ライフサイエンスコーパス: D-aspartate

1 onphysiological extracellular levels of free D-aspartate.

2 n the atypical D-configuration, D-serine and D-aspartate, activate NMDARs.

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

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

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

6 We found that MPTP treatment increases D-aspartate and D-serine in the monkey putamen while L-D

7 the geometrically different molecules L- and D-aspartate are recognized and transported by the protei

8 ed a crystal structure of Glt(Tk) with bound D-aspartate at 2.8 angstrom resolution.

9 Comparison of the L- and D-aspartate bound Glt(Tk) structures revealed that D-asp

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

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

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

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

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

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

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

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

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

19 and NS-1738 on the spontaneous and N-methyl-D-aspartate-evoked (NMDA-evoked) firing rate of rat CA1

20 5-methyl-4-isoxazole propionic acid/N-methyl-D-aspartate glutamate currents.

21 5-methyl-4-isoxazole propionic acid/N-methyl-D-aspartate glutamate ratio and spine head diameter.

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

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

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

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

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

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

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

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

30 rtate bound Glt(Tk) structures revealed that D-aspartate is accommodated with only minor rearrangemen

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

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

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

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

35 amino-5-phosphonopentanoic acid, or N-methyl-d-aspartate modulation of native or recombinant glycine

36 Over the past decade, various N-methyl-D-aspartate modulators have failed in clinical trials, u

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

38 glutamate, along with the compounds N-methyl-d-aspartate (NMDA) and d-(-)-2-amino-5-phosphonopentanoi

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

40 Here we demonstrate that the N-methyl D-aspartate (NMDA) antagonist ketamine is able to disrup

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

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

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

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

45 st of the glycine co-agonist of the N-methyl-D-aspartate (NMDA) glutamate receptor, is potentially ef

46 sumed to be mediated by blockade of N-methyl-D-aspartate (NMDA) glutamate receptors, our experiments

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

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

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

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

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

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

53 The N-methyl-D-aspartate (NMDA) receptor antagonist ketamine is assoc

54 until the discovery of ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist that produces rap

55 Ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, can rapidly alle

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

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

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

59 Animal model data suggest that N-methyl-D-aspartate (NMDA) receptor antagonists may block cortic

60 sant response to ketamine and other N-methyl-D-aspartate (NMDA) receptor antagonists.

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

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

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

64 ures, which could be reversed by an N-methyl-D-aspartate (NMDA) receptor blocker.

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

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

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

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

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

70 N-methyl-D-aspartate (NMDA) receptor-dependent LTP requires trans

71 release of H(2) O(2) resulting from N-methyl-D-aspartate (NMDA) receptor-mediated activation of nicot

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

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

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

75 N-Methyl-d-aspartate (NMDA) receptors are Ca(2+)-permeable channe

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

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

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

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

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

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

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

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

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

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

86 atory neurotransmission mediated by n-methyl-d-aspartate (NMDA) receptors following stimulation of no

87 Context-dependent inhibition of N-methyl-D-aspartate (NMDA) receptors has important therapeutic i

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

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

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

91 N-methyl-D-aspartate (NMDA) receptors mediate synaptic excitatory

92 neurotransmitter receptors, such as N-methyl-d-aspartate (NMDA) receptors, affect whole cell currents

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

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

95 e structures, and elevated synaptic N-methyl-d-aspartate (NMDA) receptors, thereby increasing synapti

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

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

98 that targets the GluN2B subunit of N-methyl-d-aspartate (NMDA) receptors.

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

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

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

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

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

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 ection of the glutamatergic agonist N-methyl-d-aspartate (NMDA).

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

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

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

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

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

112 sm is predominantly mediated by the N-methyl-d-aspartate receptor (NMDA) receptor, although NMDA-inde

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

114 naling events were dependent on the N-methyl-d-aspartate receptor (NMDA-R) and low-density lipoprotei

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

116 Increased synaptic N-methyl-d-aspartate receptor (NMDAR) activity in the hypothalami

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

118 otentiation occurred independent of N-methyl-D-aspartate receptor (NMDAR) activity, was accompanied b

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

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

121 ion and plasticity by modulation of N-methyl-d-aspartate receptor (NMDAR) and alpha-amino-3-hydroxy-5

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

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

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

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

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

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

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

129 isinhibition hypothesis posits that N-methyl-d-aspartate receptor (NMDAR) antagonists such as ketamin

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

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

132 inst the NR1 (GluN1) subunit of the N-methyl-d-aspartate receptor (NMDAR) are among the most frequent

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

134 eleton-associated protein (ARC) and N-methyl-D-aspartate receptor (NMDAR) complexes; however, larger

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

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

137 antibodies from patients with anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis alter the leve

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

139 Anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis is an immune-m

140 Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most co

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

142 on cause of autoimmune catatonia is N-methyl-D-aspartate receptor (NMDAR) encephalitis, which can acc

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

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

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

146 hlorokynurenic acid (7-Cl-KYNA), an N-methyl-D-aspartate receptor (NMDAR) glycine site antagonist, an

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

148 g this is unclear but may be due to N-methyl-D-aspartate receptor (NMDAR) hypofunction and parvalbumi

149 N-methyl-D-aspartate receptor (NMDAR) hypofunction has been impli

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

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

152 The N-methyl-d-aspartate receptor (NMDAR) is an ion channel that medi

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

154 e potentiation of excitatory GluN2B N-methyl-d-aspartate receptor (NMDAR) responses at lamina I dorsa

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

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

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

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

159 demonstrate that the developmental N-methyl-D-aspartate receptor (NMDAR) subunit switch from GluN2B

160 ionine cycle, is a known agonist of N-methyl-d-aspartate receptor (NMDAR), a glutamate receptor subty

161 gent for the GluN2B subunits of the N-methyl-d-aspartate receptor (NMDAR), a key therapeutic target f

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

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

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

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

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

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

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

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

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

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

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

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

174 mune neuroinflammation (due to anti-N-methyl-D-aspartate receptor [NMDA] encephalitis and multiple sc

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

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

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

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

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

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

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

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

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

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

185 apid antidepressant efficacy of the N-methyl-D-aspartate receptor antagonist, ketamine, for treating

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

187 ects of ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist, which produces rapid an

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

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

192 euronal autoantibodies (principally N-methyl-D-aspartate receptor antibodies) and who have responded

193 acebo-controlled clinical trials of N-methyl-D-aspartate receptor augmentation of psychotropic drug t

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

195 ting in reduced availability of the N-methyl-D-aspartate receptor coagonists glycine and D-serine and

196 ated encephalomyelitis, and 6% anti-N-methyl-d-aspartate receptor encephalitis; and 17% (95% CI, 13%-

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

198 re also present in a mouse model of N-methyl-D-aspartate receptor hypofunction (Ppp1r2cre/Grin1 knock

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

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

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

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 such deficits in humans, including N-methyl-D-aspartate receptor modulators (ketamine, D-cycloserine

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

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

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

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 ecifically successive impairment of N-methyl-d-aspartate receptor subunit 2B (NR2B), postsynaptic den

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

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

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

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

218 5-methyl-4-isoxazole propionic acid/N-methyl-D-aspartate receptor transmission.

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

220 imaging the NR2B subunit within the N-methyl-d-aspartate receptor with PET.

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

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

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

224 ediated nociception modulation, and N-methyl-D-aspartate receptor, NMDAR, antagonism.

225 1 (Sp1)-binding site resulted in an N-methyl-d-aspartate receptor-dependent enhancement of COX-2 prom

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

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

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

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

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

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

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

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

234 tightly controlled by activation of N-methyl-D-aspartate receptors (NMDAR) containing the GluN2A subu

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

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

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

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

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

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

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

242 N-methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion c

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

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

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

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

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

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

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

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

251 iole lumen diameter is regulated by N-methyl-d-aspartate receptors (NMDARs) expressed by brain endoth

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

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

254 ed by glutamate receptors including N-methyl-D-aspartate receptors (NMDARs) is pivotal to brain devel

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

256 N-Methyl-D-aspartate receptors (NMDARs) play critical roles in th

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

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

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

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

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

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

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

264 tibodies against natively expressed N-methyl-D-aspartate receptors (NMDARs), or the surface of live h

265 activation by glutamate ligands of N-methyl-D-aspartate receptors (NMDARs), which is key in model sy

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

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

268 gated the properties of presynaptic N-methyl-d-aspartate receptors (pre-NMDARs) at corticohippocampal

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

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

271 N-methyl d-aspartate receptors are ligand-gated ionotropic recept

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

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

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

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

276 inhibitors of the GluN2B subunit of N-methyl-d-aspartate receptors in the ionotropic glutamate recept

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

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

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

280 tors, and GluN2B-subunit containing N-methyl-D-aspartate receptors, but not GluA1 subunit containing

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

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

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

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

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

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

287 non-receptor tyrosine kinase Src or N-methyl-D-aspartate receptors.

288 abGCs directly excite mGCs through N-methyl-d-aspartate receptors.

289 isphosphate receptor as well as the N-methyl-d-aspartate receptors.

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

291 Localization of the N-methyl-D-aspartate type glutamate receptor (NMDAR) to dendritic

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

293 N-Methyl-d-aspartate type glutamate receptors (NMDARs) are key me

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

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

296 imilarly, USP6 expression regulates N-methyl-D-aspartate-type glutamate receptor (NMDAR)-dependent lo

297 Contributions of N-methyl-D-aspartate-type glutamate receptors (NMDARs) to cDCS-me

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

299 utamate and L-aspartate, they also recognize D-aspartate, which might participate in mammalian neurot

300 Here, we show that Glt(Tk) transports D-aspartate with identical Na(+): substrate coupling sto