ライフサイエンスコーパス: NMDAR

1 NMDAR activity in the hypothalamic paraventricular nucle

2 NMDAR antagonists act as rapid-acting antidepressants su

3 NMDAR dysfunction is involved in a variety of neurologic

4 NMDAR surface trafficking and its modulation by the sex

5 NMDAR-Ab from patients and healthy subjects do not compe

6 NMDAR-GluN2B receptor inhibitors, ifenprodil, RO 25-6981

7 NMDAR-mediated currents were eliminated in nrap-1 mutant

8 NMDAR-mediated EPSCs and puff NMDA-elicited currents wer

9 r an altered NMDAR-evoked changes in Ca(2+) (NMDAR-DeltaCa(2+) ) signalling in magnocellular neurosec

10 le having the kinetic properties of GluN1/2A NMDARs and highlight the complexity in NMDAR signaling c

11 pancy of desensitized states of the GluN1/2B NMDAR subtype.

12 These findings suggest that GluN1/2A/2B NMDARs may maintain some signaling properties of the Glu

13 GluN2 subunits in triheteromeric GluN1/2A/2B NMDARs.

14 those of diheteromeric GluN1/2A and GluN1/2B NMDARs.

15 citatory postsynaptic currents and abolished NMDAR-dependent LTP.

16 ur following synaptic input, which activates NMDARs, even when the delay between the synaptic input a

17 In addition, NMDARs have been found presynaptically, where they canno

18 rst-episode psychosis had antibodies against NMDAR that might be relevant to their illness, but did n

19 tested serum samples for antibodies against NMDAR, LGI1, CASPR2, the GABAA receptor, and the AMPA re

20 memantine and ketamine differentially alter NMDAR desensitization and that memantine stabilizes a Ca

21 that NMDAR-Ab from psychotic patients alter NMDAR synaptic transmission, supporting a pathogenically

22 However, whether an altered NMDAR-evoked changes in Ca(2+) (NMDAR-DeltaCa(2+) ) sign

23 uffering capacity contributes to the altered NMDAR-DeltaCa(2+) dynamics in this condition.

24 r, the precise mechanisms underlying altered NMDAR signalling in hypertension remain to be elucidated

25 Ca(2+) imaging to determine whether altered NMDAR-mediated changes in intracellular Ca(2+) levels (N

26 currents and decrease AMPA receptor (AMPAR)/NMDAR ratios in midbrain dopamine neurons.

27 PF-04958242, and in silico modeling of AMPAR-NMDAR interactions in the hippocampus, highlights the tr

28 urrents (IPSCs) and an increase in the AMPAR/NMDAR ratio in ventral tegmental area (VTA) dopamine neu

29 OGD causes an NMDAR- and Ca(2+)-permeable AMPAR-dependent deactivation

30 nged (24 hr) firing depressed both AMPAR and NMDAR EPSCs and eliminated spines, indicative of a synap

31 opionic acid receptors (AMPARs) as AMPAR and NMDAR functioning are coupled and interdependent.

32 that endocannabinoid/mGlu5-mediated LTD and NMDAR-dependent LTP were lacking in adult n-3-deficient

33 anistic link between the human pathology and NMDAR dysfunction is poorly understood.

34 ow an inverse distribution of spine size and NMDAR-driven calcium signals along dendritic trees, with

35 dendrite morphology, synaptic strength, and NMDAR-dependent responses.

36 s of glutamate receptors (GluRs) (AMPARs and NMDARs).

37 lease of mixed events associating AMPARs and NMDARs, as well as alpha7 and alpha*ss* nAChRs, but no e

38 Anti-NMDAR encephalitis is associated with extensive superfic

39 cases, certain autoantibodies, such as anti-NMDAR or anti-phospholipid antibodies, promote CNS lupus

40 nsecutive adult patients diagnosed with anti-NMDAR encephalitis at the French National Reference Cent

41 The prognosis of adult patients with anti-NMDAR encephalitis requiring intensive care is good, esp

42 Forty-six patients with anti-NMDAR encephalitis were included.

43 ome in patients admitted to an ICU with anti-NMDAR encephalitis.

44 ization using the inhibitors MK-801 and AP5 (NMDAR), and ivabradine and ZD7288 (HCN).

45 file paralleled activity of the compounds as NMDAR channel blockers; A-NK-amide was inactive at NMDAR

46 channel blockers; A-NK-amide was inactive at NMDARs, and norketamine and A-NK were active but ~4-fold

47 However, because NMDARs contribute to overall glutamatergic neurotransmis

48 Blocking NMDAR activity inhibited the ability of leptin to activa

49 o schizophrenia, a disorder characterized by NMDAR and cholinergic hypofunctions.

50 se changes were similar to those produced by NMDAR mutants in which the ligand-binding domains (LBDs)

51 tely distinguish between the roles played by NMDARs and neural activity in general.

52 quence-independent manner as an open-channel NMDAR antagonist at or near the Mg(2+) site, due to its

53 xin in vivo, alteration of GluN2B-containing NMDAR signaling suppresses spine density and impairs lea

54 n antagonist selective for GluN2B-containing NMDARs, reverses synapse loss when applied after Tat.

55 ncentrations and activates GluN2B-containing NMDARs.

56 increased contribution of GluN2B-containing NMDARs.

57 molecular model of mutant GluN2B-containing NMDARs.

58 GluN2D-containing NMDARs are highly expressed on cortical parvalbumin-cont

59 trates a potential role of GluN2D-containing NMDARs in the PLmPFC in alcohol-heightened aggression.

60 preferential antagonism of GluN2D-containing NMDARs.

61 e hypofunction of GluN2B(p.P553T)-containing NMDARs.

62 One strategy to correct NMDAR hypofunction is to stimulate alpha-amino-3-hydroxy

63 Modulation of Ca(2+)-dependent NMDAR desensitization is an unexplored mechanism of inhi

64 Experiments with the use-dependent NMDAR blocker, MK-801, indicate that potentiated NMDARs

65 this study, we show that PICK1 makes direct, NMDAR-dependent interactions with the core endocytic pro

66 ine and ketamine of overlapping but distinct NMDAR subpopulations.

67 ies may contribute to inhibition of distinct NMDAR subpopulations by memantine and ketamine and help

68 ms by which channel blockers may distinguish NMDAR subpopulations.

69 phorylation, which is indicative of enhanced NMDAR activation.

70 Furthermore, Y504 phosphorylation enhances NMDAR localization and injury-induced pain behavior.

71 ed alpha7nAChR agonist successfully enhances NMDAR activation.

72 dent Y504 phosphorylation modulates the EphB-NMDAR interaction in cortical and spinal cord neurons.

73 The basal amplitude of evoked NMDAR-EPSCs and puff NMDA currents in retrogradely label

74 eling, and recordings of synaptically evoked NMDAR responses in acute brain slices to investigate mec

75 ther, our results support (1) an exacerbated NMDAR-DeltaCa(2+) response in somatodendritic compartmen

76 The exacerbated NMDAR-DeltaCa(2+) responses in MNCs of RVH rats affected

77 resulting in the generation of extrasynaptic NMDAR-mediated slow inward currents (SICs) in neighborin

78 e but not ketamine may inhibit extrasynaptic NMDARs more effectively than synaptic NMDARs.

79 is responsible for recruiting extrasynaptic NMDARs.

80 ing the development of cell-based assays for NMDAR drug discovery.

81 coagonist of the NMDAR that is required for NMDAR channel opening, but which cannot mediate neurotra

82 PICK1 is a BAR domain protein required for NMDAR-dependent reductions in surface GluA2; however, th

83 ing-state network alterations may arise from NMDAR hypofunction and establish a proof of principle wh

84 Overexpression of functional NMDAR in non-neuronal cells results in cell death by exc

85 uitment of voltage-dependent currents (e.g., NMDAR-mediated Ca(2+) influx) by synaptic input.

86 and content of GluN2B-NMDAR, but not GluN2A-NMDAR, at synapses through a process requiring PDZ bindi

87 We specifically focused on the GluN2B NMDAR subunit, which is highly expressed in the hippocam

88 ntracellular C-terminal domain of the GluN2B NMDAR subunit.

89 the membrane dynamics and content of GluN2B-NMDAR, but not GluN2A-NMDAR, at synapses through a proce

90 This work suggests that targeting GluN2D-NMDARs may be of use in reducing the impact of alcohol-r

91 ulating autoantibodies against glutamatergic NMDAR in approximately 5% of patients with first-episode

92 ulating autoantibodies against glutamatergic NMDAR in psychotic disorders remains controversial, with

93 w-titer autoantibodies against glutamatergic NMDAR in seropositive patients who cannot be clinically

94 Seven (3%) patients had NMDAR antibodies compared with no controls (p=0.0204).

95 To better understand how NMDAR hypofunction affects the brain, we used magnetic r

96 However, NMDAR antibodies (n=4) or CASPR2 antibodies (n=1) were i

97 Our data suggest that hypofunctional NMDARs containing GluN2B(p.P553T) can contribute to Rett

98 th reduced NMDA-evoked currents and impaired NMDAR-dependent insertion of GluA1 at stimulated synapse

99 cKO of NL1-NL3 or single cKO of NL1 impaired NMDAR-mediated excitatory postsynaptic currents and abol

100 ogether, these findings positively implicate NMDAR-mediated neurotransmission in developmental synaps

101 Importantly, NMDAR-mediated signaling was observed in rat insulinoma

102 Changes in NMDAR-DeltaCa(2+) dynamics were observed both in somatic

103 N1/2A NMDARs and highlight the complexity in NMDAR signaling created by diversity in subunit composit

104 find that GluN2B S1413L displays deficits in NMDAR trafficking, synaptic currents, and spine density,

105 at the targeted study of certain residues in NMDARs based on rare variants identified in patients is

106 GluN1-N440 might play a potentiator role in NMDARs.

107 deficit in low-frequency stimulation-induced NMDAR-dependent long-term depression (LTD).

108 r (NMDAR) open channel blockers that inhibit NMDARs with similar potency and kinetics, but display va

109 Despite this, a prolonged and larger NMDAR-DeltaCa(2+) response was observed in the latter.

110 ion at glutamatergic synapses, while leaving NMDAR-mediated calcium influx intact.

111 electrophysiological analysis of full-length NMDARs with a glycosylation-preventing GluN1-N440Q mutat

112 ated changes in intracellular Ca(2+) levels (NMDAR-DeltaCa(2+) ) occurred in hypothalamic magnocellul

113 The mechanisms that link NMDAR activation to CME of AMPARs remain elusive.

114 nt, potent, and local mode of Abeta-mediated NMDAR impairment.

115 during early postnatal development in mice, NMDAR signaling via activity of long-range synaptic inpu

116 To date, no auxiliary proteins that modify NMDARs have been identified.

117 in kinase II (CaMKII) binds to and modulates NMDAR activity.

118 xiliary protein in C. elegans that modulates NMDAR function.

119 MDAR, plays a significant role in modulating NMDAR-mediated synaptic transmission and plasticity in m

120 Additionally, mPFC NMDAR-dependent LTP was also lacking in the n-3-deficien

121 ling predicted a reduced pore size of mutant NMDARs.

122 g increases occupancy of GluN1/2A and native NMDAR desensitized states entered after accumulation of

123 By analyzing synchronized neuronal NMDAR-mediated excitation, we found that the properties

124 e effects of specific GT release at neuronal NMDARs.

125 Vasodilation required neuronal NMDARs and NOS stimulation and subsequent guanylyl cycla

126 g memory deficits caused by the nonselective NMDAR antagonist ketamine.

127 stsynaptic, loss of vti1a and VAMP7 occludes NMDAR antagonist-induced synaptic potentiation in an int

128 ARs) resulting in a dramatic acceleration of NMDAR-mediated synaptic currents.

129 cal studies that shed light on the action of NMDAR antagonists as rapid-acting antidepressants and ho

130 The mode of action of NMDAR antagonists seemingly relies on their ability to a

131 experiments showed mechanical activation of NMDAR and inhibition by MK-801.

132 (AIP) normalized the increased amplitude of NMDAR-EPSCs and puff NMDA currents in labeled PVN neuron

133 late the trafficking and synaptic content of NMDAR subtypes.

134 onsistent with the theorized contribution of NMDAR hypofunction to predictive coding deficits in schi

135 To test the hypothesized contribution of NMDAR hypofunction to this disruption, we examined the e

136 aptic regulation via pre-synaptic control of NMDAR-mediated synaptic transmission.

137 ronic pain transition via desensitization of NMDAR.

138 dependence of the intensity and duration of NMDAR activation.

139 upports an altered spatiotemporal dynamic of NMDAR-DeltaCa(2+) signalling in MNCs from RVH rats, part

140 recently reported insulinotropic effects of NMDAR antagonists and therefore highlights the therapeut

141 ly evoked NMDA current nor the expression of NMDAR subunits were altered in RVH rats.

142 nal plasticity suggests that facilitation of NMDAR function might ameliorate CIAS.

143 AIP also normalized the higher frequency of NMDAR-mediated miniature EPSCs of PVN neurons in SHRs.

144 Our results underscore the importance of NMDAR subunit composition for memory destabilization and

145 put assay that allows for the measurement of NMDAR function in glycine/D-serine and/or glutamate sens

146 ngs concerning these unconventional modes of NMDAR action.

147 tic association between de novo mutations of NMDAR subunits and severe psychiatric diseases, little i

148 faithfully followed, even in the presence of NMDAR antagonists.

149 ntral difference in SK channel regulation of NMDAR activation has a profound effect on the transmissi

150 2B(p.P553T) coding for the GluN2B subunit of NMDAR.

151 The ability of NMDARs to regulate potassium channel surface expression

152 all molecule modulators on the activation of NMDARs at different concentrations or combinations of th

153 We show that activation of NMDARs evoked similar inward currents in MNCs of sham an

154 inement.SIGNIFICANCE STATEMENT Activation of NMDARs is critical for the activity-dependent developmen

155 Conversely, activation of NMDARs mimicked the effect of leptin, causing Ca(2+) inf

156 lar excitatory inward current, activation of NMDARs resulted in a larger and prolonged DeltaCa(2+) in

157 eve that the ability to study the biology of NMDARs rapidly and in large scale screens will enable th

158 of L-type Ca(2+)-channels during blockade of NMDARs.

159 Disruption of NMDARs causes dysfunction in predictive coding during vo

160 ycosylation on the structure and dynamics of NMDARs are largely unknown.

161 STEP reduces the surface expression of NMDARs by promoting dephosphorylation of GluN2B Y1472, w

162 PSD-95) stabilizes the surface expression of NMDARs.

163 Here, we report a novel function of NMDARs in beta-cells.

164 The expression and function of NMDARs in pancreatic beta-cells, by contrast, are poorly

165 al mechanism of facilitating the function of NMDARs.

166 and GluN2B ligand binding domains (LBDs) of NMDARs to investigate these effects.

167 Malfunction of NMDARs has been implicated in a variety of nervous syste

168 vel positive allosteric modulators (PAMs) of NMDARs have recently been identified but their effects o

169 ion UBP684 displayed greater potentiation of NMDARs with only the GluN1 LBD locked compared to NMDARs

170 obing the structure/function relationship of NMDARs.

171 The mechanical sensitivity of NMDARs may play a role in the normal physiology of fluid

172 Our assay enables the functional study of NMDARs with different subunit composition after activati

173 ion may result in functional upregulation of NMDARs, we also analyzed PrP knock-out (KO) mice.

174 nhibition by memantine and ketamine based on NMDAR location is likely to result from location depende

175 ine and ketamine have contrasting effects on NMDAR desensitization.

176 ecently been identified but their effects on NMDAR gating remain largely unknown.

177 Functionally, only patients' NMDAR-Ab prevent long-term potentiation at glutamatergic

178 the potentiated presynaptic and postsynaptic NMDAR activity of hypothalamic presympathetic neurons in

179 to potentiated presynaptic and postsynaptic NMDAR activity to elevate sympathetic vasomotor tone in

180 apses, where it associates with postsynaptic NMDARs to modify receptor gating.

181 molecular mechanism involved in potentiated NMDAR activity of hypothalamic presympathetic neurons re

182 Moreover, leptin potentiated NMDAR currents and triggered NMDAR-dependent Ca(2+) infl

183 R blocker, MK-801, indicate that potentiated NMDARs reside on the plasma membrane and are not inserte

184 However, the basis for preferential NMDAR inhibition depending on subcellular location has n

185 s, it decreases Pr by activating presynaptic NMDARs, and promotes presynaptic long-term depression.

186 eletion of postsynaptic, but not presynaptic NMDARs prevents LTD induction.

187 loss-of-function manipulations that prevent NMDAR function during development result in the disorgan

188 lcium trasport ATPase (SERCA) pump prolonged NMDAR-DeltaCa(2+) responses in sham rats, but not in RVH

189 A) pump activity with thapsigargin prolonged NMDAR-DeltaCa(2+) responses in MNCs of sham rats, but th

190 We find that quantal NMDAR calcium signals increase in amplitude as they appr

191 locker of N-Methyl-D-aspartic acid receptor (NMDAR) channels, and this occurred in the absence of ago

192 measuring N-methyl-d-aspartic acid receptor (NMDAR)-driven calcium responses in single spines, we pro

193 4 (3.6%) had N-methyl-D-aspartate receptor (NMDAR) Ab.

194 reduction in N-methyl-D-aspartate receptor (NMDAR) activity.

195 bodies to the N-methyl-D-aspartate receptor (NMDAR) and contactin-associated protein-like 2 (CASPR2)

196 he roles that N-methyl-D-aspartate receptor (NMDAR) and hyperpolarization-activated, cyclic nucleotid

197 age-dependent N-Methyl-D-aspartate receptor (NMDAR) antagonist, has been shown to have a rapid antide

198 discovery of N-methyl-D-aspartate receptor (NMDAR) antagonists as effective antidepressants, we have

199 onically with N-methyl-d-aspartate receptor (NMDAR) antagonists, we demonstrate that NMDAR synaptic c

200 aused by anti-N-methyl-d-aspartate receptor (NMDAR) antibodies is the leading cause of immune-mediate

201 research, and N-methyl-d-aspartate receptor (NMDAR) dysfunction can provide insights into the mechani

202 nts with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis.

203 ations in the N-methyl-D-aspartate receptor (NMDAR) gene GRIN2A cause epilepsy-aphasia syndrome (EAS)

204 glutamatergic N-methyl-D-aspartate receptor (NMDAR) have been reported in a proportion of patients wi

205 enia and that N-methyl-d-aspartate receptor (NMDAR) hypofunction on gamma-aminobutyric acid (GABA) in

206 vation of the N-methyl D-aspartate receptor (NMDAR) is controlled by a glutamate-binding site and a d

207 leads, in an N-methyl D-aspartate receptor (NMDAR)-dependent manner, to activation of a specific pai

208 ysfunction of N-methyl-D-aspartate receptor (NMDAR)-mediated neurotransmission.

209 s against the N-methyl-D-aspartate receptor (NMDAR)-more commonly than do healthy controls.

210 rom N-methyl-D-aspartate glutamate receptor (NMDAR) hypofunction.

211 y be dependent on concomitant NMDA receptor (NMDAR) activation during self-administration, similar to

212 Aberrant NMDA receptor (NMDAR) activity contributes to several neurological diso

213 The endogenous NMDA receptor (NMDAR) agonist D-aspartate occurs transiently in the mam

214 NT Memantine and ketamine are NMDA receptor (NMDAR) channel-blocking drugs with divergent clinical ef

215 the potential involvement of NMDA receptor (NMDAR) dysfunction, we analyzed NMDA-dependent synaptic

216 etamine are clinically useful NMDA receptor (NMDAR) open channel blockers that inhibit NMDARs with si

217 ptors (AMPARs) in response to NMDA receptor (NMDAR) stimulation causes a reduction in synaptic streng

218 KEY POINTS: NMDA receptor (NMDAR)-mediated Ca(2+) signalling plays a critical role

219 Although glutamate NMDA receptor (NMDAR)-mediated excitatory drive in the hypothalamus pla

220 evidence supports an elevated NMDA receptor (NMDAR)-mediated glutamate excitatory function in the sup

221 hostimulants acutely increase NMDA receptor (NMDAR)-mediated synaptic currents and decrease AMPA rece

222 oantibodies against glutamate NMDA receptor (NMDAR-Ab) in about 20% of psychotic patients diagnosed w

223 cially N-methyl-d-aspartate (NMDA) receptor (NMDAR)-dependent long-term potentiation (LTP), remains u

224 s, mediated by NMDA-type glutamate receptor (NMDARs) activation, form the cellular basis for inverse

225 l profile of N-methyl-d-aspartate receptors (NMDAR) in the NAc core, TLR4.KO animals exhibit a defici

226 unit composition of synaptic NMDA receptors (NMDAR), such as the relative content of GluN2A- and GluN

227 ctivation of N-methyl-D-aspartate receptors (NMDARs) and intrinsic oscillatory mechanisms.

228 B-containing N-methyl-D-aspartate receptors (NMDARs) and pathological pain are controlled by ephrin-B

229 N-methyl-D-aspartate receptors (NMDARs) are glycoproteins in the brain central to learni

230 N-methyl-d-aspartate receptors (NMDARs) are heterotetrameric ion channels assembled as d

231 le played by N-methyl-d-aspartate receptors (NMDARs) in both the pathophysiology of schizophrenia and

232 N-Methyl-D-aspartate receptors (NMDARs) play pivotal roles in synaptic development, plas

233 l may act on N-methyl-d-aspartate receptors (NMDARs) within cortical circuits to impede processing an

234 N-methyl-D-aspartate-receptors (NMDARs) are ionotropic glutamate receptors that function

235 region (BCR) associates with NMDA receptors (NMDARs) along with Tiam1 and that this protein complex i

236 ws a prominent expression of NMDA receptors (NMDARs) and nitric oxide synthase (NOS) and is therefore

237 NMDA receptors (NMDARs) are a subtype of postsynaptic ionotropic glutama

238 NMDA receptors (NMDARs) are Ca(2+)-permeant, ligand-gated ion channels a

239 NMDA receptors (NMDARs) are ion channels activated by the excitatory neu

240 NMDA receptors (NMDARs) are ionotropic glutamate receptors that are cruc

241 In the classical view, NMDA receptors (NMDARs) are stably expressed at the postsynaptic membran

242 ontrolling GluN2B-containing NMDA receptors (NMDARs) at immature excitatory synapses, via a transcrip

243 NMDA receptors (NMDARs) contribute to several neuropathological processe

244 n the subunit composition of NMDA receptors (NMDARs) resulting in a dramatic acceleration of NMDAR-me

245 ) channels, not postsynaptic NMDA receptors (NMDARs), and does not require glutamate release.

246 the functional regulation of NMDA receptors (NMDARs).

247 determined the role of CaMKII in regulating NMDAR activity of PVN presympathetic neurons in male spo

248 d that recombinant NRAP-1 can convert silent NMDARs to functional channels.

249 ordings from heterologously expressed single NMDAR subtypes, kinetic modeling, and recordings of syna

250 Strikingly, NMDAR-Ab from patients, but not from healthy subjects, s

251 ate-based, high-throughput approach to study NMDAR function.

252 tion of SK channels that strongly suppresses NMDAR activation at ventral SC synapses.

253 ion of SK-type K(+) channels that suppresses NMDAR-dependent EPSP amplification at ventral SC synapse

254 neurons, as reported in AD, alters synaptic NMDAR composition to an immature-like GluN2B-rich profil

255 Importantly, synaptic NMDAR currents in neurons transfected with GluN2B S1413L

256 amics and nanoscale organization of synaptic NMDAR and its anchoring partner the EphrinB2 receptor in

257 ouse) showed a deficit in rescue of synaptic NMDAR currents and fewer dendritic spines, consistent wi

258 cellular microenvironment regulates synaptic NMDAR signaling.

259 shed light on post-transcriptional synaptic NMDAR mediated mechanisms underlying the acute effect, b

260 ptors in tsA201 cells and of native synaptic NMDARs in cortical pyramidal neurons from mice of either

261 that astrocytes tune the gating of synaptic NMDARs to the vigilance state and demonstrate that this

262 naptic NMDARs more effectively than synaptic NMDARs.

263 Imaging agents for PET and SPECT that target NMDARs in a subtype-selective fashion may enable better

264 cell bodies and proximal dendrites, and that NMDAR activity is required for shedding of its ectodomai

265 tor (NMDAR) antagonists, we demonstrate that NMDAR synaptic currents in NRG2 KOs are augmented at hip

266 More recently, it has been established that NMDAR-mediated transmission can be dynamically regulated

267 basal-evoked NMDA currents, indicating that NMDAR-GluN2B receptors are activated by AMPH.

268 Recent evidence suggests that NMDAR antagonists relieve depressive symptoms by forming

269 We unveil that NMDAR-Ab from psychotic patients alter NMDAR synaptic tr

270 gy, and imaging techniques, we now show that NMDARs have a key role in mediating the effect of leptin

271 Together, these data suggest that NMDARs mediate cocaine-induced increases in VTA GluA1 ex

272 The NMDAR is thought to play a key role in the refinement of

273 s disruption, we examined the effects of the NMDAR antagonist, ketamine, on predictive coding during

274 This causes a full saturation of the NMDAR co-agonist site in the dark (active) phase that di

275 iotransmitter d-serine is a coagonist of the NMDAR that is required for NMDAR channel opening, but wh

276 d-Serine, a coagonist of the NMDAR, plays a significant role in modulating NMDAR-medi

277 Thus, altered spatiotemporal dynamics of the NMDAR-DeltaCa(2+) response stands as an underlying mecha

278 otting, we found that AHAs overexpressed the NMDAR GluN2D subunit in the prefrontal cortex (PFC) as c

279 In most brain regions, the NMDAR co-agonist is the astrocyte-derived gliotransmitte

280 to human MMN, along with sensitivity to the NMDAR antagonist and agonist administration.

281 Pharmacological inhibition of these NMDARs rescued spines and restored cognitive function.

282 Missense mutations distributed throughout NMDAR subunits have been associated with an array of neu

283 Furthermore, disrupting the Tiam1-NMDAR interaction with a fragment of Tiam1 blocks OGD-in

284 to ion-channel opening, which is central to NMDAR physiology and pathophysiology.

285 ix metalloprotease 3 (MMP-3), in contrast to NMDAR-dependent LTP regulated by MMP-9.

286 endocytic zones in dendrites in response to NMDAR stimulation and for consequent AMPAR internalizati

287 ies of rodent MMN, along with sensitivity to NMDAR agonist and antagonist treatments, relative to kno

288 s with only the GluN1 LBD locked compared to NMDARs with only the GluN2 LBD locked.

289 VTA neurons to study the effect of transient NMDAR inactivation on the GluA1 increases induced by chr

290 in VTA GluA1 expression, but such transient NMDAR inactivation also leads to compensatory scaling of

291 tin potentiated NMDAR currents and triggered NMDAR-dependent Ca(2+) influx.

292 The triheteromeric NMDAR structures provide the first view of the most comm

293 Unexpectedly, NMDARs have also been shown to signal metabotropically,

294 synapse to nucleus signalling, mediated via NMDAR and L-type calcium channels, results in rapid FOXP

295 ellular Ca(2+) dynamics that dictate whether NMDAR function is augmented or depressed following M1R s

296 studies and a rationale for testing whether NMDAR antagonists might be used to treat PTHS.SIGNIFICAN

297 ction with the potential to endow drugs with NMDAR selectivity that leads to superior clinical profil

298 quired for mTORC1-dependent translation with NMDAR antagonists.

299 Rare missense variants within NMDAR subunits have been identified in numerous patients

300 ss, but did not differ from patients without NMDAR antibodies in clinical characteristics.