ライフサイエンスコーパス: NMDAR

1 NMDAR activation increased spinule number, length, and c

2 NMDAR agonist responses were robustly reduced after prei

3 NMDAR antibody serostatus and titre was associated with

4 NMDAR blockers mostly decreased persistent firing associ

5 NMDAR function can be augmented by positive allosteric m

6 NMDAR IgGs were not more frequent in subjects who later

7 NMDARs are heterotetramers composed of GluN1 and GluN2 s

8 NMDARs are known to play a significant role in basic neu

9 ng alpha2delta-1 or disrupting alpha2delta-1-NMDAR interaction reduces calcineurin inhibitor-induced

10 h gabapentin or disrupting the alpha2delta-1-NMDAR interaction with alpha2delta-1Tat peptide complete

11 ely, in a breast cancer cell line MDA-MB-231 NMDAR blockade results in an increase in endosomal size

12 eral amygdala (BLA) inputs non-linearly in a NMDAR-dependent manner.

13 NMR spectroscopy to evaluate the effect of a NMDAR PAM (rapastinel) or NMDAR antagonist, ketamine on

14 utonomous function of the worm homologs of a NMDAR subunit and CaMKII.

15 grin1a (-/-) ; grin1b (-/-)), which lack all NMDAR-mediated synaptic transmission, survive until ~10

16 e, we demonstrate that zebrafish lacking all NMDAR transmission are viable through early development

17 Importantly, the dual-allosteric NMDAR antagonist NitroSynapsin, but not the FDA-approved

18 plasticity in females but may instead alter NMDAR-mediated transmission.

19 excitatory synapses, how endogenous AMPARs, NMDARs, and mGluRs are co-organized inside the synapse a

20 AGN-241751, an NMDAR positive allosteric modulator (PAM), is currently

21 ctive coding view perceptual inference as an NMDAR-dependent process of minimizing hierarchical preci

22 etitive NMDAR antagonist (DCPP-ene) or by an NMDAR channel blocker applied through the recording pipe

23 Intramuscular application of an NMDAR antagonist blocked the acquisition/maintenance of

24 a and simulations supports alterations of an NMDAR-dependent memory mechanism operating on longer tim

25 ptor activity in inhibitory neurons using an NMDAR positive allosteric modulator (PAM) elevates spiki

26 spine density, and enhanced evoked AMPAR and NMDAR EPSCs.

27 NMDAR was the most common target antigen and NMDAR IgGs were more sensitively detected with live vers

28 y of cell-surface and synaptic D1R, D2R, and NMDAR clusters were examined at different time points us

29 ment, and changes in levels of D1R, D2R, and NMDAR progressively improved several days after the infu

30 tions show temporally overlapping HVACC- and NMDAR-mediated Ca(2+)-currents during the spine spike, a

31 nt in clinical trials, but the mechanism and NMDAR subunit(s) mediating its antidepressant-like effec

32 ate the extracellular levels of D-serine and NMDAR activity.

33 ysical interaction between alpha2delta-1 and NMDARs and their synaptic trafficking in the spinal cord

34 We found that both AMPARs and NMDARs contributed to persistent activity.

35 e we compared the contribution of AMPARs and NMDARs to persistent firing in the dlPFC of male macaque

36 insight into the contribution of AMPARs and NMDARs to working memory.

37 al NMDARs: schizophrenia and autoimmune anti-NMDAR encephalitis.

38 ly serve as complementary treatment for anti-NMDAR encephalitis and deserve future investigations.

39 ebrospinal fluid (CSF) of patients with anti-NMDAR encephalitis (preabsorbed or not with GluN1) and a

40 ate receptors (NMDARs) in patients with anti-NMDAR encephalitis alter neuronal synaptic function and

41 DARs, CSF antibodies from patients with anti-NMDAR encephalitis cause reversible psychotic-like featu

42 rospinal fluid (CSF) from patients with anti-NMDAR encephalitis or controls, and the effects on clust

43 Antibodies from patients with anti-NMDAR encephalitis specifically alter the function of NM

44 what proportion of patients with FEP who are NMDAR antibody seropositive have coexisting cerebrospina

45 thin the CHR group, the relationship between NMDAR antibodies and symptoms, cognitive function and cl

46 Together, these data draw a link between NMDARs and the cytoskeleton in brain endothelial cells t

47 t on glutamate efflux, while ketamine blocks NMDAR on GABA interneurons to cause glutamate efflux and

48 r findings indicate that alpha2delta-1-bound NMDARs mediate calcineurin inhibitor-induced tonic activ

49 to schizophrenia that exceed those caused by NMDAR interneuron hypofunction alone.SIGNIFICANCE STATEM

50 sion of glucose transporter GLUT1 induced by NMDAR activity.

51 erosynaptic plasticity crosstalk mediated by NMDAR-dependent MEK/ERK signaling.

52 Excitatory signaling mediated by NMDARs has been shown to regulate mood disorders.

53 were blocked by bath applying a competitive NMDAR antagonist (DCPP-ene) or by an NMDAR channel block

54 they arise from acute effects of compromised NMDAR-mediated transmission.

55 cell-type-specific role of GluN2B-containing NMDAR in mediating antidepressant-like behavioral effect

56 indicating involvement of GluN2A-containing NMDARs.

57 ndent pathologies requires GluN2A-containing NMDARs.

58 R) subunit GluN2B and that GluN2B-containing NMDARs also regulate expression of cocaine seeking on AD

59 c compounds for GluN2A and GluN2B-containing NMDARs are well established, those that target GluN2C an

60 play between STEP, Fyn and GluN2B-containing NMDARs has been characterized by multiple groups.

61 Activin A and GluN2B-containing NMDARs have both previously been implicated in hippocamp

62 type-specific knockdown of GluN2B-containing NMDARs in mPFC demonstrates that GluN2B subunits on exci

63 re, we identify a role for GluN2D-containing NMDARs in modulating emotional behaviors and neural acti

64 e demonstrate that loss of GluN2D-containing NMDARs produces an increase in anxiety- and depressive-l

65 a loss of dendritic inhibition via decreased NMDAR currents and reduced firing of dendrite-targeting

66 ppocampus through a concentration-dependent, NMDAR-independent, and synapse-selective increase in glu

67 MDA receptor-dependent long-term depression (NMDAR-LTD) is a long-lasting form of synaptic plasticity

68 nd the broader set of mutations that disrupt NMDAR function.

69 Autophagy is inhibited during NMDAR-LTD to decrease endocytic recycling.

70 Here, we assess in vivo how an early NMDAR ablation in corticolimbic interneurons impacts on

71 Eliminating NMDARs in primary sensory neurons or alpha2delta-1 KO al

72 s that occur in the GRIN genes, which encode NMDAR subunits, and the broader set of mutations that di

73 reveal that selectively enhancing endogenous NMDAR activity on the GABAergic neurons can effectively

74 We report that mouse CNS endothelial NMDARs display the regulatory GluN3A subunit.

75 considerable interest in drugs that enhance NMDAR function and could compensate for receptor hypofun

76 emonstrate that rapastinel directly enhances NMDAR activity on principal glutamatergic neurons in med

77 AGN-241751 treatment enhances NMDAR activity of excitatory and parvalbumin-inhibitory

78 Loss of the EphB-NMDAR interaction by either mutating GluN1 or knocking d

79 ), providing a unique opportunity to explore NMDAR function during development and in generating beha

80 activity of Pin1 toward PSD-95, facilitates NMDAR synaptic expression and function.

81 These data suggest that in FEP, NMDAR antibody seropositivity alone is not an indication

82 baseline, 15 patients were seropositive for NMDAR antibodies and 372 were seronegative.

83 ials.gov number NCT01248195) were tested for NMDAR IgG antibodies using a live cell-based assay.

84 at neurodevelopmental disorders arising from NMDAR deficiency can be effectively treated in adults.

85 ts rely on magnified levels of calcium (from NMDAR, calcium channels, and/or internal release from th

86 c segments, whereas the topography of GluN2A-NMDARs remains similar along the dendritic tree.

87 t actions of ketamine were blocked by GluN2B-NMDAR knockdown on GABA (Gad1) interneurons, as well as

88 rkably, the nanoscale organization of GluN2B-NMDARs at proximal segments depends on their interaction

89 nges in the nanoscale organization of GluN2B-NMDARs between proximal and distal dendritic segments, w

90 ether, this study supports a role for GluN2D-NMDARs in regulating emotional behavior through their in

91 these results demonstrate a role for GluN2D-NMDARs in regulating the activity of stress-responsive s

92 NIFICANCE STATEMENT The authors describe how NMDARs expressed on endothelial cells regulate blood-bra

93 (preabsorbed or not with GluN1) and a human NMDAR-specific monoclonal antibody (SSM5) derived from p

94 ated diseases, both linked to hypofunctional NMDARs: schizophrenia and autoimmune anti-NMDAR encephal

95 Impaired NMDAR signalling through genetic or environmental insult

96 In NMDAR-LTD, however, they are diverted to late endosomes

97 or knocking down endogenous EphB2 increases NMDAR mobility.

98 Although calcineurin inhibition increases NMDAR activity in the spinal cord, the underlying mechan

99 the NTS to reduce food intake by increasing NMDAR-mediated currents, thus enhancing NTS sensitivity

100 s, consistent with blockade of interneuronal NMDAR blockade.

101 s provide detailed mechanistic insights into NMDAR pharmacology, activation, and inhibition, which ar

102 dentify key components of the non-ionotropic NMDAR signaling pathway driving dendritic spine shrinkag

103 erally required downstream of non-ionotropic NMDAR signaling to drive both spine shrinkage and LTD.

104 dent long-term potentiation and the isolated NMDAR potentials at the Schaffer collateral-CA1 synapses

105 cell-specific knockdown or deletion of a key NMDAR subunit, GluN2B, implicated in the actions of keta

106 subunit of the NMDAR is required to maintain NMDARs at dendritic spine synapses and mediates the dire

107 By manipulating NMDAR signaling via GluN2B knockdown, we show that ketam

108 tural consequences of mGluR and metabotropic NMDAR activation differ, and that a brake on spine struc

109 el, pannexin-1, is regulated by metabotropic NMDAR signaling through Src kinase.

110 ation of a previously described metabotropic NMDAR pathway (i.e., by preventing ligand binding to NMD

111 onstrate an unexpected role for metabotropic NMDARs and postsynaptic Panx1 in suppression of facilita

112 e alternative for regulating aberrant mGluR5/NMDAR signaling in AD without disrupting their constitut

113 This A(2A)R/mGluR5/NMDAR interaction might prove a suitable alternative for

114 In juvenile male mice, NMDAR ablation results in several pathophysiological tra

115 d brain exposures are sufficient to modulate NMDAR activity.

116 a signaling pathway wherein leptin modulates NMDARs via Src to regulate beta-cell excitability and su

117 They report that these non-neuronal NMDARs display distinct structural, functional, and phar

118 somatic locations while maintaining a normal NMDAR content.

119 ptor-mediated synaptic currents and that NTS NMDAR activation contributes to leptin-induced reduction

120 dopamine receptor subunits in the actions of NMDAR PAM vs. antagonists.

121 that underlie the antidepressant actions of NMDAR-positive modulation vs. NMDAR blockade.

122 encyclidine (a non-competitive antagonist of NMDAR), and prevented the NMDAR dysfunction caused by pa

123 the induction and developmental dampening of NMDAR-LTD.

124 tor alteration, accompanied by a decrease of NMDAR clusters and impairment of long-term potentiation.

125 reverse the mutant DISC1-induced decrease of NMDAR-mediated currents in the mPFC.

126 iation with an antibody-mediated decrease of NMDAR.

127 current work supports further evaluation of NMDAR autoantibodies as a possible prognostic biomarker

128 th FK506 failed to increase the frequency of NMDAR-mediated mEPSCs and the amplitudes of evoked EPSCs

129 t clear whether the developmental impacts of NMDAR dysfunction can be overcome by interventions in ad

130 Additionally, the inducibility of NMDAR-LTD is greatly reduced in adulthood.

131 oints, and the effects on synaptic levels of NMDAR (assessed with confocal microscopy) and plasticity

132 along with increased dopamine modulation of NMDAR-mediated current.

133 d selective positive allosteric modulator of NMDAR, reverted the memory deficit caused by phencyclidi

134 SC1 interaction and epigenetic regulation of NMDAR expression and function.

135 ings demonstrate a functional repurposing of NMDAR in the surveillance of tissue fitness.

136 es a unique opportunity to study the role of NMDAR in the development of the early vertebrate nervous

137 agal afferents, leptin increased the size of NMDAR-mediated currents, but not AMPAR-mediated currents

138 s the inducible transcription of a subset of NMDAR-sensitive genes.

139 thranilic acid (4-Cl-3-HAA), a suppressor of NMDAR agonist quinolinic acid (QUIN), is a promising pot

140 neurons SGE-301 prolonged the decay time of NMDAR-dependent spontaneous excitatory postsynaptic curr

141 , however, to study the prolonged absence of NMDARs in vertebrates, and hence their role in nervous s

142 the mechanism responsible for the action of NMDARs on BBB permeabilization.

143 Here, we show that activation of NMDARs trigger a NO-dependent pathway that strengthens i

144 Pharmacologic antagonism of NMDARs in patients with depression may reduce excitabili

145 tropic NMDA 2 (GluN2) subunit composition of NMDARs determines whether they activate the transcriptio

146 l neurons in A25 had a heightened density of NMDARs, which are the targets of novel rapid-acting anti

147 ide representing the extracellular domain of NMDARs (p < 0.0001), however, binding was retained again

148 ink between antibody-mediated dysfunction of NMDARs in oligodendrocytes and the white matter alterati

149 Given the widespread expression of NMDARs and nNOS in the mammalian brain, we speculate tha

150 N2B and strongly regulates the expression of NMDARs at synapses.

151 ephalitis specifically alter the function of NMDARs in oligodendrocytes, causing a decrease of expres

152 owever, how this bidirectional modulation of NMDARs causes similar antidepressant effects remains unk

153 Positive allosteric modulators of NMDARs include an endogenous neurosteroid pregnenolone s

154 ta reveal that the nanoscale organization of NMDARs changes along dendritic segments in a subtype-spe

155 addition to memory deficits and reduction of NMDARs, CSF antibodies from patients with anti-NMDAR enc

156 Rescue of NMDARs in adult mice yields surprisingly robust improvem

157 Here we investigated the role of NMDARs and AMPARs in working memory using iontophoresis

158 The developmental switch of NMDARs from GluN2B-containing early in development to Gl

159 To evaluate the activity of oligodendrocyte NMDARs and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepro

160 ptic turnover of D-serine and its effects on NMDAR synaptic plasticity.SIGNIFICANCE STATEMENT Despite

161 rapastinel) or NMDAR antagonist, ketamine on NMDAR function and disinhibition-mediated glutamate rele

162 lated effects of AV-101 (720 and 1440 mg) on NMDAR engagement measured by gamma-frequency band audito

163 nderlying the rescuing effects of UNC0642 on NMDAR function and social behaviors in Shank3-deficient

164 he source of excess calcium was dependent on NMDARs, L-type VGCCs, GluA2-lacking AMPARs, and internal

165 te the effect of a NMDAR PAM (rapastinel) or NMDAR antagonist, ketamine on NMDAR function and disinhi

166 ed the NMDAR dysfunction caused by patients' NMDAR antibodies in cultured neurons.

167 ion from PVI dysfunction following perinatal NMDAR blockade.

168 c activation of presynaptic and postsynaptic NMDARs at the spinal cord level and that presynaptic NMD

169 t activation of presynaptic and postsynaptic NMDARs in the spinal cord.

170 whereby Ca(2+)-entering through postsynaptic NMDARs promotes the recruitment and strengthening of GAB

171 phorylated by Src family kinases, potentiate NMDAR activity.

172 en activator, previously shown to potentiate NMDAR activity, induces metabotropic signaling via the R

173 the GluN1 helix M3, and that PES potentiates NMDAR function by stabilizing the open-state position of

174 ecular mechanism by which leptin potentiates NMDARs in beta-cells remains unknown.

175 It does so by potentiating NMDAR activity, thus enhancing Ca(2+) influx and the ens

176 This cooperative action of presynaptic NMDARs allows to implement synapse-specific, activity-de

177 t the spinal cord level and that presynaptic NMDARs play a prominent role in the development of CIPS.

178 d-serine is the primary NMDAR coagonist at mature forebrain synapses and is synt

179 spine spike, and ultrastructural data prove NMDAR presence within the GABAergic presynapse.

180 and the amplitudes of evoked EPSCs and puff NMDAR currents in spinal dorsal horn neurons.

181 c EPSCs evoked from the dorsal root and puff NMDAR currents in spinal dorsal horn neurons.

182 s posits that N-methyl-d-aspartate receptor (NMDAR) antagonists such as ketamine act preferentially o

183 nts with anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis alter the levels of dopamine 1 recep

184 Anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis is an immune-mediated disease charac

185 -Cl-KYNA), an N-methyl-D-aspartate receptor (NMDAR) glycine site antagonist, and of 4-chloro-3-hydrox

186 may be due to N-methyl-D-aspartate receptor (NMDAR) hypofunction and parvalbumin (PV) neuronal dysfun

187 N-methyl-D-aspartate receptor (NMDAR) hypofunction has been implicated in several neuro

188 The N-methyl-d-aspartate receptor (NMDAR) is an ion channel that mediates the slow, Ca(2+)-

189 d not require N-methyl-D-aspartate receptor (NMDAR) signaling and was associated with homeostatic sca

190 ounds reduced N-methyl-D-aspartate receptor (NMDAR)-mediated currents 1 week after administration.

191 -methyl-D-aspartate type glutamate receptor (NMDAR) to dendritic spines is essential for excitatory s

192 ies have shown that enhancing NMDA receptor (NMDAR) activity can exert rapid antidepressant-like effe

193 significant reduction of both NMDA receptor (NMDAR) and AMPA/kainate receptor-mediated evoked excitat

194 n of receptors, including the NMDA receptor (NMDAR) and voltage-gated Na(+) channels.

195 esthetic dose of ketamine, an NMDA receptor (NMDAR) antagonist, produces rapid and sustained antidepr

196 eduction can be achieved with NMDA receptor (NMDAR) antagonists.

197 When psychosis develops in NMDA receptor (NMDAR) antibody encephalitis, it usually has an acute or

198 NMDA receptor (NMDAR) blockade with ketamine (KET) during development c

199 This study found that NMDA receptor (NMDAR) function was significantly increased in layer V p

200 Both the NMDA receptor (NMDAR) positive allosteric modulator (PAM), and antagoni

201 regulates phosphorylation of NMDA receptor (NMDAR) subunit GluN2B and that GluN2B-containing NMDARs

202 BLA AMPA receptor (AMPAR) and NMDA receptor (NMDAR) subunit phosphorylation that likely contribute to

203 ibodies, such as those to the NMDA receptor (NMDAR), are detectable in a subgroup of patients with ps

204 ighlight a novel role for the NMDA receptor (NMDAR), independent of ion flow, in driving spine shrink

205 rons exhibited large synaptic NMDA receptor (NMDAR)-mediated currents compared with non-LepR neurons.

206 2A and GluN2B subunits of the NMDA receptor (NMDAR).

207 y showed that N Methyl D Aspartate Receptor (NMDARs), expressed on cerebral endothelial cells forming

208 ctivation of N-methyl-D-aspartate receptors (NMDAR) containing the GluN2A subunit.

209 annels (HVACCs), but also of NMDA receptors (NMDAR).

210 N-methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion channels that play criti

211 N-methyl-D-aspartate receptors (NMDARs) are required to shape activity-dependent connect

212 nst neuronal N-methyl-D-aspartate receptors (NMDARs) in patients with anti-NMDAR encephalitis alter n

213 rs including N-methyl-D-aspartate receptors (NMDARs) is pivotal to brain development and function.

214 N-Methyl-D-aspartate receptors (NMDARs) play critical roles in the central nervous syste

215 imaging the N-methyl-d-aspartate receptors (NMDARs) subtype 2B (GluN1/2B), we investigated in the cu

216 ly expressed N-methyl-D-aspartate receptors (NMDARs), or the surface of live hippocampal neurons.

217 Methyl-d-aspartate type glutamate receptors (NMDARs) are key mediators of synaptic activity-regulated

218 lling through NMDA-type glutamate receptors (NMDARs) plays a key role in synaptic plasticity in the c

219 by the NMDA subtype of glutamate receptors (NMDARs).

220 ic NMDA-type ionotropic glutamate receptors (NMDARs).

221 NMDA receptors (NMDARs) are glutamate-gated ion channels that mediate fa

222 e mice transient blockade of NMDA receptors (NMDARs) during development [subcutaneous injections of 3

223 omeostatic response in which NMDA receptors (NMDARs) play a role through nitric oxide, and the CBF in

224 s a physiologic coagonist of NMDA receptors (NMDARs) required for synaptic plasticity, but mechanisms

225 d by activation of mGluRs or NMDA receptors (NMDARs), and how this plasticity is altered in Fmr1(-/y)

226 of native GluN2A- and GluN2B-NMDA receptors (NMDARs)-which play key roles in the use-dependent adapta

227 al bedding females, concomitant with reduced NMDAR GluN1 subunit expression in the right BLA.

228 s in which STEP(61) differentially regulates NMDARs and AMPARs, as well as its role in plasticity and

229 lish a role of postsynaptic SR in regulating NMDAR function.

230 icits in Shank3-deficient mice, and restored NMDAR-mediated synaptic function.

231 very of second-generation GluN2C/D-selective NMDAR-positive allosteric modulators (PAMs) with a dihyd

232 Serum NMDAR antibodies have been reported in a minority of pat

233 se findings suggest that SGE-301, or similar NMDAR modulators, could potentially serve as complementa

234 e to outside-out patches containing a single NMDAR, we find that agonist-bound receptors transition t

235 se properties of limited inhibition and slow NMDAR-mediated currents result in strong temporal summat

236 on hypofunction alone.SIGNIFICANCE STATEMENT NMDAR hypofunction in cortical interneurons has been lin

237 de of d-serine action.SIGNIFICANCE STATEMENT NMDARs are key regulators of neurodevelopment and synapt

238 Here, we developed a model to study NMDARs in early development in zebrafish, by generating

239 r, we have developed a unique model to study NMDARs in the developing vertebrate nervous system.SIGNI

240 N-to-piriform synapses contain a substantial NMDAR-mediated current that prolongs the synaptic respon

241 regulate beta-cell excitability and suggests NMDARs as a potential target to overcome leptin resistan

242 tenuated functional hyperemia by suppressing NMDAR-dependent nitric oxide production during neural ac

243 contribute in keeping unchanged the surface NMDAR density.

244 memory impairment and a reduction of surface NMDARs, as reported in this model.

245 a feedforward mechanism to increase synaptic NMDAR activation.

246 ediated pathogenic effects (memory, synaptic NMDAR, long-term potentiation) were prevented in the ani

247 tsynaptic neuronal SR in regulating synaptic NMDAR function and suggests a possible autocrine mode of

248 utonomous role for SR in regulating synaptic NMDAR function at Schaffer collateral (CA3)-CA1 synapses

249 Interestingly, synaptic NMDARs drive degradation of the methyltransferase in a n

250 manner and differentially regulate synaptic NMDARs and AMPARs.

251 aptic inputs, yet their response to systemic NMDAR antagonism is unknown.

252 However, current treatments targeting NMDAR subtypes have shown limited success in treating pa

253 Altogether, these findings demonstrate that NMDAR autoantibodies are detectable in a subgroup of CHR

254 ll-type-specific KD in mPFC demonstrate that NMDAR-GluN2B KD on Camk2a- but not Gad1-expressing neuro

255 on of high-level PE responses, implying that NMDAR antagonism disrupts the inference on abstract stat

256 Our findings suggest that NMDAR dysfunction impairs hierarchical Bayesian inferenc

257 We observed that NMDARs form a unique cluster mainly at the center of the

258 te receptors, and it has been suggested that NMDARs are particularly important for persistent firing

259 The NMDAR was the most common target antigen and NMDAR IgGs

260 One such ligand-gated ion channel, the NMDAR, impacts nearly all forms of nervous system functi

261 , the longest isoform, dephosphorylates the NMDAR subunit GluN2B and strongly regulates the expressi

262 V-101 can penetrate the brain and engage the NMDAR and KP effectively.

263 ecent studies highlight a novel role for the NMDAR, independent of ion flow, in driving synaptic weak

264 data identify a likely binding site for the NMDAR-positive allosteric modulator PES and describe a n

265 by generating CRISPR-mediated lesions in the NMDAR genes, grin1a and grin1b, which encode the obligat

266 isms that link conformational changes in the NMDAR to changes in spine size and synaptic strength.

267 Glutamine did not increase the NMDAR potentials in slices from serine racemase knock-ou

268 Glutamine increased the NMDAR-dependent long-term potentiation and the isolated

269 strated that early postnatal ablation of the NMDAR in corticolimbic interneurons induces neurobiochem

270 in vivo that early postnatal ablation of the NMDAR in corticolimbic interneurons results in an overac

271 cellular interactions on the mobility of the NMDAR is poorly understood.

272 -terminal domain in the GluN1 subunit of the NMDAR is required to maintain NMDARs at dendritic spine

273 monstrate antidepressant-like actions of the NMDAR PAM AGN-241751 and identify GluN2B on excitatory n

274 Notably, upregulation of the NMDAR subunit GluN2B in SST interneurons corrects the ex

275 , is required for the full expression of the NMDAR-dependent component of functional hyperemia.

276 tracellular and extracellular domains of the NMDAR.

277 te (PES), but the binding site of PES on the NMDAR and the molecular mechanism of potentiation are un

278 tive antagonist of NMDAR), and prevented the NMDAR dysfunction caused by patients' NMDAR antibodies i

279 an volunteers of either sex who received the NMDAR antagonist S-ketamine in a placebo-controlled, dou

280 ses revealed that within the CHR sample, the NMDAR antibody seropositive subjects had higher levels o

281 n couples physically and functionally to the NMDAR and supports its activity.

282 replicated by short-term treatment with the NMDAR antagonist MK-801, suggesting that they arise from

283 to describe the interaction of PES with the NMDAR.

284 Blockers of the NMDARs decreased persistent firing associated with the m

285 AMPARs segregate in clusters surrounding the NMDARs.

286 increases their efficacy, and enhances their NMDAR content.

287 ion-specific manner, and suggests that these NMDARs may serve as a novel target for selectively modul

288 ium release and promote calcium flow through NMDAR and calcium channels, while in turn, calcium activ

289 TEMENT Excitatory signaling mediated through NMDARs plays an important role in shaping emotional beha

290 -ionotropic (metabotropic) signaling through NMDARs, and in wild-type mice this structural plasticity

291 consequence of a deficient signaling through NMDARs.

292 ate piriform neurons, as they are coupled to NMDAR currents and to relatively modest disynaptic inhib

293 thway (i.e., by preventing ligand binding to NMDARs with competitive antagonists or blocking downstre

294 This composition confers to NMDARs' unconventional properties: these receptors do no

295 These pathways undergo NMDAR-dependent synaptic potentiation after attack.

296 ant actions of NMDAR-positive modulation vs. NMDAR blockade.

297 These effects were NMDAR specific, as patients' CSF did not alter responses

298 escribe a novel molecular mechanism by which NMDAR activity can be augmented.SIGNIFICANCE STATEMENT T

299 scription reveals a novel mechanism by which NMDAR subunit composition confers specificity to the pro

300 We then simulated this finding with NMDAR-dependent synaptic alterations in a microcircuit m