ライフサイエンスコーパス: N-methyl-D-aspartate

1 biological basis of action of noncompetitive N-methyl-D-aspartate acid receptor (NMDA-R) antagonists

2 clear whether d-cycloserine (DCS), a partial N-methyl-d-aspartate agonist that enhances fear extincti

3 d-cycloserine (DCS), a partial glutamatergic N-methyl-D-aspartate agonist, as an augmentation strateg

4 dibenzo[a,d]cyclohepten-5,10-imine maleate]) N-methyl-d-aspartate antagonists partially decreased bot

5 apentinoids, tramadol, lidocaine, and/or the N-methyl-d-aspartate class of glutamate receptor antagon

6 methyl-4-isoxazole propionic acid (AMPA) and N-methyl-D-aspartate currents and the ability to exhibit

7 iation at these synapses as measured by AMPA/N-methyl-D-aspartate currents.

8 genic state in vitro and in vivo after NMDA (N-methyl-d-aspartate) damage in young mice.

9 We further identify N-methyl-d-aspartate-dependent long-term depression (NMD

10 N-methyl-d-aspartate-encephalitis or inborn errors of me

11 opposes synaptic strengthening by increasing N-methyl D-aspartate glutamate receptor (NMDAR) internal

12 ysfunction is further posited to result from N-methyl-D-aspartate glutamate receptor (NMDAR) hypofunc

13 Ketamine, an N-methyl-d-aspartate glutamate receptor antagonist, has

14 rapid antidepressant effects of ketamine, an N-methyl-D-aspartate glutamate receptor antagonist, have

15 At subanesthetic doses, ketamine, an N-methyl-D-aspartate glutamate receptor antagonist, incr

16 als and humans, particularly those involving N-methyl-D-aspartate glutamate receptor antagonists, to

17 izophrenia is associated with disruptions in N-methyl-D-aspartate glutamate receptor subtype (NMDAR)-

18 terious effects are very likely caused by an N-methyl-d-aspartate-mediated non-opioid mechanism as Dy

19 astric tone and motility were recorded after N-methyl-d-aspartate microinjection in the SNpc and/or o

20 N-methyl D-aspartate (NMDA) ion channels play a key role

21 ing decreases in tyrosine phosphorylation of N-methyl-D aspartate (NMDA) receptor subunit 2 (GluN2) t

22 of SFK targets, including GluN2A and GluN2B N-methyl-D-aspartate (NMDA) and GluA2 alpha-amino-3-hydr

23 In healthy subjects (HS), N-methyl-D-aspartate (NMDA) antagonists like memantine a

24 roduce low frequency tonic firing results in N-methyl-D-aspartate (NMDA) excitation balanced by gamma

25 suggests that ketamine, an antagonist of the N-methyl-d-aspartate (NMDA) glutamate receptor (GluR), h

26 In vivo imaging of N-methyl-d-aspartate (NMDA) glutamate receptor and gamma

27 probably caused by kynurenine modulation of N-methyl-d-aspartate (NMDA) glutamate receptors which ar

28 novel glutamatergic compound that acts as an N-methyl-D-aspartate (NMDA) modulator with glycine-like

29 gical concentration of KCl (5 mm or K5) plus N-methyl-d-aspartate (NMDA) or to 25 mm KCl (K25).

30 -methyl-4-isoxazole propionic acid (AMPA) to N-methyl-D-aspartate (NMDA) ratios, and matrix metallopr

31 d whether microRNAs (miRNAs) are involved in N-methyl-D-aspartate (NMDA) receptor (NMDAR)-dependent A

32 synapse function and plasticity, especially N-methyl-d-aspartate (NMDA) receptor (NMDAR)-dependent l

33 pendent on the time interval between spikes, N-methyl-D-aspartate (NMDA) receptor activation, and Cal

34 Increased postsynaptic N-methyl-D-aspartate (NMDA) receptor activity in the hyp

35 Expression of the NR1 subunit of the N-methyl-d-aspartate (NMDA) receptor and PKCgamma in the

36 The glutamate N-methyl-D-aspartate (NMDA) receptor antagonist ketamine

37 Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist that has

38 ose of ketamine, an ionotropic glutamatergic n-methyl-D-aspartate (NMDA) receptor antagonist, produce

39 antipsychotics have been shown to alleviate N-methyl-D-aspartate (NMDA) receptor antagonist-induced

40 Antidepressant activity of N-methyl-D-aspartate (NMDA) receptor antagonists and neg

41 Pretreatment with N-methyl-D-aspartate (NMDA) receptor antagonists AP5 and

42 N-methyl-D-aspartate (NMDA) receptor antagonists have be

43 view and meta-analysis of ketamine and other N-methyl-d-aspartate (NMDA) receptor antagonists in the

44 Encephalitis mediated by anti-N-methyl-D-aspartate (NMDA) receptor antibodies and herp

45 urons and cell-based assays to test for anti-N-methyl-d-aspartate (NMDA) receptor antibodies.

46 dine) has been used successfully to quantify N-methyl-d-aspartate (NMDA) receptor binding in humans.

47 Although N-methyl-d-aspartate (NMDA) receptor blockade stabilizes

48 ions in the DP were significantly reduced by N-methyl-d-aspartate (NMDA) receptor blockade.

49 N-Methyl-d-aspartate (NMDA) receptor dysfunction has bee

50 Anti-N-methyl-d-aspartate (NMDA) receptor encephalitis is a s

51 preclinical research with modulators at the N-methyl-d-aspartate (NMDA) receptor GluN2B N-terminal d

52 s in GRIN2B encoding the NR2B subunit of the N-methyl-D-aspartate (NMDA) receptor in 2 individuals wi

53 N-methyl-d-aspartate (NMDA) receptor ion channel is acti

54 the phencyclidine (PCP) binding site of the N-methyl-d-aspartate (NMDA) receptor or with sigma1 rece

55 Recent work highlights a role for altered N-methyl-d-aspartate (NMDA) receptor signaling and relat

56 wal may be due to glutamate toxicity, as the N-methyl-d-aspartate (NMDA) receptor subunit NR2B was up

57 The role of the glutamatergic N-methyl-D-aspartate (NMDA) receptor system in hedonic f

58 For we believe the first time, we show that N-methyl-d-aspartate (NMDA) receptor-dependent Ca(2+) tr

59 ng-related activity patterns known to induce N-methyl-D-aspartate (NMDA) receptor-dependent long-term

60 Evoked, N-methyl-D-aspartate (NMDA) receptor-mediated currents w

61 urodegeneration induced by the activation of N-methyl-D-aspartate (NMDA) receptors (a subtype of glut

62 pal neurons, calcium ion (Ca2+) flux through N-methyl-D-aspartate (NMDA) receptors activates Ca2+/cal

63 renic motoneuron expression of glutamatergic N-methyl-D-aspartate (NMDA) receptors and decreased expr

64 N-methyl-d-aspartate (NMDA) receptors are expressed thro

65 N-methyl-D-aspartate (NMDA) receptors are glutamate- and

66 N-methyl-d-aspartate (NMDA) receptors are glutamate- and

67 N-Methyl-D-aspartate (NMDA) receptors are glutamate-gate

68 The N-methyl-d-aspartate (NMDA) receptors are heteromeric no

69 N-methyl-D-aspartate (NMDA) receptors are known to fulfi

70 N-methyl-d-aspartate (NMDA) receptors are ligand-gated,

71 N-Methyl-D-aspartate (NMDA) receptors belong to the fami

72 taken together with the strong expression of N-methyl-D-aspartate (NMDA) receptors by its cells, are

73 Activation of extrasynaptic N-methyl-d-aspartate (NMDA) receptors causes neurodegene

74 A distinctive characteristic of N-methyl-D-aspartate (NMDA) receptors containing a GluN2

75 genetic approaches, we find that ablation of N-methyl-D-aspartate (NMDA) receptors during postnatal d

76 l studies have demonstrated that presynaptic N-methyl-d-aspartate (NMDA) receptors expressed on vagal

77 Hypofunction of N-methyl-d-aspartate (NMDA) receptors has been proposed

78 Competitive antagonists against N-methyl-D-aspartate (NMDA) receptors have played critic

79 it has been postulated that hypofunction of N-methyl-d-aspartate (NMDA) receptors in brain networks

80 The physiology of N-methyl-d-aspartate (NMDA) receptors is fundamental to

81 Our results demonstrate that activation of N-methyl-D-aspartate (NMDA) receptors is required for se

82 vel of enthusiasm to downregulate overactive N-methyl-D-aspartate (NMDA) receptors to protect neurons

83 ry that ketamine, an antagonist of glutamate/N-methyl-D-aspartate (NMDA) receptors, elicits antidepre

84 citotoxicity, mediated by overstimulation of N-methyl-D-aspartate (NMDA) receptors, is a mechanism th

85 -induced downregulation of GluN2B-containing N-methyl-D-aspartate (NMDA) receptors.

86 has been successfully used in PET imaging of N-methyl-d-aspartate (NMDA) receptors.

87 -methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors.

88 prefrontal cortex have dense populations of N-methyl-D-aspartate (NMDA) receptors.

89 eficits in glutamatergic transmission at the N-methyl-d-aspartate (NMDA) receptors.

90 lutamate release activating Ca(2+)-permeable N-methyl-D-aspartate (NMDA) receptors.

91 ne implicated in influencing learning is the N-methyl-D-aspartate (NMDA) subtype 2B glutamate recepto

92 s was mediated by glutamate receptors of the N-methyl-d-aspartate (NMDA) subtype and resulted in remo

93 The N-methyl-d-aspartate (NMDA) subtype of the ionotropic gl

94 ontactin-associated protein-like 2 (CASPR2), N-methyl-d-aspartate (NMDA), and glycine (GlY) receptors

95 ceptor (iGluR) agonists, kainic acid (KA) or N-methyl-D-aspartate (NMDA), contributed to significant,

96 traocular) unimNPs with the glutamate analog N-methyl-d-aspartate (NMDA), which is excito-toxic and i

97 tive confocal immunofluorescence showed that N-methyl-D-aspartate (NMDA)-receptor labeling was presen

98 e quantitated the cell surface expression of N-methyl-D-aspartate (NMDA)-type and alpha-amino-3-hydro

99 methylisoxazole-4-propionic acid (AMPA)- and N-methyl-D-aspartate (NMDA)-type glutamate receptors (AM

100 N-methyl-d-aspartate (NMDA)-type ionotropic glutamate re

101 ommissural pathways mimicking the effects of N-methyl-D-aspartate on locomotor frequency in isolated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

295 manipulations were employed to determine how N-methyl-D-aspartate transmission in the medial PFC chan

296 pharmacological manipulation targeted at the N-methyl-D-aspartate type glutamate receptor (NMDAR).

297 Specifically, an increase in the N-methyl-d-aspartate-type 1 receptor (NMDA-NR1) expressi

298 We found that N-methyl-d-aspartate-type glutamate receptor (NMDAR) act

299 Antagonists of N-methyl-D-aspartate-type glutamate receptors (NMDAR) in

300 While overstimulation of N-methyl-d-aspartate-type glutamate receptors (NMDARs) i