ライフサイエンスコーパス: N-methyl-D-aspartate receptor

1 amine is a non-competitive antagonist at the N-methyl-d-aspartate receptor.

2 a postsynaptic form (post-LTP) that requires N-methyl-D-aspartate receptors.

3 ts, and inhibited both glutamate release and N-methyl-d-aspartate receptors.

4 l is an allosteric inhibitor of GluN1/GluN2B N-methyl-D-aspartate receptors.

5 y and Rho kinases as well as NR2B-containing N-methyl-D-aspartate receptors.

6 ations between domain layers, reminiscent of N-methyl-D-aspartate receptors.

7 roxy-5-methyl-4-isoxazole propionic acid and N-methyl-D-aspartate receptors.

8 eltaC synergistically augmented signaling by N-methyl-d-aspartate receptors.

9 t of both alpha7 nicotinic acetylcholine and N-methyl-D-aspartate receptors.

10 potential or intracellular blockade of NMDA (N-methyl-d-aspartate) receptors.

11 m/calmodulin-dependent protein kinase II and N-methyl-D-aspartate receptor 2A and increased N-methyl-

12 es, Kal7(KO) females had decreased levels of N-methyl-d-aspartate receptor 2B in hippocampal PSD frac

13 methyl-D-aspartate receptor 2A and increased N-methyl-D-aspartate receptor 2B levels and were indepen

14 e subset of antibody-positive patients, anti-N-methyl-d-aspartate receptor (5 patients), had normal M

15 ective activity through its effects on NMDA (N-methyl-D-aspartate) receptors, a determined effort has

16 nses in CA2 pyramidal neurons that relied on N-methyl-d-aspartate receptor activation and calcium/cal

17 l of the effects of stress is independent of N-methyl-D-aspartate receptor activation in PW animals.

18 ptic rules which may determine the extent of N-methyl-D-aspartate receptor activation in the amygdala

19 te overshoot and hyperalgesia) that required N-methyl-D-aspartate receptor activation of adenylyl cyc

20 N-methyl-D-aspartate receptor activation requires the bi

21 , including acetylcholinesterase inhibition, N-methyl-D-aspartate receptor activation, and calcium dy

22 The findings implicate dysfunction of N-methyl-D-aspartate receptor and glutamatergic neurotra

23 m/calmodulin-dependent protein kinase II and N-methyl-D-aspartate receptors and suggest that NA suppl

24 stent firing of 'Delay cells' is mediated by N-methyl-d-aspartate receptors and weakened by cAMP-PKA-

25 the stimulated spine that depends on NMDAR (N-methyl-d-aspartate receptor) and CaMKII signalling and

26 ha7 nicotinic acetylcholine receptor and the N-methyl-D-aspartate receptor, and 3-hydroxykynurenine (

27 sed neuronal or glial proteins such as LGI1, N-methyl-D-aspartate receptor, and aquaporin-4.

28 as potent inihitors of both cholinesterases, N-methyl-D-aspartate receptors, and monoamine oxidases.

29 Furthermore, NMDA (N-methyl-d-aspartate) receptor antagonism by ketamine ha

30 o stabilize cellular calcium homeostasis via N-methyl-D-aspartate-receptor antagonism.

31 Ketamine, a noncompetitive N-methyl-D-aspartate receptor antagonist has shown poten

32 The N-methyl-D-aspartate receptor antagonist ketamine can im

33 suggests a single sub-anesthetic dose of the N-methyl-D-aspartate receptor antagonist ketamine may wo

34 of striatal DeltaFosB overexpression and the N-methyl-D-aspartate receptor antagonist ketamine, both

35 number of compounds, including the glutamate N-methyl-D-aspartate receptor antagonist ketamine, have

36 influx that can be partially blocked by the N-methyl-d-aspartate receptor antagonist MK-801.

37 al striatal function by local infusion of an N-methyl-D-aspartate receptor antagonist or an antisense

38 Ketamine is a potent N-methyl-D-aspartate receptor antagonist with a potentia

39 of inflammatory genes, and that ketamine (an N-methyl-D-aspartate receptor antagonist) would reduce o

40 We found that administration of ketamine, an N-methyl-D-aspartate receptor antagonist, in monkeys cau

41 Recent clinical trials have shown that the N-methyl-D-aspartate receptor antagonist, ketamine, can

42 xide, an inhalational general anesthetic and N-methyl-D-aspartate receptor antagonist, may also be a

43 Subchronic treatment with the N-methyl-D-aspartate receptor antagonist, phencyclidine

44 able recent discovery shows that ketamine, a N-methyl-D-aspartate receptor antagonist, produces rapid

45 Ketamine is an N-methyl-D-aspartate receptor antagonist, which on admin

46 The non-competitive, glutamatergic NMDAR (N-methyl-d-aspartate receptor) antagonist (R,S)-ketamine

47 ketamine, an ionotropic glutamatergic NMDAR (N-methyl-D-aspartate receptor) antagonist, produces fast

48 epines are considered first-line therapy and N-Methyl-d-aspartate receptor antagonists also appears t

49 Additionally, the NR2B-selective N-methyl-D-aspartate receptor antagonists ifenprodil and

50 The robust antidepressant effects of the N-methyl-D-aspartate receptor antagonists ketamine and t

51 N-methyl-D-aspartate receptor antagonists, such as ketam

52 transmission, and synaptogenesis, similar to N-methyl-D-aspartate receptor antagonists.

53 have been implicated in the rapid actions of N-methyl-D-aspartate receptor antagonists.

54 ates the cognitive and behavioral effects of N-methyl-D-aspartate receptor antagonists.

55 They include anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis,

56 ncephalitis, began identifying cases of anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis.

57 findings demonstrate the epileptogenicity of N-methyl D-aspartate receptor antibodies in vivo, and su

58 th teratoma-associated encephalitis, 211 had N-methyl-D-aspartate receptor antibodies and 38 were neg

59 ody testing confirmed identification of anti-N-methyl-D-aspartate receptor antibodies in the cerebros

60 receptor antibodies, the absolute levels of N-methyl-d-aspartate receptor antibodies were higher in

61 gh there was marked intrathecal synthesis of N-methyl-d-aspartate receptor antibodies, the absolute l

62 Most patients with N-methyl D-aspartate-receptor antibody encephalitis deve

63 ied Rankin scores, correlated with decreased N-methyl-d-aspartate receptor antibody levels and were a

64 ctivation dynamics due to synaptic input via n-methyl-d-aspartate receptors are qualitatively account

65 ecular assay suggests that protein levels of N-methyl-D-aspartate receptors are reduced in this trans

66 Tonic activation of N-methyl-D-aspartate receptors at synapses in the amygda

67 rine, a partial agonist at the glutamatergic N-methyl-d-aspartate receptor, augments and accelerates

68 There are now a large number of requests for N-methyl-D-aspartate receptor autoantibody (NMDAR-Ab) te

69 Parenchymal administration of the N-methyl-d-aspartate receptor blocker MK-801 directly in

70 low-frequency stimulation, and is blocked by N-methyl-D-aspartate receptor blockers in rats.

71 Glycine acts as an N-methyl-D-aspartate receptor coagonist.

72 ells, NR1 and NR2B receptors, Src within the N-methyl-D-aspartate receptor complex, and the subsequen

73 protein-1 (Sp1)-binding site resulted in an N-methyl-d-aspartate receptor-dependent enhancement of C

74 specific GSK3 inhibitors improve deficits in N-methyl-D-aspartate receptor-dependent long-term potent

75 ng an essential function in the induction of N-methyl-D-aspartate receptor-dependent long-term potent

76 N-methyl-D-aspartate receptor-dependent plasticity in th

77 Mechanisms of N-methyl-D-aspartate receptor-dependent synaptic plastic

78 Here we report that hippocampal N-methyl-d-aspartate receptor-dependent synaptic plastic

79 tatory synaptic activity and was shown to be N-methyl-d-aspartate receptor-dependent.

80 rengthening of synaptic connections by NMDA (N-methyl-d-aspartate) receptor-dependent long-term poten

81 These data implicate NR2A-related N-methyl-D-aspartate receptor development in adolescent

82 st-mortem, surprisingly, the total number of N-methyl D-aspartate receptors did not differ between te

83 t impaired sensory memory that might reflect N-methyl-D-aspartate receptor dysfunction in chronic can

84 he characteristic laboratory finding of anti-N-methyl-D-aspartate receptor encephalitis.

85 promotes depolarization, thereby augmenting N-methyl-d-aspartate receptor function and contributing

86 hizophrenia thought to reflect glutamatergic N-methyl-d-aspartate receptor function and excitatory-in

87 Inhibition of neuronal activity, N-methyl-d-aspartate receptor function, or glycogen synt

88 ia, consistent with hypothesized deficits in N-methyl-D-aspartate receptor function.

89 Here we show that the identity of the N-methyl-D-aspartate receptor glycine site agonist at sy

90 sion (over expression and phosphorylation of N-methyl-D-aspartate receptors) have been associated wit

91 abnormal glutamateric neurotransmission and N-methyl-D-aspartate receptor hypofunction in the pathop

92 The N-methyl-D-aspartate receptor hypofunction model of schi

93 most common and was predicted best when both N-methyl-D-aspartate receptor-IgG and aquaporin-4-IgG co

94 Here, we show that blockage of the N-methyl-D-aspartate receptor impairs the cycling of syn

95 nts, glycine receptor (GLY-R) in 5 patients, N-methyl-d-aspartate receptor in 4 patients and gamma-am

96 chosis patients (3 IgG, 1 IgM, 0 IgA) and to N-methyl-D-aspartate receptor in 6 of 43 patients (5 IgG

97 others have recently found antibodies to the N-methyl-D-aspartate receptor in first-episode psychosis

98 The expression of the NR2B subunit of the N-methyl-D-aspartate receptor in the amygdala was examin

99 d-cycloserine, a partial agonist at the N-methyl-d-aspartate receptor in the amygdala, has been

100 on and downregulated the NR2B subunit of the N-methyl-D-aspartate receptor in the lateral and basal n

101 lpha-syn modulation of the GluN2D-expressing N-methyl-D-aspartate receptors in cholinergic interneuro

102 eleased glutamate that selectively activated N-methyl-d-aspartate receptors in homotypic, but not het

103 in a significant upregulation of excitatory N-methyl-D-aspartate receptors in the BLA.

104 pression of the essential NR1 subunit of the N-methyl-D-aspartate receptor increased during downstrea

105 erates the rate of AMPAR recycling following N-methyl-D-aspartate receptor-induced internalization.

106 ed by sustained activation of synaptic NMDA (N-methyl-d-aspartate) receptors, induces physical associ

107 r gamma-aminobutyric acid type A receptor or N-methyl-D-aspartate receptor inhibition.

108 n emission tomography, a marker of activated N-methyl-D-aspartate receptor ion channels, to compare i

109 We have probed NMDA (N-methyl-D-aspartate) receptor ion channel in live HEK-2

110 Deficient signaling through the N-methyl-D-aspartate receptor is hypothesized to underli

111 antidepressant effects of ketamine and other N-methyl-D-aspartate receptor ligands, which occur withi

112 nstrated that this effect was independent of N-methyl-D-aspartate receptor, low-density lipoprotein-r

113 N-Methyl-D-aspartate receptors mediate the slow componen

114 nge detection thought to index glutamatergic N-methyl-D-aspartate receptor-mediated neurotransmission

115 es in afferent activity levels into enhanced N-methyl-D-aspartate receptor-mediated synaptic events,

116 th MoCD, and demonstrated that it acts as an N-methyl D-aspartate receptor (NMDA-R) agonist, leading

117 Furthermore, inhibition of N-methyl-d-aspartate receptor (NMDA) activity blocks spi

118 N-methyl-D-aspartate receptor (NMDA-R) hypofunction play

119 The expression of N-methyl-d-aspartate receptor (NMDA-R) subunit 2b mRNA e

120 N-Methyl-D-aspartate receptors (NMDA-Rs) are ion channel

121 titative model of glutamate spillover on the N-methyl-d-aspartate receptors (NMDA-Rs) at the cerebell

122 signaling (glutamate transporter-I [GLT-I], N-methyl-D-aspartate receptors [NMDA-R] and alpha-3-hydr

123 n for ketamine is mediated primarily through N-methyl d-aspartate receptor (NMDAR) antagonism; howeve

124 NSFT following EtOH abstinence utilizing the N-methyl D-aspartate receptor (NMDAR) antagonist and ant

125 Anti-N-methyl D-aspartate receptor (NMDAR) encephalitis is a

126 ynaptic transmission that is contingent upon N-methyl d-aspartate receptor (NMDAR) function contribut

127 The activation of the N-methyl D-aspartate receptor (NMDAR) is controlled by a

128 KYNA depletion then leads, in an N-methyl D-aspartate receptor (NMDAR)-dependent manner,

129 to its central role in learning and memory, N-methyl D-aspartate receptor (NMDAR)-dependent signalin

130 y explained by enrichment for members of the N-methyl-D-aspartate receptor (NMDAR) (P=4.24 x 10(-)(6)

131 vated protein 1 [LGI1] Ab), and 4 (3.6%) had N-methyl-D-aspartate receptor (NMDAR) Ab.

132 T-CBD3, but not CBD3 without TAT, attenuated N-methyl-d-aspartate receptor (NMDAR) activity and prote

133 CK2 (formerly casein kinase II) in increased N-methyl-d-aspartate receptor (NMDAR) activity in spinal

134 Increased N-methyl-d-aspartate receptor (NMDAR) activity in the pa

135 The hippocampal N-methyl-D-aspartate receptor (NMDAR) activity plays imp

136 Increased glutamatergic input, particularly N-methyl-D-aspartate receptor (NMDAR) activity, in the p

137 sis in human primary neurons is dependent on N-methyl-D-aspartate receptor (NMDAR) activity.

138 F2K) activity subsequent to the reduction in N-methyl-D-aspartate receptor (NMDAR) activity.

139 a neuron-specific phosphatase that regulates N-methyl-D-aspartate receptor (NMDAR) and alpha-amino-3-

140 The N-methyl-d-aspartate receptor (NMDAR) and alpha-amino-3-

141 We recorded N-methyl-D-aspartate receptor (NMDAR) and alpha-amino-3-

142 de registers to search for antibodies to the N-methyl-D-aspartate receptor (NMDAR) and contactin-asso

143 von Frey filaments to examine the roles that N-methyl-D-aspartate receptor (NMDAR) and hyperpolarizat

144 The psychotomimetic effect of the N-methyl-D-aspartate receptor (NMDAR) antagonist ketamin

145 tamine, a non-competitive, voltage-dependent N-Methyl-D-aspartate receptor (NMDAR) antagonist, has be

146 nical evidence that ketamine, a nonselective N-methyl-D-aspartate receptor (NMDAR) antagonist, has th

147 The uncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonist, ketami

148 Through the fortuitous discovery of N-methyl-D-aspartate receptor (NMDAR) antagonists as eff

149 Competitive N-methyl-d-aspartate receptor (NMDAR) antagonists bind t

150 A single injection of N-methyl-D-aspartate receptor (NMDAR) antagonists produc

151 of schizophrenia are based on the ability of N-methyl-D-aspartate receptor (NMDAR) antagonists to ind

152 Here, we utilized four subtype-selective N-methyl-d-aspartate receptor (NMDAR) antagonists to inv

153 Similar to mice treated chronically with N-methyl-d-aspartate receptor (NMDAR) antagonists, we de

154 RATIONALE: Encephalitis caused by anti-N-methyl-d-aspartate receptor (NMDAR) antibodies is the

155 N-Methyl-D-aspartate receptor (NMDAR) antibodies of the

156 sing post-herpes simplex encephalitis (HSE), N-methyl-D-aspartate receptor (NMDAR) antibodies were id

157 N-methyl-D-aspartate receptor (NMDAR) antibody encephali

158 CHPG-LTD and NLDE-LTD were insensitive to N-methyl-D-aspartate receptor (NMDAR) block, even though

159 udies have documented the effects of chronic N-methyl-D-aspartate receptor (NMDAR) blockade on excita

160 e inhibition of neurotransmitter release and N-methyl-D-aspartate receptor (NMDAR) blockade, which is

161 Ketamine, an N-methyl-D-aspartate receptor (NMDAR) channel blocker, h

162 ot alter the density of excitatory synapses, N-methyl-D-aspartate receptor (NMDAR) clusters, or cell

163 The N-methyl-D-aspartate receptor (NMDAR) coagonists glycine

164 ed cytoskeleton-associated protein (ARC) and N-methyl-d-aspartate receptor (NMDAR) complexes.

165 The N-methyl-d-aspartate receptor (NMDAR) controls synaptic

166 amplitude and prolongs the decay kinetics of N-methyl-d-aspartate receptor (NMDAR) currents in male r

167 Our previous studies indicated that N-methyl-D-aspartate receptor (NMDAR) deletion from a su

168 ly overlooked in schizophrenia research, and N-methyl-d-aspartate receptor (NMDAR) dysfunction can pr

169 Because N-methyl-D-aspartate receptor (NMDAR) dysfunction has be

170 ted the glutamate system and, in particular, N-methyl-D-aspartate receptor (NMDAR) dysfunction in the

171 Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a

172 Anti- N-methyl-D-aspartate receptor (NMDAR) encephalitis is a

173 Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is an

174 Patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis often

175 The majority of patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis suffe

176 as are frequently described in patients with N-methyl-d-aspartate receptor (NMDAR) encephalitis, yet

177 normal in the majority of patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis.

178 Mutations in the N-methyl-D-aspartate receptor (NMDAR) gene GRIN2A cause

179 ulating autoantibodies against glutamatergic N-methyl-D-aspartate receptor (NMDAR) have been reported

180 N-methyl-D-aspartate receptor (NMDAR) hypofunction in pa

181 s glutamate excess in schizophrenia and that N-methyl-d-aspartate receptor (NMDAR) hypofunction on ga

182 netic and neurobiological findings that link N-methyl-D-aspartate receptor (NMDAR) hypofunction to th

183 es support the theory of hypofunction of the N-methyl-D-aspartate receptor (NMDAR) in SCZ, as well as

184 The N-methyl-D-aspartate receptor (NMDAR) is a member of the

185 The N-methyl-D-aspartate receptor (NMDAR) is a prime target

186 Preclinical studies suggest that augmenting N-methyl-d-aspartate receptor (NMDAR) signaling may prom

187 Abnormal activity of various N-methyl-d-aspartate receptor (NMDAR) subtypes has been

188 Early postnatal experience shapes N-methyl-D-aspartate receptor (NMDAR) subunit compositio

189 The RNA sequencing screen revealed that the N-methyl-D-aspartate receptor (NMDAR) subunit Grin2B was

190 ncoded by GRIN2A and GRIN2B) subunits of the N-methyl-D-aspartate receptor (NMDAR), a ligand-gated io

191 a list of AD-relevant targets, including the N-methyl-d-aspartate receptor (NMDAR), acetylcholinester

192 usly known types of autoimmune encephalitis [N-methyl-D-aspartate receptor (NMDAR), alpha-amino-3-hyd

193 able samples were retested for antibodies to N-methyl-d-aspartate receptor (NMDAR), the glycine recep

194 mples were tested/retested for antibodies to N-methyl-D-aspartate receptor (NMDAR), VGKC-complex, LGI

195 N-Methyl-D-Aspartate receptor (NMDAR)-Ab was found in tw

196 ansmitter molecules, is its manifestation as N-methyl-d-aspartate receptor (NMDAR)-dependent slow inw

197 degeneration of primary cortical neurons via N-methyl-d-aspartate receptor (NMDAR)-dependent suppress

198 es that prior experience and hippocampal CA3 N-Methyl-D-aspartate receptor (NMDAR)-dependent synaptic

199 associations is known to rely on hippocampal N-methyl-D-aspartate receptor (NMDAR)-dependent synaptic

200 Surprisingly, recovery of Kv4.2 after N-methyl-D-aspartate receptor (NMDAR)-induced degradatio

201 These biochemical events potentiate N-methyl-D-aspartate receptor (NMDAR)-mediated currents

202 al-anxiety is associated with a reduction in N-methyl-D-aspartate receptor (NMDAR)-mediated currents

203 -isoxazolepropionic acid receptor (AMPAR) or N-methyl-D-aspartate receptor (NMDAR)-mediated excitator

204 impairments are thought to be due to reduced N-methyl-D-aspartate receptor (NMDAR)-mediated inhibitio

205 and are linked to underlying dysfunction of N-methyl-D-aspartate receptor (NMDAR)-mediated neurotran

206 In particular, a robust decrease in N-methyl-D-aspartate receptor (NMDAR)-mediated synaptic

207 antibodies-especially antibodies against the N-methyl-D-aspartate receptor (NMDAR)-more commonly than

208 llosteric antagonists of ion channels of the N-methyl-d-aspartate receptor (NMDAR).

209 D-serine is an endogenous co-agonist for the N-methyl-D-aspartate receptor (NMDAR).

210 fluid (CSF) against the GluN1 subunit of the N-methyl-D-aspartate receptor (NMDAR).

211 eacts with the NR2A and NR2B subunits of the N-methyl-d-aspartate receptor (NMDAR).

212 ing neurons as a result of inhibition of the N-methyl-d-aspartate receptor (NMDAR).

213 present in the NR2A and NR2B subunits of the N-methyl-d-aspartate receptor (NMDAR).

214 cysteine (Hcy) is an agonist of the neuronal N-methyl-D-aspartate receptor (NMDAr).

215 or D-serine are obligatory coagonists of the N-methyl-D-aspartate receptor (NMDAR).

216 ifferences in the pharmacological profile of N-methyl-d-aspartate receptors (NMDAR) in the NAc core,

217 N-methyl-D-aspartate receptors (NMDAR) regulate synaptic

218 d-Serine modulates N-methyl d-aspartate receptors (NMDARs) and regulates sy

219 The subunit composition of N-methyl D-aspartate receptors (NMDARs) is tightly regul

220 ntly enriched in conantokins, antagonists of N-methyl d-aspartate receptors (NMDARs).

221 Synaptically evoked Ca(2+) influx through N-methyl-D-aspartate receptors (NMDARs) activates spine

222 development and synaptic plasticity through N-methyl-D-aspartate receptors (NMDARs) and calcium-depe

223 PS modulates N-methyl-D-aspartate receptors (NMDARs) and has been sho

224 n interaction between synaptic activation of N-methyl-D-aspartate receptors (NMDARs) and intrinsic os

225 quivocal uncompetitive inhibitory effects on N-methyl-d-aspartate receptors (NMDARs) and may preferen

226 t synaptic accumulation of GluN2B-containing N-methyl-D-aspartate receptors (NMDARs) and pathological

227 We found that coactivation of N-methyl-D-aspartate receptors (NMDARs) and type 1 canna

228 N-Methyl-d-aspartate receptors (NMDARs) are Ca(2+)-perme

229 N-Methyl-D-aspartate receptors (NMDARs) are glutamate-ga

230 N-methyl-D-aspartate receptors (NMDARs) are glutamate-ga

231 N-methyl-D-aspartate receptors (NMDARs) are glutamate-ga

232 N-methyl-d-aspartate receptors (NMDARs) are glutamate-ga

233 N-methyl-D-aspartate receptors (NMDARs) are glycoprotein

234 N-methyl-d-aspartate receptors (NMDARs) are heterotetram

235 N-Methyl-D-aspartate receptors (NMDARs) are involved in

236 N-methyl-d-aspartate receptors (NMDARs) are ionotropic g

237 N-methyl-D-aspartate receptors (NMDARs) are ligand-gated

238 N-methyl-D-aspartate receptors (NMDARs) are necessary fo

239 Regulation of the activity of N-methyl-d-aspartate receptors (NMDARs) at glutamatergic

240 The N-methyl-d-aspartate receptors (NMDARs) constitute an im

241 N-Methyl-d-aspartate receptors (NMDARs) display a critic

242 The present study evaluated the role of N-methyl-D-aspartate receptors (NMDARs) expressed in the

243 Although antagonists to GluN2B-containing N-methyl-D-aspartate receptors (NMDARs) have been widely

244 l upregulation of cortical GluN2C-containing N-methyl-D-aspartate receptors (NMDARs) in an mTOR-depen

245 The significant role played by N-methyl-d-aspartate receptors (NMDARs) in both the path

246 Glutamate N-methyl-D-aspartate receptors (NMDARs) in the medial pr

247 n deficit is hyperfunction of glutamate-type N-methyl-d-aspartate receptors (NMDARs) in the selective

248 N-methyl-d-aspartate receptors (NMDARs) mediate critical

249 N-methyl-D-aspartate receptors (NMDARs) mediate synaptic

250 Postsynaptic N-methyl-d-aspartate receptors (NMDARs) phasically activ

251 N-Methyl-D-aspartate receptors (NMDARs) play pivotal rol

252 Synaptic activation of N-methyl-d-aspartate receptors (NMDARs) plays a key role

253 Preclinical studies revealed contribution of N-methyl-D-aspartate receptors (NMDARs) to a variety of

254 Coactivation of N-methyl-D-aspartate receptors (NMDARs) together with AM

255 Alcohol may act on N-methyl-d-aspartate receptors (NMDARs) within cortical

256 The ionotropic glutamate receptors (N-methyl-D-aspartate receptors (NMDARs)) are composed of

257 Both memantine and ketamine antagonize N-methyl-D-aspartate receptors (NMDARs), a glutamate rec

258 Here, we investigate the role of N-methyl-D-aspartate receptors (NMDARs), AMPARs, and sma

259 SAP102 binds directly to N-methyl-D-aspartate receptors (NMDARs), anchors recepto

260 N-methyl-D-aspartate receptors (NMDARs), critical mediat

261 TBI occurs largely due to hyperactivation of N-methyl-d-aspartate receptors (NMDARs), leading to toxi

262 The short-term form depends on activation of N-methyl-d-aspartate receptors (NMDARs), whereas the rap

263 understood, particularly the involvement of N-methyl-D-aspartate receptors (NMDARs), which are criti

264 -isoxazole-propionate receptors (AMPARs) and N-methyl-d-aspartate receptors (NMDARs).

265 rine models have shown altered expression of N-methyl-D-aspartate receptors (NMDARs).

266 apse require stimulation of both betaARs and N-methyl-D-aspartate receptors (NMDARs).

267 N-methyl-D-aspartate-receptors (NMDARs) are ionotropic g

268 c density-95 (PSD-95) with the glutamatergic N-methyl-d-aspartate receptor NR2B subunit and the subse

269 Blocking N-methyl-D-aspartate receptors or activation of extracel

270 in G either reduced synaptic localization of N-methyl D-aspartate receptors, or had a direct effect o

271 cytoskeleton-associated protein (P=0.23) or N-methyl-D-aspartate receptor (P=0.74) post-synaptic sig

272 ications for understanding D-serine-mediated N-methyl-D-aspartate receptor plasticity in the amygdala

273 We emphasize the key role of N-methyl-D-aspartate receptor potentiation by D1 recepto

274 inct subdivisions of ACC with different AMPA/N-methyl-D-aspartate receptor profiles.

275 reas stimulating predominantly extrasynaptic N-methyl-D-aspartate receptors promoted the proteasomal

276 -5-methyl-4-isoxazolepropionic acid receptor/N-methyl-D-aspartate receptor ratio.

277 tion between alpha-syn and GluN2D-expressing N-methyl-D-aspartate receptors, represents a precocious

278 DCS), a partial agonist at the glutamatergic N-methyl-D-aspartate receptor, showed promise in enhanci

279 gic synapses, particularly components of the N-methyl-D-aspartate receptor signaling complex, includi

280 r bound to compound 1 (Cmpd-1), a novel A2AR/N-methyl d-aspartate receptor subtype 2B (NR2B) dual ant

281 ed Ags (microtubule-associated protein-2 and N-methyl d-aspartate receptor subunit NR-2A), and myelin

282 d number of key synaptic proteins, including N-methyl-d-aspartate receptor subunit 2B (NR2B) and PSD-

283 ts, with the GRIN2A gene encoding the GluN2A N-methyl-d-aspartate receptor subunit being most often a

284 Autoantibodies (AB) against N-methyl-D-aspartate receptor subunit NR1 (NMDAR1) are h

285 ing impaired spine pruning and switch in the N-methyl-D-aspartate receptor subunit, which are relevan

286 n unexpectedly high seroprevalence (~10%) of N-methyl-D-aspartate-receptor subunit-NR1 (NMDAR1) autoa

287 We detected down-regulation of N-methyl-D-aspartate receptor subunits 2A and 2B (GluN2A

288 memory circuitry were assessed by measuring N-methyl-D-aspartate receptor subunits and glutamic acid

289 le propionic acid receptor (AMPAR) and GluN1 N-methyl-D-aspartate receptor subunits.

290 TH-induced decreased expression of AMPAR and N-methyl-D-aspartate receptor subunits.

291 of IgG antibodies to the NR1 subunit of the N-methyl-D-aspartate receptor, that is, the characterist

292 long term potentiation through regulation of N-methyl-d-aspartate receptor trafficking.

293 We found that only N-methyl-D-aspartate receptor transmission onto the apic

294 represents an effective strategy to enhance N-methyl-D-aspartate receptor transmission.

295 -hydroxy-5-methyl-4-isoxazole propionic acid/N-methyl-D-aspartate receptor transmission.

296 mine-2 receptor (D2R) and NR1 subunit of the N-methyl-D-aspartate receptor using a flow cytometry liv

297 ion of CXCR4, the IL-1beta receptor, and the N-methyl-d-aspartate receptor was required.

298 d modulation of extinction and plasticity on N-methyl-D-aspartate receptors was examined as well.

299 roxy-5-methyl-4-isoxazole propionic acid and N-methyl-D-aspartate receptors were not regulated after

300 ls the activity and synaptic localization of N-methyl-d-aspartate receptors, which activity is impair

301 opioid facilitation, and interactions of the N-methyl D-aspartate receptor with opioids at the level