ライフサイエンスコーパス: NMDA

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

2 NMDA receptor antagonists prevented medullary SD and apn

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

4 NMDA receptor-mediated synaptic currents in heterozygous

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

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

7 NMDA receptors are excitatory ion channels with fundamen

8 NMDA receptors are ionotropic calcium-permeable glutamat

9 NMDA receptors are neurotransmitter-gated ion channels t

10 NMDA receptors play crucial roles in excitatory synaptic

11 NMDA-evoked NO release peaked at 1.1 muM and lasted more

12 NMDA-type glutamate receptors act as voltage- and ligand

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

14 ing from hippocampal slices showed no Mg(2+)/NMDA-mediated epileptiform events in knockouts.

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

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

17 alphaPBN), and the N-methyl-D-aspartic acid (NMDA) antagonist MK801-in mouse and rat models of focal

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

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

20 an brain endothelial cells by NMDA agonists (NMDA or glycine) and the serine protease tissue plasmino

21 MDA receptor subunit composition and altered NMDA-dependent synaptic plasticity.

22 aspartate receptor (NMDA) receptor, although NMDA-independent mechanisms are not ruled out.

23 elin is able to rescue the deficits in AMPA, NMDA, GABA(A) receptors, mTOR and p-mTOR induced by CORT

24 the incentive stimulus depended on NAcC AMPA/NMDA and dopamine D1 receptors, but the retrieval of the

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

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

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

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

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

30 of a GABA(A) receptor antagonist, but not an NMDA/AMPA/kainate receptor antagonist, suggesting that t

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

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

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

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

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

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

37 ckade of glutamate receptors of the AMPA and NMDA types in hippocampal neurons in culture induces cha

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

39 produce the finding that glutamate, AP5, and NMDA positively modulate glycine receptor currents.

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

41 The identification of AMPA, kainate and NMDA glutamate receptor subtypes by Watkins and colleagu

42 xcitatory postsynaptic currents (mEPSCs) and NMDA-evoked currents in CA1 pyramidal neurons of rat hip

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

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

45 in additive increase of both spontaneous and NMDA-evoked firing rate.

46 ation of Fyn kinase and its targets, tau and NMDA-NR2B, and decreased Rho kinase signaling changes an

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

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

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

50 create a novel mouse model in which SCs are NMDA-R-deficient (GluN1- mice).

51 ong with the compounds N-methyl-d-aspartate (NMDA) and d-(-)-2-amino-5-phosphonopentanoic acid (AP5),

52 e demonstrate that the N-methyl D-aspartate (NMDA) antagonist ketamine is able to disrupt MRMs in haz

53 ediated by blockade of N-methyl-D-aspartate (NMDA) glutamate receptors, our experiments demonstrate t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 glutamatergic agonist N-methyl-d-aspartate (NMDA).

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

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

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

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

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

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

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

77 ct as an opiate but its effects require both NMDA and opiate receptor signaling, suggesting that inte

78 oked saline mice, it is able to restore both NMDA-dependent and mGluR5-dependent LTD in animals after

79 mulation of human brain endothelial cells by NMDA agonists (NMDA or glycine) and the serine protease

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

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

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

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

84 elective targeting of either GluN2B-carrying NMDA or sigma(1)-receptors.

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

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

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

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

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

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

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

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

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

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

95 In striking contrast, NMDA-induced spine plasticity in Fmr1(-/y) mice was no l

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

97 n hiNPC were treated with EI-tPA in culture, NMDA-R-dependent cell signaling was initiated, expressio

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

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

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

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

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

103 TNFR1 was shown to be critical for elevated NMDA-mediated excitatory currents in sympathoexcitatory

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

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

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

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

108 7 amacrines express clustered, extrasynaptic NMDA receptors, with different and complementary subunit

109 following Ca(2+) entry through extrasynaptic NMDA-type ionotropic glutamate receptors (NMDARs).

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

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

112 Further, TNFR1 activation was essential for NMDA signaling and the heightening NMDA currents during

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

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

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

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

117 cortical excitation/inhibition balance from NMDA-R hypofunction predominantly onto excitatory neuron

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

119 targeted grin1 encoding the essential GluN1 NMDA-R subunit, conditionally in SCs, to create a novel

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

121 tic plasmalemmal density of obligatory GluN1-NMDA subunits in dendrites of all sizes and (2) a shift

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

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

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

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

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

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

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

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

130 risingly, the blockade of both glutamatergic NMDA and GABA(A) receptors improved neuronal selectivity

131 ntial for NMDA signaling and the heightening NMDA currents during hypertension.

132 the magnitude of an NMDAR-evoked current (I(NMDA) ).

133 r BAPTA (10 mM) increased the magnitude of I(NMDA) in MNNs from both sham and HF rats, and occluded t

134 oisomer were evaluated on the following: (i) NMDA-induced lethality in mice, (ii) NMDAR-mediated fiel

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

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

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

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

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

140 conclusion, these results show a decrease in NMDA neurotoxicity by NBCn1 deletion.

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

142 a cellular pathway involving an increase in NMDA-mediated currents in the PVN following AngII infusi

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

144 infections, but were low or undetectable in NMDA encephalitis, multiple sclerosis, and controls.

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

146 g antidepressant drug development, including NMDA channel blockers, glycine site agents, and alloster

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

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

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

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

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

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

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

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

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

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

157 erences in the glutamate receptor ionotropic NMDA 2 (GluN2) subunit composition of NMDARs determines

158 Non-ketamine NMDA antagonists lacked efficacy and we also found that

159 tures of hippocampal neurons from knockouts, NMDA had no neurotoxic effects, determined by lactate de

160 cularly of slow subthreshold potentials like NMDA spikes or trains of EPSPs from dendrite to soma.

161 oupling of slow subthreshold potentials like NMDA spikes or trains of EPSPs from the distal apical de

162 chwann cells, S-PrP interacted with the LRP1/NMDA-R system to activate extracellular signal-regulated

163 aused by other proteins that engage the LRP1/NMDA-R system, including activated alpha(2)-macroglobuli

164 us system by serving as ligands for the LRP1/NMDA-R system.

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

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

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

168 4 suppressed AMPA-receptor-mediated, but not NMDA-receptor-mediated, synaptic responses, while altern

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

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

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

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

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

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

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

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

177 We observe that antagonism of NMDA and AMPA type glutamate receptors protects neurons

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

179 the ICc, we found that local application of NMDA enhances sound-driven activity in a concentration-d

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

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

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

183 This effect can be mimicked by blockade of NMDA-type glutamate receptors but not voltage-gated calc

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

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

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

187 ditive over the sum of the single effects of NMDA and NS-1738.

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

189 this behaviour, we simulated the effects of NMDA-R hypofunction onto either excitatory or inhibitory

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

191 Although inhibition of NMDA-type glutamate receptors (NMDARs) is one mechanism

192 Introduction of NMDA receptor antagonists was correlated with a decrease

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

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

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

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

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

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

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

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

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

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

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

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

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

206 licing of neurexin-2 at SS4 had no effect on NMDA- or AMPA-receptor-mediated responses.

207 2A(N615K) variant has substantial effects on NMDA receptor properties fundamental to the roles of the

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

209 ction rostral to DMH, blocked cold-evoked or NMDA in MnPO-evoked BAT thermogenesis.

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

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

212 Other NMDA antagonist did not translocate Galpha(s) from lipid

213 ese effects by comparing ketamine with other NMDA antagonists using this decision-making task.

214 ut the same effects were not seen with other NMDA antagonists.

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

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

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

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

219 n mice, the ED(50) of (2R,6R)-HNK to prevent NMDA-induced lethality was found to be 228 mg/kg, compar

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

221 entiating effect of AngII on mEPSCs and puff NMDA currents of labelled PVN neurons in SHRs.

222 currents (mEPSCs) and the amplitude of puff NMDA currents of retrogradely labelled spinally projecti

223 of its targets glutamate ionotropic receptor NMDA-type subunit 2B (GRIN2B) and glutamate ionotropic r

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

225 endent on the N-methyl-d-aspartate receptor (NMDA-R) and low-density lipoprotein receptor-related pro

226 To model possible effects of NMDA receptor (NMDA-R) antagonism on this behaviour, we simulated the e

227 n1, the gene that encodes the NMDA receptor (NMDA-R) GluN1 subunit, is deleted in SCs.

228 reported that SCs express the NMDA receptor (NMDA-R), which activates cell signaling in response to g

229 (due to anti-N-methyl-D-aspartate receptor [NMDA] encephalitis and multiple sclerosis), and noninfla

230 1 or D2 receptors, GABAA or GABAB receptors, NMDA receptors, P2Y1 ATP receptors, metabotropic glutama

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

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

233 s, enhanced dendritic inhibition and reduced NMDA currents strongly decreased burst-induced NMDAR-med

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

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

236 More recently, indirect ways to regulate NMDA that would be less disruptive have been proposed an

237 municating through endocannabinoid-regulated NMDA receptors.

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

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

240 ectively, these findings demonstrate that SC NMDA-R is essential for normal PNS development and for p

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

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

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

244 amma2 GABA(A) receptors akin to that of slow NMDA and fast AMPA EPSCs at glutamate synapses.

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

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

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

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

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

250 d that PCDH7 overexpression reduces synaptic NMDA receptor currents.

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

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

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

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

255 l computation based on our data predict that NMDA-induced sodium increases drive the NCX into reverse

256 We show that NMDA-R modulation of sound-driven activity in the ICc is

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

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

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

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

261 hat this effect of leptin is mediated by the NMDA subtype of glutamate receptors (NMDARs).

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

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

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

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

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

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

268 monstration of the dramatic influence of the NMDA activated NO pathway on sound-driven neuronal activ

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

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

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

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

273 While Zn(2+) inhibition of the NMDA subtype of the ionotropic glutamate receptors is we

274 The increase of the NMDA-evoked firing rate exerted by NS-1738 was superaddi

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

276 This response required the NMDA-R, LRP1, Src family kinases, and Trk receptors.

277 blockade of nNOS or sGC, indicating that the NMDA effect is mediated solely via the NO and cGMP signa

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

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

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

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

282 se were then tested experimentally using the NMDA-R antagonist ketamine, a pharmacological model of s

283 We examined if combined treatment with the NMDA antagonist memantine and the opioid antagonist nalt

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

285 Calcium signalling through NMDA-type glutamate receptors (NMDARs) plays a key role

286 opose that glutamate activates TRESK through NMDA and AMPA mediated calcium influx and calcineurin ac

287 hold, and decreased depolarizing response to NMDA in deep-layer PL-PFC neurons analyzed by current-cl

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

289 bited marked sodium increases in response to NMDA.

290 to leptin but hyperpolarized in response to NMDA.

291 Triheteromeric NMDA receptors contain two GluN1 and two distinct GluN2

292 Triheteromeric NMDA-type glutamate receptors that contain two GluN1 and

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

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

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

296 ors, for example, kainate receptors on which NMDA acts as a competitive antagonist, and high affinity

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

298 e therapeutic in pathologies associated with NMDA receptor dysfunction.

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

300 ypes (6-8 weeks old) were then injected with NMDA (75 mg/kg; ip) and hippocampal neuronal damages wer

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