ライフサイエンスコーパス: aspartate receptor

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

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

3 ibited both glutamate release and N-methyl-d-aspartate receptors.

4 osteric inhibitor of GluN1/GluN2B N-methyl-D-aspartate receptors.

5 inases as well as NR2B-containing N-methyl-D-aspartate receptors.

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

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

8 gistically augmented signaling by N-methyl-d-aspartate receptors.

9 lpha7 nicotinic acetylcholine and N-methyl-D-aspartate receptors.

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

11 n-dependent protein kinase II and N-methyl-D-aspartate receptor 2A and increased N-methyl-D-aspartate

12 ) females had decreased levels of N-methyl-d-aspartate receptor 2B in hippocampal PSD fractions with

13 partate receptor 2A and increased N-methyl-D-aspartate receptor 2B levels and were independent of amy

14 antibody-positive patients, anti-N-methyl-d-aspartate receptor (5 patients), had normal MRI results

15 vity through its effects on NMDA (N-methyl-D-aspartate) receptors, a determined effort has been made

16 pyramidal neurons that relied on N-methyl-d-aspartate receptor activation and calcium/calmodulin-dep

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

18 which may determine the extent of N-methyl-D-aspartate receptor activation in the amygdala, a key str

19 t and hyperalgesia) that required N-methyl-D-aspartate receptor activation of adenylyl cyclase type 1

20 N-methyl-D-aspartate receptor activation requires the binding of a

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

22 findings implicate dysfunction of N-methyl-D-aspartate receptor and glutamatergic neurotransmission i

23 n-dependent protein kinase II and N-methyl-D-aspartate receptors and suggest that NA supplementation

24 g of 'Delay cells' is mediated by N-methyl-d-aspartate receptors and weakened by cAMP-PKA-potassium c

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

26 ic acetylcholine receptor and the N-methyl-D-aspartate receptor, and 3-hydroxykynurenine (3-HK), a ge

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

28 nihitors of both cholinesterases, N-methyl-D-aspartate receptors, and monoamine oxidases.

29 Furthermore, NMDA (N-methyl-d-aspartate) receptor antagonism by ketamine had an opposi

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

31 Ketamine, a noncompetitive N-methyl-D-aspartate receptor antagonist has shown potential as a r

32 The N-methyl-D-aspartate receptor antagonist ketamine can improve major

33 single sub-anesthetic dose of the N-methyl-D-aspartate receptor antagonist ketamine may work to corre

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

35 ompounds, including the glutamate N-methyl-D-aspartate receptor antagonist ketamine, have spurred ren

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

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

38 Ketamine is a potent N-methyl-D-aspartate receptor antagonist with a potentially novel m

39 tory genes, and that ketamine (an N-methyl-D-aspartate receptor antagonist) would reduce or block thi

40 at administration of ketamine, an N-methyl-D-aspartate receptor antagonist, in monkeys caused a dose-

41 inical trials have shown that the N-methyl-D-aspartate receptor antagonist, ketamine, can induce an a

42 halational general anesthetic and N-methyl-D-aspartate receptor antagonist, may also be a rapidly act

43 Subchronic treatment with the N-methyl-D-aspartate receptor antagonist, phencyclidine (PCP), indu

44 discovery shows that ketamine, a N-methyl-D-aspartate receptor antagonist, produces rapid (within ho

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

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

47 n ionotropic glutamatergic NMDAR (N-methyl-D-aspartate receptor) antagonist, produces fast-acting ant

48 considered first-line therapy and N-Methyl-d-aspartate receptor antagonists also appears to be effect

49 Additionally, the NR2B-selective N-methyl-D-aspartate receptor antagonists ifenprodil and CP-101,606

50 ust antidepressant effects of the N-methyl-D-aspartate receptor antagonists ketamine and traxoprodil

51 N-methyl-D-aspartate receptor antagonists, such as ketamine, have r

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

53 mplicated in the rapid actions of N-methyl-D-aspartate receptor antagonists.

54 gnitive and behavioral effects of N-methyl-D-aspartate receptor antagonists.

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

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

57 -associated encephalitis, 211 had N-methyl-D-aspartate receptor antibodies and 38 were negative for t

58 confirmed identification of anti-N-methyl-D-aspartate receptor antibodies in the cerebrospinal fluid

59 monstrate the epileptogenicity of N-methyl D-aspartate receptor antibodies in vivo, and suggest that

60 scores, correlated with decreased N-methyl-d-aspartate receptor antibody levels and were associated w

61 Most patients with N-methyl D-aspartate-receptor antibody encephalitis develop seizure

62 ynamics due to synaptic input via n-methyl-d-aspartate receptors are qualitatively accounted for in t

63 y suggests that protein levels of N-methyl-D-aspartate receptors are reduced in this transgenic mouse

64 Tonic activation of N-methyl-D-aspartate receptors at synapses in the amygdala under lo

65 tial agonist at the glutamatergic N-methyl-d-aspartate receptor, augments and accelerates a full cour

66 ow a large number of requests for N-methyl-D-aspartate receptor autoantibody (NMDAR-Ab) tests, and it

67 Parenchymal administration of the N-methyl-d-aspartate receptor blocker MK-801 directly into the caud

68 cy stimulation, and is blocked by N-methyl-D-aspartate receptor blockers in rats.

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

70 nd NR2B receptors, Src within the N-methyl-D-aspartate receptor complex, and the subsequent Ca(2+)-de

71 (Sp1)-binding site resulted in an N-methyl-d-aspartate receptor-dependent enhancement of COX-2 promot

72 K3 inhibitors improve deficits in N-methyl-D-aspartate receptor-dependent long-term potentiation at m

73 tial function in the induction of N-methyl-D-aspartate receptor-dependent long-term potentiation in f

74 N-methyl-D-aspartate receptor-dependent plasticity in the amygdala

75 Mechanisms of N-methyl-D-aspartate receptor-dependent synaptic plasticity contrib

76 Here we report that hippocampal N-methyl-d-aspartate receptor-dependent synaptic plasticity is elim

77 ptic activity and was shown to be N-methyl-d-aspartate receptor-dependent.

78 of synaptic connections by NMDA (N-methyl-d-aspartate) receptor-dependent long-term potentiation (LT

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

80 surprisingly, the total number of N-methyl D-aspartate receptors did not differ between test and cont

81 sensory memory that might reflect N-methyl-D-aspartate receptor dysfunction in chronic cannabis users

82 ristic laboratory finding of anti-N-methyl-D-aspartate receptor encephalitis.

83 epolarization, thereby augmenting N-methyl-d-aspartate receptor function and contributing to the indu

84 thought to reflect glutamatergic N-methyl-d-aspartate receptor function and excitatory-inhibitory ne

85 Inhibition of neuronal activity, N-methyl-d-aspartate receptor function, or glycogen synthase kinase

86 ent with hypothesized deficits in N-methyl-D-aspartate receptor function.

87 we show that the identity of the N-methyl-D-aspartate receptor glycine site agonist at synapses in t

88 expression and phosphorylation of N-methyl-D-aspartate receptors) have been associated with the devel

89 lutamateric neurotransmission and N-methyl-D-aspartate receptor hypofunction in the pathophysiology o

90 The N-methyl-D-aspartate receptor hypofunction model of schizophrenia p

91 and was predicted best when both N-methyl-D-aspartate receptor-IgG and aquaporin-4-IgG coexisted (71

92 ere, we show that blockage of the N-methyl-D-aspartate receptor impairs the cycling of synaptic vesic

93 e receptor (GLY-R) in 5 patients, N-methyl-d-aspartate receptor in 4 patients and gamma-aminobutyric

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

95 recently found antibodies to the N-methyl-D-aspartate receptor in first-episode psychosis.

96 ession of the NR2B subunit of the N-methyl-D-aspartate receptor in the amygdala was examined after be

97 oserine, a partial agonist at the N-methyl-d-aspartate receptor in the amygdala, has been associated

98 regulated the NR2B subunit of the N-methyl-D-aspartate receptor in the lateral and basal nuclei of th

99 dulation of the GluN2D-expressing N-methyl-D-aspartate receptors in cholinergic interneurons.

100 tamate that selectively activated N-methyl-d-aspartate receptors in homotypic, but not heterotypic, M

101 ficant upregulation of excitatory N-methyl-D-aspartate receptors in the BLA.

102 the essential NR1 subunit of the N-methyl-D-aspartate receptor increased during downstream migration

103 rate of AMPAR recycling following N-methyl-D-aspartate receptor-induced internalization.

104 ined activation of synaptic NMDA (N-methyl-d-aspartate) receptors, induces physical association betwe

105 nobutyric acid type A receptor or N-methyl-D-aspartate receptor inhibition.

106 tomography, a marker of activated N-methyl-D-aspartate receptor ion channels, to compare in vivo glut

107 We have probed NMDA (N-methyl-D-aspartate) receptor ion channel in live HEK-293 cell, es

108 Deficient signaling through the N-methyl-D-aspartate receptor is hypothesized to underlie many sign

109 Fusions of the Escherichia coli aspartate receptor KCM to HAMP domains of defined struct

110 ant effects of ketamine and other N-methyl-D-aspartate receptor ligands, which occur within <2 hours,

111 at this effect was independent of N-methyl-D-aspartate receptor, low-density lipoprotein-related prot

112 N-Methyl-D-aspartate receptors mediate the slow component of excita

113 on thought to index glutamatergic N-methyl-D-aspartate receptor-mediated neurotransmission, which is

114 ent activity levels into enhanced N-methyl-D-aspartate receptor-mediated synaptic events, serving an

115 Furthermore, inhibition of N-methyl-d-aspartate receptor (NMDA) activity blocks spinophilin-me

116 d demonstrated that it acts as an N-methyl D-aspartate receptor (NMDA-R) agonist, leading to calcium

117 N-methyl-D-aspartate receptor (NMDA-R) hypofunction plays an import

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

119 N-Methyl-D-aspartate receptors (NMDA-Rs) are ion channels that are

120 del of glutamate spillover on the N-methyl-d-aspartate receptors (NMDA-Rs) at the cerebellar glomerul

121 (glutamate transporter-I [GLT-I], N-methyl-D-aspartate receptors [NMDA-R] and alpha-3-hydroxy-5-methy

122 by enrichment for members of the N-methyl-D-aspartate receptor (NMDAR) (P=4.24 x 10(-)(6)) and neuro

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

124 not CBD3 without TAT, attenuated N-methyl-d-aspartate receptor (NMDAR) activity and protected neuron

125 ly casein kinase II) in increased N-methyl-d-aspartate receptor (NMDAR) activity in spinally projecti

126 Increased N-methyl-d-aspartate receptor (NMDAR) activity in the paraventricul

127 The hippocampal N-methyl-D-aspartate receptor (NMDAR) activity plays important role

128 glutamatergic input, particularly N-methyl-D-aspartate receptor (NMDAR) activity, in the paraventricu

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

130 ecific phosphatase that regulates N-methyl-D-aspartate receptor (NMDAR) and alpha-amino-3-hydroxy-5-m

131 We recorded N-methyl-D-aspartate receptor (NMDAR) and alpha-amino-3-hydroxy-5-m

132 The N-methyl-d-aspartate receptor (NMDAR) and alpha-amino-3-hydroxyl-5-

133 s to search for antibodies to the N-methyl-D-aspartate receptor (NMDAR) and contactin-associated prot

134 laments to examine the roles that N-methyl-D-aspartate receptor (NMDAR) and hyperpolarization-activat

135 ine is mediated primarily through N-methyl d-aspartate receptor (NMDAR) antagonism; however, normal (

136 ing EtOH abstinence utilizing the N-methyl D-aspartate receptor (NMDAR) antagonist and antidepressant

137 The psychotomimetic effect of the N-methyl-D-aspartate receptor (NMDAR) antagonist ketamine is though

138 on-competitive, voltage-dependent N-Methyl-D-aspartate receptor (NMDAR) antagonist, has been shown to

139 nce that ketamine, a nonselective N-methyl-D-aspartate receptor (NMDAR) antagonist, has therapeutic e

140 The uncompetitive N-methyl-D-aspartate receptor (NMDAR) antagonist, ketamine, induces

141 rough the fortuitous discovery of N-methyl-D-aspartate receptor (NMDAR) antagonists as effective anti

142 Competitive N-methyl-d-aspartate receptor (NMDAR) antagonists bind to the GluN2

143 A single injection of N-methyl-D-aspartate receptor (NMDAR) antagonists produces a rapid

144 renia are based on the ability of N-methyl-D-aspartate receptor (NMDAR) antagonists to induce schizop

145 e utilized four subtype-selective N-methyl-d-aspartate receptor (NMDAR) antagonists to investigate wh

146 to mice treated chronically with N-methyl-d-aspartate receptor (NMDAR) antagonists, we demonstrate t

147 NALE: Encephalitis caused by anti-N-methyl-d-aspartate receptor (NMDAR) antibodies is the leading cau

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

149 erpes simplex encephalitis (HSE), N-methyl-D-aspartate receptor (NMDAR) antibodies were identified.

150 N-methyl-D-aspartate receptor (NMDAR) antibody encephalitis is an a

151 and NLDE-LTD were insensitive to N-methyl-D-aspartate receptor (NMDAR) block, even though LFS-LTD re

152 documented the effects of chronic N-methyl-D-aspartate receptor (NMDAR) blockade on excitatory circui

153 n of neurotransmitter release and N-methyl-D-aspartate receptor (NMDAR) blockade, which is consistent

154 Ketamine, an N-methyl-D-aspartate receptor (NMDAR) channel blocker, has been fou

155 e density of excitatory synapses, N-methyl-D-aspartate receptor (NMDAR) clusters, or cell viability.

156 The N-methyl-D-aspartate receptor (NMDAR) coagonists glycine, D-serine

157 eton-associated protein (ARC) and N-methyl-d-aspartate receptor (NMDAR) complexes.

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

159 nd prolongs the decay kinetics of N-methyl-d-aspartate receptor (NMDAR) currents in male rat infralim

160 r previous studies indicated that N-methyl-D-aspartate receptor (NMDAR) deletion from a subset of cor

161 ed in schizophrenia research, and N-methyl-d-aspartate receptor (NMDAR) dysfunction can provide insig

162 Because N-methyl-D-aspartate receptor (NMDAR) dysfunction has been strongly

163 tamate system and, in particular, N-methyl-D-aspartate receptor (NMDAR) dysfunction in the pathophysi

164 Anti- N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe auto

165 Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe but

166 Anti-N-methyl D-aspartate receptor (NMDAR) encephalitis is a severe neur

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

168 Patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis often develop pr

169 he majority of patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis suffer from pers

170 uently described in patients with N-methyl-d-aspartate receptor (NMDAR) encephalitis, yet NMDAR encep

171 he majority of patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis.

172 nsmission that is contingent upon N-methyl d-aspartate receptor (NMDAR) function contributes to core

173 Mutations in the N-methyl-D-aspartate receptor (NMDAR) gene GRIN2A cause epilepsy-ap

174 oantibodies against glutamatergic N-methyl-D-aspartate receptor (NMDAR) have been reported in a propo

175 N-methyl-D-aspartate receptor (NMDAR) hypofunction in parvalbumin-e

176 excess in schizophrenia and that N-methyl-d-aspartate receptor (NMDAR) hypofunction on gamma-aminobu

177 eurobiological findings that link N-methyl-D-aspartate receptor (NMDAR) hypofunction to the etiology

178 the theory of hypofunction of the N-methyl-D-aspartate receptor (NMDAR) in SCZ, as well as the conver

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

180 The N-methyl-D-aspartate receptor (NMDAR) is a prime target for the dev

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

182 l studies suggest that augmenting N-methyl-d-aspartate receptor (NMDAR) signaling may promote experie

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

184 Early postnatal experience shapes N-methyl-D-aspartate receptor (NMDAR) subunit composition and kinet

185 quencing screen revealed that the N-methyl-D-aspartate receptor (NMDAR) subunit Grin2B was elevated i

186 RIN2A and GRIN2B) subunits of the N-methyl-D-aspartate receptor (NMDAR), a ligand-gated ion channel w

187 D-relevant targets, including the N-methyl-d-aspartate receptor (NMDAR), acetylcholinesterase (AChE),

188 types of autoimmune encephalitis [N-methyl-D-aspartate receptor (NMDAR), alpha-amino-3-hydroxy-5-meth

189 s were retested for antibodies to N-methyl-d-aspartate receptor (NMDAR), the glycine receptor (GlyR),

190 tested/retested for antibodies to N-methyl-D-aspartate receptor (NMDAR), VGKC-complex, LGI1, CASPR2 a

191 N-Methyl-D-Aspartate receptor (NMDAR)-Ab was found in two; one pres

192 for learning and memory, includingN-methyl-d-aspartate receptor (NMDAR)-dependent long-term potentiat

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

194 tral role in learning and memory, N-methyl D-aspartate receptor (NMDAR)-dependent signaling regulates

195 olecules, is its manifestation as N-methyl-d-aspartate receptor (NMDAR)-dependent slow inward current

196 n of primary cortical neurons via N-methyl-d-aspartate receptor (NMDAR)-dependent suppression of the

197 or experience and hippocampal CA3 N-Methyl-D-aspartate receptor (NMDAR)-dependent synaptic plasticity

198 s is known to rely on hippocampal N-methyl-D-aspartate receptor (NMDAR)-dependent synaptic plasticity

199 risingly, recovery of Kv4.2 after N-methyl-D-aspartate receptor (NMDAR)-induced degradation also requ

200 is associated with a reduction in N-methyl-D-aspartate receptor (NMDAR)-mediated currents and subunit

201 ese biochemical events potentiate N-methyl-D-aspartate receptor (NMDAR)-mediated currents that underl

202 ropionic acid receptor (AMPAR) or N-methyl-D-aspartate receptor (NMDAR)-mediated excitatory postsynap

203 are thought to be due to reduced N-methyl-D-aspartate receptor (NMDAR)-mediated inhibition from parv

204 nked to underlying dysfunction of N-methyl-D-aspartate receptor (NMDAR)-mediated neurotransmission.

205 particular, a robust decrease in N-methyl-D-aspartate receptor (NMDAR)-mediated synaptic responses i

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

207 ntagonists of ion channels of the N-methyl-d-aspartate receptor (NMDAR).

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

209 against the GluN1 subunit of the N-methyl-D-aspartate receptor (NMDAR).

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

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

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

213 cy) is an agonist of the neuronal N-methyl-D-aspartate receptor (NMDAr).

214 are obligatory coagonists of the N-methyl-D-aspartate receptor (NMDAR).

215 in the pharmacological profile of N-methyl-d-aspartate receptors (NMDAR) in the NAc core, TLR4.KO ani

216 N-methyl-D-aspartate receptors (NMDAR) regulate synaptic plasticity

217 ally evoked Ca(2+) influx through N-methyl-D-aspartate receptors (NMDARs) activates spine SK channels

218 t and synaptic plasticity through N-methyl-D-aspartate receptors (NMDARs) and calcium-dependent signa

219 PS modulates N-methyl-D-aspartate receptors (NMDARs) and has been shown to have

220 on between synaptic activation of N-methyl-D-aspartate receptors (NMDARs) and intrinsic oscillatory m

221 competitive inhibitory effects on N-methyl-d-aspartate receptors (NMDARs) and may preferentially alte

222 accumulation of GluN2B-containing N-methyl-D-aspartate receptors (NMDARs) and pathological pain are c

223 d-Serine modulates N-methyl d-aspartate receptors (NMDARs) and regulates synaptic plas

224 We found that coactivation of N-methyl-D-aspartate receptors (NMDARs) and type 1 cannabinoid rece

225 N-Methyl-d-aspartate receptors (NMDARs) are Ca(2+)-permeable glutam

226 N-Methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion cha

227 N-methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion cha

228 N-methyl-d-aspartate receptors (NMDARs) are glutamate-gated ion cha

229 N-methyl-D-aspartate receptors (NMDARs) are glutamate-gated, calciu

230 N-methyl-D-aspartate receptors (NMDARs) are glycoproteins in the br

231 N-methyl-d-aspartate receptors (NMDARs) are heterotetrameric ion ch

232 N-Methyl-D-aspartate receptors (NMDARs) are involved in learning an

233 N-methyl-d-aspartate receptors (NMDARs) are ionotropic glutamatergi

234 N-methyl-D-aspartate receptors (NMDARs) are ligand-gated cation cha

235 N-methyl-D-aspartate receptors (NMDARs) are necessary for the induc

236 Regulation of the activity of N-methyl-d-aspartate receptors (NMDARs) at glutamatergic synapses i

237 The N-methyl-d-aspartate receptors (NMDARs) constitute an important cla

238 N-Methyl-d-aspartate receptors (NMDARs) display a critical role in

239 esent study evaluated the role of N-methyl-D-aspartate receptors (NMDARs) expressed in the dorsal roo

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

241 ion of cortical GluN2C-containing N-methyl-D-aspartate receptors (NMDARs) in an mTOR-dependent manner

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

243 Glutamate N-methyl-D-aspartate receptors (NMDARs) in the medial prefrontal co

244 s hyperfunction of glutamate-type N-methyl-d-aspartate receptors (NMDARs) in the selectively vulnerab

245 The subunit composition of N-methyl D-aspartate receptors (NMDARs) is tightly regulated during

246 N-methyl-d-aspartate receptors (NMDARs) mediate critical CNS functi

247 N-methyl-D-aspartate receptors (NMDARs) mediate synaptic plasticity

248 Postsynaptic N-methyl-d-aspartate receptors (NMDARs) phasically activated by pre

249 N-Methyl-D-aspartate receptors (NMDARs) play pivotal roles in synap

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

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

252 Coactivation of N-methyl-D-aspartate receptors (NMDARs) together with AMPARs and GA

253 Alcohol may act on N-methyl-d-aspartate receptors (NMDARs) within cortical circuits to

254 e ionotropic glutamate receptors (N-methyl-D-aspartate receptors (NMDARs)) are composed of large comp

255 memantine and ketamine antagonize N-methyl-D-aspartate receptors (NMDARs), a glutamate receptor subfa

256 Here, we investigate the role of N-methyl-D-aspartate receptors (NMDARs), AMPARs, and small conducta

257 SAP102 binds directly to N-methyl-D-aspartate receptors (NMDARs), anchors receptors at synap

258 N-methyl-D-aspartate receptors (NMDARs), critical mediators of both

259 largely due to hyperactivation of N-methyl-d-aspartate receptors (NMDARs), leading to toxic levels of

260 erm form depends on activation of N-methyl-d-aspartate receptors (NMDARs), whereas the rapid form doe

261 , particularly the involvement of N-methyl-D-aspartate receptors (NMDARs), which are critical for exc

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

263 ed in conantokins, antagonists of N-methyl d-aspartate receptors (NMDARs).

264 have shown altered expression of N-methyl-D-aspartate receptors (NMDARs).

265 e stimulation of both betaARs and N-methyl-D-aspartate receptors (NMDARs).

266 N-methyl-D-aspartate-receptors (NMDARs) are ionotropic glutamate re

267 5 (PSD-95) with the glutamatergic N-methyl-d-aspartate receptor NR2B subunit and the subsequent NR2B

268 Blocking N-methyl-D-aspartate receptors or activation of extracellular signa

269 reduced synaptic localization of N-methyl D-aspartate receptors, or had a direct effect on receptor

270 on-associated protein (P=0.23) or N-methyl-D-aspartate receptor (P=0.74) post-synaptic signalling gen

271 r understanding D-serine-mediated N-methyl-D-aspartate receptor plasticity in the amygdala and how th

272 We emphasize the key role of N-methyl-D-aspartate receptor potentiation by D1 receptor to trigge

273 isions of ACC with different AMPA/N-methyl-D-aspartate receptor profiles.

274 ating predominantly extrasynaptic N-methyl-D-aspartate receptors promoted the proteasomal degradation

275 -isoxazolepropionic acid receptor/N-methyl-D-aspartate receptor ratio.

276 n alpha-syn and GluN2D-expressing N-methyl-D-aspartate receptors, represents a precocious biological

277 tial agonist at the glutamatergic N-methyl-D-aspartate receptor, showed promise in enhancing treatmen

278 s, particularly components of the N-methyl-D-aspartate receptor signaling complex, including the PSD-

279 compound 1 (Cmpd-1), a novel A2AR/N-methyl d-aspartate receptor subtype 2B (NR2B) dual antagonist and

280 key synaptic proteins, including N-methyl-d-aspartate receptor subunit 2B (NR2B) and PSD-95.

281 e GRIN2A gene encoding the GluN2A N-methyl-d-aspartate receptor subunit being most often affected.

282 rotubule-associated protein-2 and N-methyl d-aspartate receptor subunit NR-2A), and myelin-derived Ag

283 Autoantibodies (AB) against N-methyl-D-aspartate receptor subunit NR1 (NMDAR1) are highly serop

284 d spine pruning and switch in the N-methyl-D-aspartate receptor subunit, which are relevant to autism

285 dly high seroprevalence (~10%) of N-methyl-D-aspartate-receptor subunit-NR1 (NMDAR1) autoantibodies (

286 We detected down-regulation of N-methyl-D-aspartate receptor subunits 2A and 2B (GluN2A and GluN2B

287 cuitry were assessed by measuring N-methyl-D-aspartate receptor subunits and glutamic acid decarboxyl

288 c acid receptor (AMPAR) and GluN1 N-methyl-D-aspartate receptor subunits.

289 decreased expression of AMPAR and N-methyl-D-aspartate receptor subunits.

290 ibodies to the NR1 subunit of the N-methyl-D-aspartate receptor, that is, the characteristic laborato

291 otentiation through regulation of N-methyl-d-aspartate receptor trafficking.

292 We found that only N-methyl-D-aspartate receptor transmission onto the apical dendrite

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

294 methyl-4-isoxazole propionic acid/N-methyl-D-aspartate receptor transmission.

295 ptor (D2R) and NR1 subunit of the N-methyl-D-aspartate receptor using a flow cytometry live cell-base

296 4, the IL-1beta receptor, and the N-methyl-d-aspartate receptor was required.

297 n of extinction and plasticity on N-methyl-D-aspartate receptors was examined as well.

298 yl-4-isoxazole propionic acid and N-methyl-D-aspartate receptors were not regulated after the 30-min

299 vity and synaptic localization of N-methyl-d-aspartate receptors, which activity is impaired by prolo

300 litation, and interactions of the N-methyl D-aspartate receptor with opioids at the level of the spin