ライフサイエンスコーパス: D-aspartate

1 onphysiological extracellular levels of free D-aspartate.

2 ther d-cycloserine (DCS), a partial N-methyl-d-aspartate agonist that enhances fear extinction, can a

3 rine (DCS), a partial glutamatergic N-methyl-D-aspartate agonist, as an augmentation strategy for exp

4 ices are incubated with low concentration of d-aspartate (an EAAT2 substrate), axon terminals accumul

5 roach enabled the relative quantification of d-aspartate and d-glutamate in individual neurons mechan

6 nd enhanced selectivity for L-aspartate over D-aspartate and L-glutamate, and lost their selectivity

7 ,d]cyclohepten-5,10-imine maleate]) N-methyl-d-aspartate antagonists partially decreased both basal a

8 EAAT2 substrate), axon terminals accumulate d-aspartate as quickly as astroglia.

9 ds, tramadol, lidocaine, and/or the N-methyl-d-aspartate class of glutamate receptor antagonists have

10 In the present work, we show that d-aspartate content in the mouse brain drastically decre

11 isoxazole propionic acid (AMPA) and N-methyl-D-aspartate currents and the ability to exhibit long-ter

12 these synapses as measured by AMPA/N-methyl-D-aspartate currents.

13 Exposing brain slices to Glut and D-aspartate (D-Asp) before recording resulted in an incr

14 d by exogenous preexposure to the amino acid D-aspartate (D-Asp).

15 te in vitro and in vivo after NMDA (N-methyl-d-aspartate) damage in young mice.

16 We further identify N-methyl-d-aspartate-dependent long-term depression (NMDA-LTD) at

17 N-methyl-d-aspartate-encephalitis or inborn errors of metabolism

18 n is further posited to result from N-methyl-D-aspartate glutamate receptor (NMDAR) hypofunction.

19 ynaptic strengthening by increasing N-methyl D-aspartate glutamate receptor (NMDAR) internalization t

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

21 idepressant effects of ketamine, an N-methyl-D-aspartate glutamate receptor antagonist, have not been

22 t subanesthetic doses, ketamine, an N-methyl-D-aspartate glutamate receptor antagonist, increases glu

23 umans, particularly those involving N-methyl-D-aspartate glutamate receptor antagonists, to illustrat

24 a is associated with disruptions in N-methyl-D-aspartate glutamate receptor subtype (NMDAR)-mediated

25 tantially increased extracellular content of d-aspartate in the brain.

26 DAR overstimulation, persistent elevation of D-aspartate levels in Ddo(-/-) brains is associated with

27 blished that postnatal reduction of cerebral D-aspartate levels is due to the concomitant onset of D-

28 ffects are very likely caused by an N-methyl-d-aspartate-mediated non-opioid mechanism as Dyn A pepti

29 ne and motility were recorded after N-methyl-d-aspartate microinjection in the SNpc and/or optogeneti

30 ases in tyrosine phosphorylation of N-methyl-D aspartate (NMDA) receptor subunit 2 (GluN2) that is cr

31 argets, including GluN2A and GluN2B N-methyl-D-aspartate (NMDA) and GluA2 alpha-amino-3-hydroxy-5-met

32 In healthy subjects (HS), N-methyl-D-aspartate (NMDA) antagonists like memantine and ketami

33 w frequency tonic firing results in N-methyl-D-aspartate (NMDA) excitation balanced by gamma-Aminobut

34 that ketamine, an antagonist of the N-methyl-d-aspartate (NMDA) glutamate receptor (GluR), has rapid

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

36 caused by kynurenine modulation of N-methyl-d-aspartate (NMDA) glutamate receptors which are activat

37 N-methyl D-aspartate (NMDA) ion channels play a key role in a wid

38 tamatergic compound that acts as an N-methyl-D-aspartate (NMDA) modulator with glycine-like partial a

39 centration of KCl (5 mm or K5) plus N-methyl-d-aspartate (NMDA) or to 25 mm KCl (K25).

40 -isoxazole propionic acid (AMPA) to N-methyl-D-aspartate (NMDA) ratios, and matrix metalloproteinase

41 microRNAs (miRNAs) are involved in N-methyl-D-aspartate (NMDA) receptor (NMDAR)-dependent AMPAR expr

42 function and plasticity, especially N-methyl-d-aspartate (NMDA) receptor (NMDAR)-dependent long-term

43 n the time interval between spikes, N-methyl-D-aspartate (NMDA) receptor activation, and Calcium/calm

44 Increased postsynaptic N-methyl-D-aspartate (NMDA) receptor activity in the hypothalamic

45 xpression of the NR1 subunit of the N-methyl-d-aspartate (NMDA) receptor and PKCgamma in the spinal c

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

47 Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist that has been fou

48 tamine, an ionotropic glutamatergic n-methyl-D-aspartate (NMDA) receptor antagonist, produces a fast-

49 hotics have been shown to alleviate N-methyl-D-aspartate (NMDA) receptor antagonist-induced BOLD sign

50 Antidepressant activity of N-methyl-D-aspartate (NMDA) receptor antagonists and negative all

51 Pretreatment with N-methyl-D-aspartate (NMDA) receptor antagonists AP5 and CGP78608

52 N-methyl-D-aspartate (NMDA) receptor antagonists have been used e

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

54 Encephalitis mediated by anti-N-methyl-D-aspartate (NMDA) receptor antibodies and herpes simple

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

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

57 Although N-methyl-d-aspartate (NMDA) receptor blockade stabilizes spines i

58 he DP were significantly reduced by N-methyl-d-aspartate (NMDA) receptor blockade.

59 N-Methyl-d-aspartate (NMDA) receptor dysfunction has been linked

60 Anti-N-methyl-d-aspartate (NMDA) receptor encephalitis is a severe but

61 cal research with modulators at the N-methyl-d-aspartate (NMDA) receptor GluN2B N-terminal domain (NT

62 2B encoding the NR2B subunit of the N-methyl-D-aspartate (NMDA) receptor in 2 individuals with West s

63 N-methyl-d-aspartate (NMDA) receptor ion channel is activated by

64 cyclidine (PCP) binding site of the N-methyl-d-aspartate (NMDA) receptor or with sigma1 receptors, re

65 work highlights a role for altered N-methyl-d-aspartate (NMDA) receptor signaling and related impair

66 e due to glutamate toxicity, as the N-methyl-d-aspartate (NMDA) receptor subunit NR2B was up-regulate

67 The role of the glutamatergic N-methyl-D-aspartate (NMDA) receptor system in hedonic feeding is

68 elieve the first time, we show that N-methyl-d-aspartate (NMDA) receptor-dependent Ca(2+) transients

69 d activity patterns known to induce N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentia

70 Evoked, N-methyl-D-aspartate (NMDA) receptor-mediated currents were recor

71 ns, calcium ion (Ca2+) flux through N-methyl-D-aspartate (NMDA) receptors activates Ca2+/calmodulin s

72 oneuron expression of glutamatergic N-methyl-D-aspartate (NMDA) receptors and decreased expression of

73 N-methyl-d-aspartate (NMDA) receptors are expressed throughout th

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

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

76 N-Methyl-D-aspartate (NMDA) receptors are glutamate-gated excitat

77 The N-methyl-d-aspartate (NMDA) receptors are heteromeric non-selecti

78 N-methyl-D-aspartate (NMDA) receptors are known to fulfill crucia

79 N-methyl-d-aspartate (NMDA) receptors are ligand-gated, cation-se

80 N-Methyl-D-aspartate (NMDA) receptors belong to the family of ion

81 ether with the strong expression of N-methyl-D-aspartate (NMDA) receptors by its cells, are consisten

82 Activation of extrasynaptic N-methyl-d-aspartate (NMDA) receptors causes neurodegeneration an

83 A distinctive characteristic of N-methyl-D-aspartate (NMDA) receptors containing a GluN2A subunit

84 pproaches, we find that ablation of N-methyl-D-aspartate (NMDA) receptors during postnatal developmen

85 have demonstrated that presynaptic N-methyl-d-aspartate (NMDA) receptors expressed on vagal afferent

86 Hypofunction of N-methyl-d-aspartate (NMDA) receptors has been proposed to have a

87 Competitive antagonists against N-methyl-D-aspartate (NMDA) receptors have played critical roles

88 een postulated that hypofunction of N-methyl-d-aspartate (NMDA) receptors in brain networks supportin

89 The physiology of N-methyl-d-aspartate (NMDA) receptors is fundamental to brain dev

90 ults demonstrate that activation of N-methyl-D-aspartate (NMDA) receptors is required for sensory-evo

91 thusiasm to downregulate overactive N-methyl-D-aspartate (NMDA) receptors to protect neurons from exc

92 etamine, an antagonist of glutamate/N-methyl-D-aspartate (NMDA) receptors, elicits antidepressant act

93 ity, mediated by overstimulation of N-methyl-D-aspartate (NMDA) receptors, is a mechanism that causes

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

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

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

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

98 ated in influencing learning is the N-methyl-D-aspartate (NMDA) subtype 2B glutamate receptor (NR2B).

99 iated by glutamate receptors of the N-methyl-d-aspartate (NMDA) subtype and resulted in removal of gl

100 The N-methyl-d-aspartate (NMDA) subtype of the ionotropic glutamate r

101 GluR) agonists, kainic acid (KA) or N-methyl-D-aspartate (NMDA), contributed to significant, progress

102 ) unimNPs with the glutamate analog N-methyl-d-aspartate (NMDA), which is excito-toxic and induces RG

103 ocal immunofluorescence showed that N-methyl-D-aspartate (NMDA)-receptor labeling was present more fr

104 ated the cell surface expression of N-methyl-D-aspartate (NMDA)-type and alpha-amino-3-hydroxy-5-meth

105 N-methyl-d-aspartate (NMDA)-type ionotropic glutamate receptors m

106 The endogenous NMDA receptor (NMDAR) agonist D-aspartate occurs transiently in the mammalian brain be

107 l pathways mimicking the effects of N-methyl-D-aspartate on locomotor frequency in isolated rodent sp

108 te levels is due to the concomitant onset of D-aspartate oxidase (DDO) activity, a flavoenzyme that s

109 of antibody-positive patients, anti-N-methyl-d-aspartate receptor (5 patients), had normal MRI result

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

111 and demonstrated that it acts as an N-methyl D-aspartate receptor (NMDA-R) agonist, leading to calciu

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

113 ut not CBD3 without TAT, attenuated N-methyl-d-aspartate receptor (NMDAR) activity and protected neur

114 Increased N-methyl-d-aspartate receptor (NMDAR) activity in the paraventric

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

116 specific phosphatase that regulates N-methyl-D-aspartate receptor (NMDAR) and alpha-amino-3-hydroxy-5

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

118 ers to search for antibodies to the N-methyl-D-aspartate receptor (NMDAR) and contactin-associated pr

119 filaments to examine the roles that N-methyl-D-aspartate receptor (NMDAR) and hyperpolarization-activ

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

121 owing EtOH abstinence utilizing the N-methyl D-aspartate receptor (NMDAR) antagonist and antidepressa

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

123 non-competitive, voltage-dependent N-Methyl-D-aspartate receptor (NMDAR) antagonist, has been shown

124 Through the fortuitous discovery of N-methyl-D-aspartate receptor (NMDAR) antagonists as effective an

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

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

127 IONALE: Encephalitis caused by anti-N-methyl-d-aspartate receptor (NMDAR) antibodies is the leading c

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

129 ion of neurotransmitter release and N-methyl-D-aspartate receptor (NMDAR) blockade, which is consiste

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

131 the density of excitatory synapses, N-methyl-D-aspartate receptor (NMDAR) clusters, or cell viability

132 The N-methyl-D-aspartate receptor (NMDAR) coagonists glycine, D-serin

133 eleton-associated protein (ARC) and N-methyl-d-aspartate receptor (NMDAR) complexes.

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

135 and prolongs the decay kinetics of N-methyl-d-aspartate receptor (NMDAR) currents in male rat infral

136 oked in schizophrenia research, and N-methyl-d-aspartate receptor (NMDAR) dysfunction can provide ins

137 Because N-methyl-D-aspartate receptor (NMDAR) dysfunction has been strong

138 Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe bu

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

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

141 equently described in patients with N-methyl-d-aspartate receptor (NMDAR) encephalitis, yet NMDAR enc

142 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 epilepsy-

144 utoantibodies against glutamatergic N-methyl-D-aspartate receptor (NMDAR) have been reported in a pro

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

146 te excess in schizophrenia and that N-methyl-d-aspartate receptor (NMDAR) hypofunction on gamma-amino

147 neurobiological findings that link N-methyl-D-aspartate receptor (NMDAR) hypofunction to the etiolog

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

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

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

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

152 cal studies suggest that augmenting N-methyl-d-aspartate receptor (NMDAR) signaling may promote exper

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

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

155 sequencing screen revealed that the N-methyl-D-aspartate receptor (NMDAR) subunit Grin2B was elevated

156 GRIN2A and GRIN2B) subunits of the N-methyl-D-aspartate receptor (NMDAR), a ligand-gated ion channel

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

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

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

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

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

162 entral role in learning and memory, N-methyl D-aspartate receptor (NMDAR)-dependent signaling regulat

163 molecules, is its manifestation as N-methyl-d-aspartate receptor (NMDAR)-dependent slow inward curre

164 ons is known to rely on hippocampal N-methyl-D-aspartate receptor (NMDAR)-dependent synaptic plastici

165 ts are thought to be due to reduced N-methyl-D-aspartate receptor (NMDAR)-mediated inhibition from pa

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

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

168 s-especially antibodies against the N-methyl-D-aspartate receptor (NMDAR)-more commonly than do healt

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

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

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

172 eton-associated protein (P=0.23) or N-methyl-D-aspartate receptor (P=0.74) post-synaptic signalling g

173 A2 pyramidal neurons that relied on N-methyl-d-aspartate receptor activation and calcium/calmodulin-d

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

175 N-methyl-D-aspartate receptor activation requires the binding of

176 ng acetylcholinesterase inhibition, N-methyl-D-aspartate receptor activation, and calcium dysregulati

177 e findings implicate dysfunction of N-methyl-D-aspartate receptor and glutamatergic neurotransmission

178 The N-methyl-D-aspartate receptor antagonist ketamine can improve maj

179 a single sub-anesthetic dose of the N-methyl-D-aspartate receptor antagonist ketamine may work to cor

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

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

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

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

184 matory genes, and that ketamine (an N-methyl-D-aspartate receptor antagonist) would reduce or block t

185 inhalational general anesthetic and N-methyl-D-aspartate receptor antagonist, may also be a rapidly a

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

187 e considered first-line therapy and N-Methyl-d-aspartate receptor antagonists also appears to be effe

188 Additionally, the NR2B-selective N-methyl-D-aspartate receptor antagonists ifenprodil and CP-101,6

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

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

191 ng confirmed identification of anti-N-methyl-D-aspartate receptor antibodies in the cerebrospinal flu

192 demonstrate the epileptogenicity of N-methyl D-aspartate receptor antibodies in vivo, and suggest tha

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

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

195 d sensory memory that might reflect N-methyl-D-aspartate receptor dysfunction in chronic cannabis use

196 teristic laboratory finding of anti-N-methyl-D-aspartate receptor encephalitis.

197 ia thought to reflect glutamatergic N-methyl-d-aspartate receptor function and excitatory-inhibitory

198 Inhibition of neuronal activity, N-methyl-d-aspartate receptor function, or glycogen synthase kina

199 glutamateric neurotransmission and N-methyl-D-aspartate receptor hypofunction in the pathophysiology

200 The N-methyl-D-aspartate receptor hypofunction model of schizophrenia

201 ine receptor (GLY-R) in 5 patients, N-methyl-d-aspartate receptor in 4 patients and gamma-aminobutyri

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

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

204 closerine, a partial agonist at the N-methyl-d-aspartate receptor in the amygdala, has been associate

205 of the essential NR1 subunit of the N-methyl-D-aspartate receptor increased during downstream migrati

206 minobutyric acid type A receptor or N-methyl-D-aspartate receptor inhibition.

207 Deficient signaling through the N-methyl-D-aspartate receptor is hypothesized to underlie many si

208 for understanding D-serine-mediated N-methyl-D-aspartate receptor plasticity in the amygdala and how

209 ivisions of ACC with different AMPA/N-methyl-D-aspartate receptor profiles.

210 ses, particularly components of the N-methyl-D-aspartate receptor signaling complex, including the PS

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

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

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

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

215 red spine pruning and switch in the N-methyl-D-aspartate receptor subunit, which are relevant to auti

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

217 nic acid receptor (AMPAR) and GluN1 N-methyl-D-aspartate receptor subunits.

218 We found that only N-methyl-D-aspartate receptor transmission onto the apical dendri

219 5-methyl-4-isoxazole propionic acid/N-methyl-D-aspartate receptor transmission.

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

221 ceptor (D2R) and NR1 subunit of the N-methyl-D-aspartate receptor using a flow cytometry live cell-ba

222 cilitation, and interactions of the N-methyl D-aspartate receptor with opioids at the level of the sp

223 ulated spine that depends on NMDAR (N-methyl-d-aspartate receptor) and CaMKII signalling and on posts

224 n-competitive, glutamatergic NMDAR (N-methyl-d-aspartate receptor) antagonist (R,S)-ketamine exerts r

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

226 that this effect was independent of N-methyl-D-aspartate receptor, low-density lipoprotein-related pr

227 ntibodies to the NR1 subunit of the N-methyl-D-aspartate receptor, that is, the characteristic labora

228 1 (Sp1)-binding site resulted in an N-methyl-d-aspartate receptor-dependent enhancement of COX-2 prom

229 N-methyl-D-aspartate receptor-dependent plasticity in the amygdal

230 Here we report that hippocampal N-methyl-d-aspartate receptor-dependent synaptic plasticity is el

231 naptic activity and was shown to be N-methyl-d-aspartate receptor-dependent.

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

233 tion thought to index glutamatergic N-methyl-D-aspartate receptor-mediated neurotransmission, which i

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

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

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

237 Most patients with N-methyl D-aspartate-receptor antibody encephalitis develop seizu

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

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

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

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

242 tion between synaptic activation of N-methyl-D-aspartate receptors (NMDARs) and intrinsic oscillatory

243 uncompetitive inhibitory effects on N-methyl-d-aspartate receptors (NMDARs) and may preferentially al

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

245 d-Serine modulates N-methyl d-aspartate receptors (NMDARs) and regulates synaptic pl

246 N-methyl-d-aspartate receptors (NMDARs) are glutamate-gated ion c

247 N-Methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion c

248 N-methyl-D-aspartate receptors (NMDARs) are glutamate-gated, calc

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

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

251 N-methyl-d-aspartate receptors (NMDARs) are ionotropic glutamater

252 N-methyl-D-aspartate receptors (NMDARs) are ligand-gated cation c

253 N-methyl-D-aspartate receptors (NMDARs) are necessary for the ind

254 The N-methyl-d-aspartate receptors (NMDARs) constitute an important c

255 N-Methyl-d-aspartate receptors (NMDARs) display a critical role i

256 present study evaluated the role of N-methyl-D-aspartate receptors (NMDARs) expressed in the dorsal r

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

258 is hyperfunction of glutamate-type N-methyl-d-aspartate receptors (NMDARs) in the selectively vulner

259 N-methyl-D-aspartate receptors (NMDARs) mediate synaptic plastici

260 Postsynaptic N-methyl-d-aspartate receptors (NMDARs) phasically activated by p

261 N-Methyl-D-aspartate receptors (NMDARs) play pivotal roles in syn

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

263 al studies revealed contribution of N-methyl-D-aspartate receptors (NMDARs) to a variety of neuropsyc

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

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

266 The ionotropic glutamate receptors (N-methyl-D-aspartate receptors (NMDARs)) are composed of large co

267 h memantine and ketamine antagonize N-methyl-D-aspartate receptors (NMDARs), a glutamate receptor sub

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

269 ire stimulation of both betaARs and N-methyl-D-aspartate receptors (NMDARs).

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

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

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

273 ing of 'Delay cells' is mediated by N-methyl-d-aspartate receptors and weakened by cAMP-PKA-potassium

274 dynamics due to synaptic input via n-methyl-d-aspartate receptors are qualitatively accounted for in

275 say suggests that protein levels of N-methyl-D-aspartate receptors are reduced in this transgenic mou

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

277 modulation of the GluN2D-expressing N-methyl-D-aspartate receptors in cholinergic interneurons.

278 lutamate that selectively activated N-methyl-d-aspartate receptors in homotypic, but not heterotypic,

279 N-Methyl-D-aspartate receptors mediate the slow component of exci

280 Blocking N-methyl-D-aspartate receptors or activation of extracellular sig

281 ulating predominantly extrasynaptic N-methyl-D-aspartate receptors promoted the proteasomal degradati

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

283 inihitors of both cholinesterases, N-methyl-D-aspartate receptors, and monoamine oxidases.

284 er reduced synaptic localization of N-methyl D-aspartate receptors, or had a direct effect on recepto

285 een alpha-syn and GluN2D-expressing N-methyl-D-aspartate receptors, represents a precocious biologica

286 thyl-4-isoxazole propionic acid and N-methyl-D-aspartate receptors.

287 alpha7 nicotinic acetylcholine and N-methyl-D-aspartate receptors.

288 ergistically augmented signaling by N-methyl-d-aspartate receptors.

289 aptic form (post-LTP) that requires N-methyl-D-aspartate receptors.

290 kinases as well as NR2B-containing N-methyl-D-aspartate receptors.

291 tween domain layers, reminiscent of N-methyl-D-aspartate receptors.

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

293 ly, application of the transporter substrate d-aspartate reversed the TTX-induced increase in the per

294 ions were employed to determine how N-methyl-D-aspartate transmission in the medial PFC changes durin

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

296 Specifically, an increase in the N-methyl-d-aspartate-type 1 receptor (NMDA-NR1) expression within

297 We found that N-methyl-d-aspartate-type glutamate receptor (NMDAR) activation d

298 Antagonists of N-methyl-D-aspartate-type glutamate receptors (NMDAR) induce symp

299 While overstimulation of N-methyl-d-aspartate-type glutamate receptors (NMDARs) is thought

300 Conversely, release of charged osmolytes (d-aspartate) was strongly reduced by deletion of LRRC8A