeting NMDA receptors.

6 een GluN2A(N615K) diheteromers and wild-type NMDA receptors.

7 ription, expression and function of AMPA and NMDA receptors.

8 bility, and increased levels of postsynaptic NMDA receptors.

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

10 le food via downstream communication to mPFC NMDA receptors.

11 municating through endocannabinoid-regulated NMDA receptors.

12 nd TrkB-mediated tyrosine phosphorylation of NMDA receptors.

13 tramolecular potentiating role of glycans on NMDA receptors.

14 riatal spiny projection neurons (SPNs) - not NMDA receptors.

15 modulation of GluN2C- and GluN2D-containing NMDA receptors.

16 uit to the impact of transient disruption of NMDA receptors.

17 subunit composition or the protein levels of NMDA-receptors.

18 the GluN2B subunit of N-methyl-d-aspartate (NMDA) receptors.

19 NMDA receptor activation also increased the frequency of

20 This translocation depended on NMDA receptor activation and Ras-MAPK signaling.

21 A key role for NMDA receptor activation in impairing plasticity followi

22 NMDA receptor activation is accompanied by local calcium

23 ic, to inhibitory synapses, quashing further NMDA receptor activation necessary for inducing more exc

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

25 a novel role of SULT4A1 in the modulation of NMDA receptor activity and strongly contributes to expla

26 Here, we show that selectively increasing NMDA receptor activity in inhibitory neurons using an NM

27 rmalizes the increased pre- and postsynaptic NMDA receptor activity of hypothalamic presympathetic ne

28 ter receptors, such as N-methyl-d-aspartate (NMDA) receptors, affect whole cell currents only after s

29 ologous cells, mutant receptors had enhanced NMDA receptor agonist potency and slow deactivation foll

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

31 of 192 healthy participants received either NMDA receptor agonists/antagonists (D-cycloserine/dextro

32 t and efficacious co-agonist of GluN1/GluN2C NMDA receptors, AICP, was found to reduce the spike freq

33 diated by the N-methyl-d-aspartate receptor (NMDA) receptor, although NMDA-independent mechanisms are

34 es compound binding site in the GluN1-GluN2B NMDA receptor amino terminal domain and show that the in

35 f postsynaptic response occurrence acting at NMDA receptors and decreases this probability acting at

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

37 erneurons in stratum oriens does not require NMDA receptors and the induction mechanisms are incomple

38 ent on extracellular glutamate diffusion and NMDA receptors and the other dependent on extracellular

39 ating action potential due to the opening of NMDA receptors and voltage dependent calcium channels.

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

41 The findings suggest that an NMDA receptor antagonist attenuates corticosteroid effec

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

43 We administered the NMDA receptor antagonist MK-801 and the GABA(A) receptor

44 xtromethadone; REL-1017) is a noncompetitive NMDA receptor antagonist with an apparently favorable sa

45 r administration of either dextromethorphan (NMDA receptor antagonist) or placebo across two sessions

46 Ketamine, an NMDA receptor antagonist, has emerged as a new rapid-act

47 The uncompetitive low-affinity NMDA receptor antagonist, memantine, acutely increases e

48 ave demonstrated the ability of ketamine, an NMDA receptor antagonist, to induce rapid (within hours)

49 The N-methyl-D-aspartate (NMDA) receptor antagonist ketamine is associated with ra

50 covery of ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist that produces rapid and sustai

51 Ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, can rapidly alleviate depress

52 c glutamate signaling using subtype-specific NMDA receptor antagonists in vitro and in vivo We report

53 Moreover, NMDA receptor antagonists MK-801 and memantine prevented

54 This action was not replicated by NMDA receptor antagonists or a chemical variant of ketam

55 NMDA receptor antagonists prevented medullary SD and apn

56 onic treatment of homozygous mouse pups with NMDA receptor antagonists significantly delayed the onse

57 Introduction of NMDA receptor antagonists was correlated with a decrease

58 odel data suggest that N-methyl-D-aspartate (NMDA) receptor antagonists may block corticosteroid effe

59 to ketamine and other N-methyl-D-aspartate (NMDA) receptor antagonists.

60 odulatory effects on signals elicited by the NMDA-receptor antagonists phencyclidine (PCP) and ketami

61 .SIGNIFICANCE STATEMENT At central synapses, NMDA receptors are a major class of excitatory glutamate

62 NMDA receptors are also implicated in psychiatric and ne

63 The GluN2C- and GluN2D-containing NMDA receptors are distinct from GluN2A- and GluN2B-cont

64 NMDA receptors are excitatory ion channels with fundamen

65 NMDA receptors are ionotropic calcium-permeable glutamat

66 NMDA receptors are neurotransmitter-gated ion channels t

67 N-Methyl-d-aspartate (NMDA) receptors are Ca(2+)-permeable channels gated by g

68 A receptor influences the activity of nearby NMDA receptors, as a possible coupling mechanism.

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

70 neuronal nitric oxide synthase (nNOS) and of NMDA receptors blocked potentiation, indicating that NO

71 ould be reversed by an N-methyl-D-aspartate (NMDA) receptor blocker.

72 ral excitability and the effects of AMPA and NMDA receptor blockers on functional connectivity.

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

74 uggest GluN2C-selective in vivo targeting of NMDA receptors by AICP.

75 C-containing receptors because inhibition of NMDA receptors by AP5 did not affect spike frequency in

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

77 rrents in rod bipolar cells, suggesting that NMDA receptors can drive release of GABA from A17 amacri

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

79 We also found that NMDA receptor channel blocker produced a deficit in prep

80 We also examined the response to NMDA receptor channel blockers in these mouse strains an

81 rapid-acting antidepressants that act at the NMDA receptor complex, but without dissociative and psyc

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

83 Triheteromeric NMDA receptors contain two GluN1 and two distinct GluN2

84 Here, we identified NMDA receptors containing the 2A subunit (GluN2A) on par

85 s in physiologically relevant triheteromeric NMDA receptors containing two GluN1 and two distinct Glu

86 from female rats, we found no evidence that NMDA receptors contribute to postsynaptic currents evoke

87 Here we report that the NMDA receptor controls cell competition of epithelial ce

88 Together, these new results demonstrate that NMDA receptor currents are negatively coupled through CD

89 Synaptic NMDA receptor currents are subject to Ca(2+)-dependent i

90 We found that, like ketamine, HNK reduced NMDA receptor currents in a dose-, pH-, and voltage-depe

91 ts show that 2R,6R-hydroxynorketamine blocks NMDA receptor currents with low affinity and weak voltag

92 system, ketamine acts primarily by blocking NMDA receptor currents.

93 d that PCDH7 overexpression reduces synaptic NMDA receptor currents.

94 nfluence the activity-dependent reduction in NMDA receptor currents.SIGNIFICANCE STATEMENT At central

95 nstrate that glutamate signaling through the NMDA receptor, cytosolic phospholipase A2, COX-2, and mP

96 Crucially, we show that histamine permits NMDA receptor-dependent corticostriatal synaptic plastic

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

98 We now directly address this question for NMDA receptor-dependent long-term depression (LTD) in th

99 NMDA receptor-dependent long-term depression (NMDAR-LTD)

100 synapses and show that histamine facilitates NMDA receptor-dependent LTP via H(3) receptors during th

101 te that the growth of these signals requires NMDA receptor-dependent plasticity within the NAc, revea

102 elta9-THC and endocannabinoids that regulate NMDA receptor-dependent synaptic plasticity of glutamate

103 N-methyl-D-aspartate (NMDA) receptor-dependent LTP requires trans-synaptic bin

104 ll-diameter afferents predominantly evoke an NMDA-receptor-dependent form of PSI that inhibits large-

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

106 Surprisingly, inhibition of NMDA receptors during HFS "uncovered" a persistent form

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

108 Here, we study the role of glutamate and NMDA receptor dynamics in the context of an ionic electr

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

110 cations for neurological disorders involving NMDA receptor dysfunction such as schizophrenia and depr

111 y, such as dopamine dysregulation, glutamate/NMDA receptor dysfunction, neuroinflammation or redox im

112 e therapeutic in pathologies associated with NMDA receptor dysfunction.

113 Anti-IgLON5 and anti-NMDA receptor encephalitis exemplify two diseases in whi

114 description of this disease, whereas in anti-NMDA receptor encephalitis, sleep disorders vary accordi

115 induced damage caused by toxic extrasynaptic NMDA receptor (eNMDAR) signaling.

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

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

118 all LAR-RPTPs led to a reduction in synaptic NMDA-receptor EPSCs, without changing the subunit compos

119 (2+) imaging, we verified that activation of NMDA receptors evoked an increase of intracellular Ca(2+

120 ectrophysiological recordings of recombinant NMDA receptors expressed in HEK-293 cells.

121 roscopic responses elicited from recombinant NMDA receptors expressed in human embryonic kidney 293 c

122 ansmission mediated by n-methyl-d-aspartate (NMDA) receptors following stimulation of non-motor regio

123 atergic transmission that does not depend on NMDA receptors for its induction but, instead, requires

124 tPA deficiency prevents NMDA receptors from triggering nitric oxide production,

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

126 on, perineural net degradation, and impaired NMDA receptor function.

127 ility to the impact of transient blockade of NMDA receptor function.

128 Whereas NMDA receptors gate channels with slow kinetics, respons

129 This was accompanied by increased NMDA receptor gating, dependent on mGluR5 and linked to

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

131 In the CNS, NMDA receptors generate large and highly regulated Ca(2+

132 Hypofunction of NMDA receptors has been considered a possible cause for

133 ependent inhibition of N-methyl-D-aspartate (NMDA) receptors has important therapeutic implications f

134 alamus are endogenously activated to sustain NMDA receptor hyperactivity and elevated sympathetic out

135 The changes reported here are centered on NMDA receptor hyperactivity, hyperplasticity, and hypere

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

137 Cul3 deficiency in forebrain or PFC induces NMDA receptor hypofunction, while Cul3 loss in striatum

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

139 ds on the human DG/CA3 region implicates the NMDA receptor in human hippocampal volume losses with co

140 of intragastric sucrose, and deletion of the NMDA receptor in these neurons, which affects bursting a

141 ognitive benefit of the direct antagonism of NMDA receptors in AD, we here focus on an alternative wa

142 GluN1/2B/2D receptors are also observed for NMDA receptors in hippocampal interneurons but not CA1 p

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

144 , shows greater potency against GluN1-GluN2B NMDA receptors in such low pH environments, allowing tar

145 r resting membrane potentials, activation of NMDA receptors in the absence of depolarization or Ca(2+

146 se the functional expression and activity of NMDA receptors in the mature PL-PFC.

147 ransients were reduced by ~50% upon blocking NMDA receptors in the neocortex, but not hippocampus.

148 reatment were reduced by inhibiting AMPA and NMDA receptors in the spinal cord.

149 logical blockade of GluN2C/GluN2D-containing NMDA receptors in vivo during the period of tonic intern

150 to the list of sources of Ca(2+) that induce NMDA receptor independent LTP in hippocampal oriens inte

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

152 knocking out the NMDA receptor indicating an NMDA receptor-independent effect.

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

154 llular cAMP persisted after knocking out the NMDA receptor indicating an NMDA receptor-independent ef

155 asked whether Ca(2+) influx through a single NMDA receptor influences the activity of nearby NMDA rec

156 The GluN2C subunit of the NMDA receptor is enriched in the neurons in nucleus reti

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

158 e role, but that glutamatergic signaling via NMDA receptors is required for OSN synaptic refinement.

159 es on neurons, but the role of extrasynaptic NMDA receptors is unclear.

160 Ca(2+) influx through NMDA receptors leads to channel inactivation through a p

161 How postsynaptic AMPA- and NMDA-receptor levels are regulated, however, remains unc

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

163 GluN2C/GluN2D-containing NMDA receptors mediate the majority of this current and

164 N-methyl-D-aspartate (NMDA) receptors mediate synaptic excitatory signaling in

165 These observations suggest that (1) NMDA receptor mediated LTP is observed in nociceptors ac

166 Specifically, the NMDA receptor mediated processes may suppress endocannab

167 itored in juvenile mice, but again decreased NMDA-receptor mediated synaptic transmission.

168 and (2) there may be an interaction between NMDA receptor-mediated and endocannabinoid-mediated form

169 synaptic transmission and this LTP was both NMDA receptor-mediated and synapse-specific.

170 , a key molecule necessary for iMF, bypasses NMDA receptor-mediated constraints, thereby rescuing pla

171 IB2 KO granule cells showed a larger NMDA receptor-mediated current and enhanced intrinsic ex

172 Electrophysiological studies showed reduced NMDA receptor-mediated currents in cholinergic neurons o

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

174 hese synapses have larger AMPA receptor- and NMDA receptor-mediated events.

175 this remodeling requires neural activity and NMDA receptor-mediated glutamatergic transmission.

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

177 innervation of D2 SPNs and stronger cortical NMDA receptor-mediated inputs to D1 SPNs, both in the se

178 ty that is largely insensitive to changes in NMDA receptor-mediated neurotransmission.

179 results show that seizures are initiated by NMDA receptor-mediated NOX-induced oxidative stress and

180 essing neurons to vagal inputs by increasing NMDA receptor-mediated synaptic currents and that NTS NM

181 NMDA receptor-mediated synaptic currents in heterozygous

182 suggest that PirB is an integral part of an NMDA receptor-mediated synaptic mechanism that maintains

183 In addition, SPARCL1 but not THBS4 tripled NMDA receptor-mediated synaptic responses.

184 2) O(2) resulting from N-methyl-D-aspartate (NMDA) receptor-mediated activation of nicotinamide adeni

185 ansporters, boosting glutamate spillover and NMDA-receptor-mediated inter-synaptic cross-talk.

186 Deletion of LAR-RPTPs decreased NMDA-receptor-mediated responses by a trans-synaptic mec

187 in cultured neurons or in vivo, but impaired NMDA-receptor-mediated responses.

188 y also suggest a close interrelation between NMDA-receptor-mediated sodium influx and calcium signali

189 Moreover, neocortical astrocytes experience NMDA-receptor-mediated sodium influx, which hippocampal

190 e 4 (SS4) dramatically enhanced postsynaptic NMDA-receptor-mediated, but not AMPA-receptor-mediated,

191 4 suppressed AMPA-receptor-mediated, but not NMDA-receptor-mediated, synaptic responses, while altern

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

193 , a newly identified glycine-site agonist of NMDA receptors, modulates the function of reticular thal

194 onnexin 36 on AII amacrines, suggesting that NMDA receptor modulation of gap junction coupling betwee

195 es a variety of synaptic proteins, including NMDA receptors (NAMDRs).

196 ors expressed in human HEK293 cells and from NMDA receptors native to hippocampal neurons from male a

197 To model possible effects of NMDA receptor (NMDA-R) antagonism on this behaviour, we

198 N) in which grin1, the gene that encodes the NMDA receptor (NMDA-R) GluN1 subunit, is deleted in SCs.

199 We previously reported that SCs express the NMDA receptor (NMDA-R), which activates cell signaling i

200 atergic synapses in a complex with glutamate NMDA receptors (NMDA-Rs), soluble guanylyl cyclase (sGC,

201 For example, NMDA receptor (NMDAR) activation is typically required f

202 tly potentiated when firing was triggered by NMDA receptor (NMDAR) activation.

203 reclinical studies have shown that enhancing NMDA receptor (NMDAR) activity can exert rapid antidepre

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

205 resulted in a significant reduction of both NMDA receptor (NMDAR) and AMPA/kainate receptor-mediated

206 verse collection of receptors, including the NMDA receptor (NMDAR) and voltage-gated Na(+) channels.

207 A single subanesthetic dose of ketamine, an NMDA receptor (NMDAR) antagonist, produces rapid and sus

208 a similar MMN reduction can be achieved with NMDA receptor (NMDAR) antagonists.

209 When psychosis develops in NMDA receptor (NMDAR) antibody encephalitis, it usually

210 NMDA receptor (NMDAR) blockade with ketamine (KET) durin

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

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

213 The identification of anti-NMDA receptor (NMDAR) encephalitis about 12 years ago ma

214 This study found that NMDA receptor (NMDAR) function was significantly increas

215 urther demonstrate that Lnx1 deletion causes NMDA receptor (NMDAR) hypofunction and this is attributa

216 d genetic and chemogenetic tools to modulate NMDA receptor (NMDAR) integrity and function, CREB-media

217 SIGNIFICANCE STATEMENT Signaling through the NMDA receptor (NMDAR) is vitally important for the synap

218 Both the NMDA receptor (NMDAR) positive allosteric modulator (PAM

219 that activin A regulates phosphorylation of NMDA receptor (NMDAR) subunit GluN2B and that GluN2B-con

220 and changes in BLA AMPA receptor (AMPAR) and NMDA receptor (NMDAR) subunit phosphorylation that likel

221 euronal autoantibodies, such as those to the NMDA receptor (NMDAR), are detectable in a subgroup of p

222 ecent studies highlight a novel role for the NMDA receptor (NMDAR), independent of ion flow, in drivi

223 rs and LepR neurons exhibited large synaptic NMDA receptor (NMDAR)-mediated currents compared with no

224 given frequency was robustly potentiated by NMDA receptor (NMDAR)-mediated firing.

225 In contrast, postsynaptic NMDA receptor (NMDAR)-mediated responses involve a neure

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

227 Dysfunction of NMDA receptor (NMDAR)-mediated transmission is supposed

228 t with the GluN2A and GluN2B subunits of the NMDA receptor (NMDAR).

229 ivated Ca(2+)-channels (HVACCs), but also of NMDA receptors (NMDAR).

230 The cytosolic C-terminal domains of both NMDA receptors (NMDARs) and AMPA receptors (AMPARs) have

231 L2/3 neurons and depends on the activity of NMDA receptors (NMDARs) and group I metabotropic glutama

232 Glutamatergic NMDA receptors (NMDARs) and small conductance Ca(2+) -ac

233 Glutamatergic NMDA receptors (NMDARs) and small conductance Ca(2+) -ac

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

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

236 NMDA receptors (NMDARs) are glutamate-gated ion channels

237 NMDA receptors (NMDARs) are glutamate-gated ion channels

238 NMDA receptors (NMDARs) are ionotropic glutamate recepto

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

240 hown that in male mice transient blockade of NMDA receptors (NMDARs) during development [subcutaneous

241 s of either GABA(A) receptors (GABA(A)Rs) or NMDA receptors (NMDARs) in primary afferents leads to ta

242 The majority of NMDA receptors (NMDARs) in the brain are composed of 2 G

243 emia), a vital homeostatic response in which NMDA receptors (NMDARs) play a role through nitric oxide

244 D-serine is a physiologic coagonist of NMDA receptors (NMDARs) required for synaptic plasticity

245 uring LTD induced by activation of mGluRs or NMDA receptors (NMDARs), and how this plasticity is alte

246 ast, the functional significance of PV+ cell NMDA receptors (NMDARs), which generate relatively slow

247 cale topography of native GluN2A- and GluN2B-NMDA receptors (NMDARs)-which play key roles in the use-

248 nt/beta-catenin-regulated FKN expression via NMDA receptors (NMDARs).

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

250 ptors on AII amacrines and GluN2A-containing NMDA receptors on A17 amacrines.

251 g experiments, which found GluN2B-containing NMDA receptors on AII amacrines and GluN2A-containing NM

252 Instead, NMDA receptors on both amacrine cells were activated by

253 ng also revealed a clustered organization of NMDA receptors on both amacrines and a close spatial ass

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

255 1 or D2 receptors, GABAA or GABAB receptors, NMDA receptors, P2Y1 ATP receptors, metabotropic glutama

256 pression and protein kinase C (PKC)-mediated NMDA receptor phosphorylation levels in the hypothalamus

257 NMDA receptors play crucial roles in excitatory synaptic

258 2A(N615K) variant has substantial effects on NMDA receptor properties fundamental to the roles of the

259 vidence suggests that both amacrines express NMDA receptors, raising questions concerning molecular c

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

261 s highlight its effectiveness to a subset of NMDA receptor responses and recommend it for further inv

262 feedback mechanism that reduces GluN2A-type NMDA receptor responses in an activity-dependent manner.

263 The blockade of NMDA receptors resulted in a slight enhancement of selec

264 Here we show that activation of NMDA receptors results in prominent sodium transients in

265 xic effects in part through their effects on NMDA receptor signaling and glutamatergic neurotransmiss

266 Collectively, the results indicate NMDA receptor signaling during adolescence enables the g

267 ulin resistance and T2D as well as disrupted NMDA receptor signaling in the hippocampus, resulting in

268 Here we found that NMDA receptor signaling is critical to enable the gain o

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

270 uires olfactory reception, OSN activity, and NMDA receptor signaling.

271 larization-activated currents, and increased NMDA receptor signaling.

272 This NMDA receptor-signaling is prerequisite for developmenta

273 undermines iMF by enhancing NR2B-containing NMDA receptor signalling, which can be rescued by exogen

274 tonic activation of GluN2C/GluN2D-containing NMDA receptors.SIGNIFICANCE STATEMENT Inhibitory GABAerg

275 nNOS puncta form multiprotein complexes with NMDA receptors, soluble guanylyl cyclase (sGC), and PSD9

276 of the receptor mGluR5 in the fine-tuning of NMDA receptors, specifically in the context of sensorimo

277 e GluN1 subunit (GluN1-NTD) is important for NMDA receptor structure and function, but the interactin

278 properties of the triheteromeric GluN1/2B/2D NMDA receptor subtype that is expressed in distinct neur

279 of EAAT3(glo)/CMKII mice revealed changes in NMDA receptor subunit composition and altered NMDA-depen

280 revealed decreased expression levels of the NMDA receptor subunit GluN1 and the postsynaptic density

281 ction with NRF1, leading to suppression of a NMDA receptor subunit Grin2A.

282 While clonal depletion of the NMDA receptor subunit NR2 results in their rapid elimina

283 ocated in the ion channel pore of the GluN2A NMDA receptor subunit.

284 gulation of membrane expression of the GluN1 NMDA receptor subunit.

285 novo variant in the gene encoding the GluN2A NMDA receptor subunit: a N615K missense variant in the M

286 rneuron function under redox control include NMDA receptor subunits GluN1 and GluN2A as well as KEAP1

287 l communication Variations in genes encoding NMDA receptor subunits have been found in a range of neu

288 ered that SorCS2 is a selective regulator of NMDA receptor surface trafficking in hippocampal neurons

289 and elevated synaptic N-methyl-d-aspartate (NMDA) receptors, thereby increasing synaptic connectivit

290 er than remaining trapped at synaptic sites, NMDA receptors undergo constant cycling into and out of

291 ation of tonic activity of GluN2C subtype of NMDA receptors using AICP, a newly identified glycine-si

292 ynapse properties by regulating postsynaptic NMDA-receptors via a trans-synaptic mechanism that likel

293 tput in rats in which spinal NR2B-containing NMDA receptors were inhibited.

294 nsport block and the resulting activation of NMDA receptors were regarded as reliable evidence for a

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

296 d the impact of the variant in diheteromeric NMDA receptors with two GluN1 and two identical GluN2 su

297 es, express extrasynaptic (but not synaptic) NMDA receptors, with different and complementary GluN2 s

298 7 amacrines express clustered, extrasynaptic NMDA receptors, with different and complementary subunit

299 mechanism, which coordinates the activity of NMDA receptors within a cluster, may cause signaling alt

300 in the recurrent excitation mediated by slow NMDA receptors within a selective population and mutual