ライフサイエンスコーパス: N-methyl-D-aspartate

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

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

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

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

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

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

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

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

9 NU-120596 and NS-1738 on the spontaneous and N-methyl-D-aspartate-evoked (NMDA-evoked) firing rate of

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

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

12 -hydroxy-5-methyl-4-isoxazole propionic acid/N-methyl-D-aspartate glutamate ratio and spine head diam

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

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

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

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

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

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

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

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

21 d-(-)-2-amino-5-phosphonopentanoic acid, or N-methyl-d-aspartate modulation of native or recombinant

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

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

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

25 nsmitter glutamate, along with the compounds N-methyl-d-aspartate (NMDA) and d-(-)-2-amino-5-phosphon

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

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

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

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

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

31 ial agonist of the glycine co-agonist of the N-methyl-D-aspartate (NMDA) glutamate receptor, is poten

32 widely assumed to be mediated by blockade of N-methyl-D-aspartate (NMDA) glutamate receptors, our exp

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

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

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

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

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

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

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

40 e 1950's until the discovery of ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist that pro

41 Ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, can rap

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

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

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

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

46 Animal model data suggest that N-methyl-D-aspartate (NMDA) receptor antagonists may blo

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

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

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

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

51 lice cultures, which could be reversed by an N-methyl-D-aspartate (NMDA) receptor blocker.

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

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

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

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

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

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 N-methyl-D-aspartate (NMDA) receptor-dependent LTP requi

60 a rapid release of H(2) O(2) resulting from N-methyl-D-aspartate (NMDA) receptor-mediated activation

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

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 Ca(2+)-permeab

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

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

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

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

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

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

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

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

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

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

75 in excitatory neurotransmission mediated by n-methyl-d-aspartate (NMDA) receptors following stimulat

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

77 Context-dependent inhibition of N-methyl-D-aspartate (NMDA) receptors has important ther

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 N-methyl-D-aspartate (NMDA) receptors mediate synaptic e

82 ther CNS neurotransmitter receptors, such as N-methyl-d-aspartate (NMDA) receptors, affect whole cell

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 spine-like structures, and elevated synaptic N-methyl-d-aspartate (NMDA) receptors, thereby increasin

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

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

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

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

90 ing probe that targets the GluN2B subunit of 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 ceptor (iGluR) agonists, kainic acid (KA) or N-methyl-D-aspartate (NMDA), contributed to significant,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 llosteric antagonists of ion channels 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 s, autoimmune neuroinflammation (due to anti-N-methyl-D-aspartate receptor [NMDA] encephalitis and mu

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

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

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

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

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

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

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

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

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

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

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

186 169 (49%) patients and measurements of anti-N-methyl-D-aspartate receptor antibodies were taken in 4

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

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

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

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

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

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

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

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

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

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

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

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

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

205 as reduced substantially upon addition of an N-methyl-D-aspartate receptor peptide analog but not ATP

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

236 3A1, are tightly controlled by activation of N-methyl-D-aspartate receptors (NMDAR) containing the Gl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

258 N-Methyl-D-aspartate receptors (NMDARs) play critical ro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

291 1,4,5-trisphosphate receptor as well as the N-methyl-d-aspartate receptors.

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

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

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

295 N-Methyl-d-aspartate type glutamate receptors (NMDARs) a

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

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

298 Similarly, USP6 expression regulates N-methyl-D-aspartate-type glutamate receptor (NMDAR)-dep

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

300 Contributions of N-methyl-D-aspartate-type glutamate receptors (NMDARs) t