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 probe for imaging the GluN2B subunits of the N-methyl-d-aspartate receptor.

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

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

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

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

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

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

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

10 h as the non-receptor tyrosine kinase Src or N-methyl-D-aspartate receptors.

11 ) inputs, abGCs directly excite mGCs through N-methyl-d-aspartate receptors.

12 1,4,5-trisphosphate receptor as well as the N-methyl-d-aspartate receptors.

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

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

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

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

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

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

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

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 roinflammation as well as restored levels of N-methyl-d-aspartate receptors and post-synaptic markers

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

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

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

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

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

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

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

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

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

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

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

38 sthetic doses of ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist(2,3), provide r

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 rts the rapid antidepressant efficacy of the N-methyl-D-aspartate receptor antagonist, ketamine, for

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

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

44 -like effects of ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist, which produces

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

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

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

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

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

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

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

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

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

54 169 (49%) patients and measurements of anti-N-methyl-D-aspartate receptor antibodies were taken in 4

55 ive for neuronal autoantibodies (principally N-methyl-D-aspartate receptor antibodies) and who have r

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

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

58 N-methyl d-aspartate receptors are ligand-gated ionotrop

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

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

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

62 blind, placebo-controlled clinical trials of N-methyl-D-aspartate receptor augmentation of psychotrop

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

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

65 d that this effect requires open presynaptic N-methyl-d-aspartate receptors but not plasmin generatio

66 cid receptors, and GluN2B-subunit containing N-methyl-D-aspartate receptors, but not GluA1 subunit co

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

68 bly resulting in reduced availability of the N-methyl-D-aspartate receptor coagonists glycine and D-s

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

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

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

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

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

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

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

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

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

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

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

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

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

82 disseminated encephalomyelitis, and 6% anti-N-methyl-d-aspartate receptor encephalitis; and 17% (95%

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

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

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

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

87 alities are also present in a mouse model of N-methyl-D-aspartate receptor hypofunction (Ppp1r2cre/Gr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 elective inhibitors of the GluN2B subunit of N-methyl-d-aspartate receptors in the ionotropic glutama

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

104 r gamma-aminobutyric 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-2

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

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

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

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

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

111 o reverse such deficits in humans, including N-methyl-D-aspartate receptor modulators (ketamine, D-cy

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

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

114 ced by two mechanisms-induced emigration via N-methyl-D-aspartate receptor (NMDA) dependence and rest

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

116 cell-signaling events were dependent on the N-methyl-d-aspartate receptor (NMDA-R) and low-density l

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

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

119 s, autoimmune neuroinflammation (due to anti-N-methyl-D-aspartate receptor [NMDA] encephalitis and mu

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

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

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

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

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

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

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

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

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

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

130 Increased synaptic N-methyl-d-aspartate receptor (NMDAR) activity in the hy

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

132 induced potentiation occurred independent of N-methyl-D-aspartate receptor (NMDAR) activity, was acco

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

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

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

136 tic function and plasticity by modulation of N-methyl-d-aspartate receptor (NMDAR) and alpha-amino-3-

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

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

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

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

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

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

143 vailing disinhibition hypothesis posits that N-methyl-d-aspartate receptor (NMDAR) antagonists such a

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

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

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

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

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

149 (ABs) against the NR1 (GluN1) subunit of the N-methyl-d-aspartate receptor (NMDAR) are among the most

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

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

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

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

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

155 ed cytoskeleton-associated protein (ARC) and N-methyl-D-aspartate receptor (NMDAR) complexes; however

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

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

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

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

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

161 rate that antibodies from patients with anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis alter

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

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

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

165 Anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis is an

166 Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is th

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

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

169 most common cause of autoimmune catatonia is N-methyl-D-aspartate receptor (NMDAR) encephalitis, whic

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

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

172 Of these, the N-methyl-d-aspartate receptor (NMDAR) family has many cr

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

174 ug of 7-chlorokynurenic acid (7-Cl-KYNA), an N-methyl-D-aspartate receptor (NMDAR) glycine site antag

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

176 underlying this is unclear but may be due to N-methyl-D-aspartate receptor (NMDAR) hypofunction and p

177 N-methyl-D-aspartate receptor (NMDAR) hypofunction has b

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

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

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

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

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

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

184 The N-methyl-d-aspartate receptor (NMDAR) is an ion channel

185 gates the potentiation of excitatory GluN2B N-methyl-d-aspartate receptor (NMDAR) responses at lamin

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

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

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

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

190 Alterations of the N-methyl-d-aspartate receptor (NMDAR) subunit GluN2A, en

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

192 We demonstrate that the developmental N-methyl-D-aspartate receptor (NMDAR) subunit switch fro

193 the methionine cycle, is a known agonist of N-methyl-d-aspartate receptor (NMDAR), a glutamate recep

194 imaging agent for the GluN2B subunits of the N-methyl-d-aspartate receptor (NMDAR), a key therapeutic

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

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

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

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

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

200 istration improves outcomes in patients with N-methyl-D-aspartate receptor (NMDAR)-antibody encephali

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

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

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

204 All three compounds reduced N-methyl-D-aspartate receptor (NMDAR)-mediated currents

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

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

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

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

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

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

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

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

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

214 3A1, are tightly controlled by activation of N-methyl-D-aspartate receptors (NMDAR) containing the Gl

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

216 ephrine mediated nociception modulation, and N-methyl-D-aspartate receptor, NMDAR, antagonism.

217 We previously showed that N Methyl D Aspartate Receptor (NMDARs), expressed on cer

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 cal arteriole lumen diameter is regulated by N-methyl-d-aspartate receptors (NMDARs) expressed by bra

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

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

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

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

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

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 meditated by glutamate receptors including N-methyl-D-aspartate receptors (NMDARs) is pivotal to br

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 critical ro

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

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

254 ith improved characteristics for imaging the N-methyl-d-aspartate receptors (NMDARs) subtype 2B (GluN

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

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

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

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

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

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

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

262 wed no antibodies against natively expressed N-methyl-D-aspartate receptors (NMDARs), or the surface

263 involving activation by glutamate ligands of N-methyl-D-aspartate receptors (NMDARs), which is key in

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

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

266 -isoxazole-propionate receptors (AMPARs) 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 as reduced substantially upon addition of an N-methyl-D-aspartate receptor peptide analog but not ATP

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

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

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

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

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

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

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

282 diated specifically successive impairment of N-methyl-d-aspartate receptor subunit 2B (NR2B), postsyn

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

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

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

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

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

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

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

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

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

300 ates for imaging the NR2B subunit within the N-methyl-d-aspartate receptor with PET.