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 maging the GluN2B subunits of the N-methyl-d-aspartate receptor.

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

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

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

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

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

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

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

10 n-receptor tyrosine kinase Src or N-methyl-D-aspartate receptors.

11 bGCs directly excite mGCs through N-methyl-d-aspartate receptors.

12 phosphate receptor as well as the N-methyl-d-aspartate receptors.

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

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

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

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

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

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

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

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 ion as well as restored levels of N-methyl-d-aspartate receptors and post-synaptic markers compared w

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

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

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

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

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

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

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

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

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

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

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

38 es of ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist(2,3), provide rapid and lo

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 id antidepressant efficacy of the N-methyl-D-aspartate receptor antagonist, ketamine, for treating ma

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

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

44 ts of ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist, which produces rapid and

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

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

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

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

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

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

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

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

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

54 patients and measurements of anti-N-methyl-D-aspartate receptor antibodies were taken in 49 (14%) pat

55 ronal autoantibodies (principally N-methyl-D-aspartate receptor antibodies) and who have responded to

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

57 CSF from patients with either N-methyl-D-aspartate-receptor-antibody (pCSF(NMDAR), n = 7) or Leuc

58 N-methyl d-aspartate receptors are ligand-gated ionotropic receptor

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

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

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

62 ebo-controlled clinical trials of N-methyl-D-aspartate receptor augmentation of psychotropic drug tre

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

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

65 effect requires open presynaptic N-methyl-d-aspartate receptors but not plasmin generation.

66 rs, and GluN2B-subunit containing N-methyl-D-aspartate receptors, but not GluA1 subunit containing al

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

68 ng in reduced availability of the N-methyl-D-aspartate receptor coagonists glycine and D-serine and N

69 alcium signaling, and presynaptic N-methyl-D-aspartate receptors coupled with calcineurin signaling,

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

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

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

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

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

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

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

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

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

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

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

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

82 ed encephalomyelitis, and 6% anti-N-methyl-d-aspartate receptor encephalitis; and 17% (95% CI, 13%-21

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

87 also present in a mouse model of N-methyl-D-aspartate receptor hypofunction (Ppp1r2cre/Grin1 knockou

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

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

90 ostsynaptic current frequency and N-methyl-D-aspartate receptor hypofunction.

91 agonists glycine and D-serine and N-methyl-D-aspartate receptor hypofunction.

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

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

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

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

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

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

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

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

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

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

102 hibitors of the GluN2B subunit of N-methyl-d-aspartate receptors in the ionotropic glutamate receptor

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

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

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

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

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

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

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

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

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

112 uch deficits in humans, including N-methyl-D-aspartate receptor modulators (ketamine, D-cycloserine),

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

114 mechanisms-induced emigration via N-methyl-D-aspartate receptor (NMDA) dependence and restriction via

115 is predominantly mediated by the N-methyl-d-aspartate receptor (NMDA) receptor, although NMDA-indepe

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

117 ling events were dependent on the N-methyl-d-aspartate receptor (NMDA-R) and low-density lipoprotein

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 ne neuroinflammation (due to anti-N-methyl-D-aspartate receptor [NMDA] encephalitis and multiple scle

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

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

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

124 Increased synaptic N-methyl-d-aspartate receptor (NMDAR) activity in the hypothalamic

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

126 entiation occurred independent of N-methyl-D-aspartate receptor (NMDAR) activity, was accompanied by

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

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

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

130 n and plasticity by modulation of N-methyl-d-aspartate receptor (NMDAR) and alpha-amino-3-hydroxy-5-m

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

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

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

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

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

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

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

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

139 inhibition hypothesis posits that N-methyl-d-aspartate receptor (NMDAR) antagonists such as ketamine

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

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

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

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

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

145 st the NR1 (GluN1) subunit of the N-methyl-d-aspartate receptor (NMDAR) are among the most frequently

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

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

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

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

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

151 eton-associated protein (ARC) and N-methyl-D-aspartate receptor (NMDAR) complexes; however, larger sa

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

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

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

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

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

157 ntibodies from patients with anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis alter the levels

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

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

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

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

162 Anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis is an immune-med

163 Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most comm

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

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

166 cause of autoimmune catatonia is N-methyl-D-aspartate receptor (NMDAR) encephalitis, which can accou

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

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

169 Of these, the N-methyl-d-aspartate receptor (NMDAR) family has many critical role

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

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

172 orokynurenic acid (7-Cl-KYNA), an N-methyl-D-aspartate receptor (NMDAR) glycine site antagonist, and

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

174 this is unclear but may be due to N-methyl-D-aspartate receptor (NMDAR) hypofunction and parvalbumin

175 N-methyl-D-aspartate receptor (NMDAR) hypofunction has been implica

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

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

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

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

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

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

182 The N-methyl-d-aspartate receptor (NMDAR) is an ion channel that mediat

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

184 potentiation of excitatory GluN2B N-methyl-d-aspartate receptor (NMDAR) responses at lamina I dorsal

185 Downward FRH did not require N-methyl-D-aspartate receptor (NMDAR) signaling and was associated

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

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

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

189 Alterations of the N-methyl-d-aspartate receptor (NMDAR) subunit GluN2A, encoded by GR

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

191 emonstrate that the developmental N-methyl-D-aspartate receptor (NMDAR) subunit switch from GluN2B to

192 nine cycle, is a known agonist of N-methyl-d-aspartate receptor (NMDAR), a glutamate receptor subtype

193 nt for the GluN2B subunits of the N-methyl-d-aspartate receptor (NMDAR), a key therapeutic target for

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

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

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

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

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

199 mproves outcomes in patients with N-methyl-D-aspartate receptor (NMDAR)-antibody encephalitis.

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

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

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

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

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

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

206 All three compounds reduced N-methyl-D-aspartate receptor (NMDAR)-mediated currents 1 week afte

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

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

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

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

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

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

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

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

215 ghtly controlled by activation of N-methyl-D-aspartate receptors (NMDAR) containing the GluN2A subuni

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

217 iated nociception modulation, and N-methyl-D-aspartate receptor, NMDAR, antagonism.

218 We previously showed that N Methyl D Aspartate Receptor (NMDARs), expressed on cerebral endot

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

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

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

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

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

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

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 ion cha

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

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

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

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 N-methyl-D-aspartate receptors (NMDARs) are required to shape activ

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

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

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

240 le lumen diameter is regulated by N-methyl-d-aspartate receptors (NMDARs) expressed by brain endothel

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

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

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

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

245 Antibodies against neuronal N-methyl-D-aspartate receptors (NMDARs) in patients with anti-NMDAR

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

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

248 by glutamate receptors including N-methyl-D-aspartate receptors (NMDARs) is pivotal to brain develop

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

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

251 N-Methyl-D-aspartate receptors (NMDARs) play critical roles in the

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

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

254 d characteristics for imaging the N-methyl-d-aspartate receptors (NMDARs) subtype 2B (GluN1/2B), we i

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

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

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

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

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

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

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

262 bodies against natively expressed N-methyl-D-aspartate receptors (NMDARs), or the surface of live hip

263 ctivation by glutamate ligands of N-methyl-D-aspartate receptors (NMDARs), which is key in model syst

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

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

268 5 (PSD-95) with the glutamatergic N-methyl-d-aspartate receptor NR2B subunit and the subsequent NR2B

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

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

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

272 substantially upon addition of an N-methyl-D-aspartate receptor peptide analog but not ATP.

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

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

275 ted the properties of presynaptic N-methyl-d-aspartate receptors (pre-NMDARs) at corticohippocampal e

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

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

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

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

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

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

282 ifically successive impairment of N-methyl-d-aspartate receptor subunit 2B (NR2B), postsynaptic densi

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

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

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

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

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

288 related to an upregulation of the N-methyl-D-aspartate receptor subunits NR1 and NR2A.

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

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

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

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

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

294 an effective strategy to enhance 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 n of extinction and plasticity on N-methyl-D-aspartate receptors was examined as well.

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

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

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

300 aging the NR2B subunit within the N-methyl-d-aspartate receptor with PET.