ライフサイエンスコーパス: glutamate

1 , and intracellular- lactate, glutamine, and glutamate).

2 all molecules aligned by poly(gamma-benzyl-l-glutamate).

3 d hyperpolarizing K(+) currents triggered by glutamate.

4 aptic vesicles promotes vesicle filling with glutamate.

5 ice after applying various concentrations of glutamate.

6 eviously undescribed spontaneous "plumes" of glutamate.

7 ite some crowding in the binding site by the glutamates.

8 etabolites implicated in insulin resistance (glutamate, -29%; P=1.5x10(-55); dimethylguanidino valeri

9 s in the C-terminal domain, tyrosine 351 and glutamate 355, that influence pH gating properties, as w

10 BD filament comprises residues lysine 274 to glutamate 380 of tau, spanning the last residue of the R

11 The metabotropic glutamate 5 (mGlu(5)) receptor is important in many brai

12 lar milieu acts through the deprotonation of glutamate 8 to release the hormone from the amyloid.

13 by transmitters released by vagal afferents, glutamate acting at AMPA receptors and 5-HT acting at 5-

14 his affects PAPs and therefore extrasynaptic glutamate actions is poorly understood.

15 We propose that glutamate activates TRESK through NMDA and AMPA mediated

16 and Ser845 sites at the GluA1 subunit of the glutamate AMPA receptors, which has been characterized a

17 have found evidence of robust alterations in glutamate and dopamine receptors within brain regions th

18 Responses to glutamate and endogenous inhibitory responses were routi

19 Reductions in the neurotransmitters glutamate and GABA correlate with impulsive behaviour in

20 We measured glutamate and GABA levels using semi-LASER magnetic reso

21 , as well as functional changes in forebrain glutamate and GABA systems, recapitulating aspects of th

22 n dorsal anterior cingulate cortex (ACC) and glutamate and Glx levels in left thalamus.

23 ative cooperativity between the two agonists glutamate and glycine in the NMDA receptor.

24 d the effects of excitatory neurotransmitter glutamate and inhibitory neurotransmitter GABA in regula

25 l-Theanine is an amino acid analog of l-glutamate and l-glutamine derived from various plant sou

26 cave bears based on the delta(15)N values of glutamate and phenylalanine.

27 st and significant increase in extracellular glutamate and phospho-cFos expression.

28 hich activates cell signaling in response to glutamate and specific protein ligands, such as tissue-t

29 ds, beta-citryl-glutamate, N-acetyl-aspartyl-glutamate, and ophthalmate-a marker of gamma-glutamyl cy

30 ia would exhibit a reduction in glutathione, glutamate, and/or glutamine in the cerebral cortex, cons

31 dd glycines post-translationally to internal glutamates, and we find that the same active-site residu

32 notable because SLC7A11 codes for a cysteine-glutamate anti-porter regulating levels of the antioxida

33 their protective scaffolding, gain of glial glutamate antiporter xCT expression, and reactive astroc

34 we were unable to reproduce the finding that glutamate, AP5, and NMDA positively modulate glycine rec

35 Rapid l-glutamate application under forward transport conditions

36 synaptic transmission, when large amounts of glutamate are released, Na(+) accumulated in the termina

37 Gamma-aminobutyric acid (GABA) and glutamate are the most abundant amino acid neurotransmit

38 ate transporter 2 (VGluT2) and thus releases glutamate as a second neurotransmitter in the striatum.

39 Mutation of alanine 53 to glutamate, as found in patients with early-onset PD, wea

40 ic metabolism, the innate immune system, and glutamate-associated proteins while simultaneously provi

41 Initially, a conserved glutamate at the active site was believed to generate th

42 Glutamate, ATP, Arabidopsis PLANT ELICITOR PEPTIDE, and

43 a defect linked with decreased extracellular glutamate availability.

44 y through covalent attachment of a synthetic glutamate-based photoswitch via a self-labelling SNAP ta

45 In contrast, for iGlu(h) and Fl-GluBP, glutamate binding is followed by isomerization.

46 ion pathway for chloride intersects with the glutamate binding site.

47 Remarkably, glutamate binding with a diffusion-limited rate constant

48 methyl-4-isoxazolepropionic acid receptor by glutamate binding.

49 These findings show that glutamate can be used as a noninvasive, imageable metabo

50 We identify mechanisms through which excess glutamate can negatively influence synaptic plasticity,

51 Glutamate carboxypeptidase II (GCPII), coded by the gene

52 y-like activation via two-photon uncaging of glutamate causes GC spines to release GABA both synchron

53 the DA signal, optogenetic activation of VTA glutamate cell bodies or axon terminals in NAc was suffi

54 Higher glutamate change tended to associate with longer emotion

55 oles in this fast-timescale behavior through glutamate co-release and convergent output to spinal-pro

56 ventral tegmental area dopamine neurons via glutamate co-transmission and that this co-transmission

57 eurons modulate dopamine neuron activity via glutamate co-transmission and that this pathway is devel

58 ropic receptors for acetylcholine, GABA, and glutamate, completing a map of this communication networ

59 was not significantly related to hippocampal glutamate concentration (p = 0.13).

60 urther identified a significant reduction in glutamate concentration and glutamate turnover (glutamat

61 tion status on the association between local glutamate concentration and WM activation in left DLPFC,

62 -wise difference in partial volume corrected glutamate concentration between patients and controls.

63 Crucially, glutamate concentration correlated negatively with the i

64 t WM-dependent activation is associated with glutamate concentration in unmedicated patients with sch

65 We found no group difference in local glutamate concentration.

66 s, but is not strongly linked to hippocampal glutamate concentrations.

67 ume, focal atrophy, and evidence of elevated glutamate concentrations.

68 Interestingly, interference with glutamine-glutamate conversion preferentially blocked proliferatio

69 uT3(+)INTs) has prompted speculation of GABA/glutamate corelease from these cells for almost two deca

70 -serine synaptic turnover, and the glutamine-glutamate cycle.

71 to replicate the results and did not observe glutamate, d-(-)-2-amino-5-phosphonopentanoic acid, or N

72 GAD1 encodes the glutamate decarboxylase enzyme GAD67, a critical actor o

73 amus in the mutant larvae, and expression of glutamate decarboxylase was reduced throughout the brain

74 upregulated after EGFR activation in a GDH1 (glutamate dehydrogenase 1)-dependent manner.

75 sympathoadrenal activity and reduced hepatic glutamate dehydrogenase enzymatic activity.

76 eling, we identified decreased intracellular glutamate density in presynaptic terminals, presynaptic

77 to hypertension via heightened hypothalamic glutamate-dependent signaling.SIGNIFICANCE STATEMENT Inf

78 To define how glutamate drives these conformations, we decoupled the l

79 t increase the availability of extracellular glutamate during neural activity can have profoundly neg

80 uous as the fundamental relationship between glutamate dynamics and plasticity, and the mechanisms li

81 r, non-heme iron center through the bridging glutamate E205 and subsequent catalysis occurs only in t

82 he molecular basis of the so-called bridging glutamate (E205) residue in intersubunit electron transf

83 e GLT-1 expression and a lack of increase in glutamate efflux during reinstatement of cocaine-seeking

84 ssion of the glutamate transporter GLT-1 and glutamate efflux in the nucleus accumbens (NA) core duri

85 racellular lifetime of synaptically released glutamate estimated with uptake measurements.

86 This imbalance could potentiate glutamate excitotoxicity and contribute to neuronal dysf

87 ons of the viscoelastic properties caused by glutamate excitotoxicity were similar to those induced b

88 OHB entry into the neuron, and protects from glutamate excitotoxicity.

89 en occurs in pathological conditions such as glutamate excitotoxicity.

90 osine triphosphate (ATP), but the reason for glutamate excretion is unclear.

91 Silencing glutamate favored goal-directed behaviors and had no imp

92 the importance of the co-release of GABA and glutamate from immature glycinergic MNTB terminals.

93 SCN neurons are exposed to glutamate from multiple sources including from the retin

94 Release of glutamate from nanoclusters in vivo caused enhanced c-Fo

95 mising potential antidepressant that targets glutamate functioning via the KP.

96 ion of metabolites and enzymes from the GABA-glutamate, GABA-putrescine, and the glyoxylate pathways

97 as a slow glutamate transporter and also as glutamate-gated chloride channel, the chloride conductan

98 king analysis supports allosteric binding to glutamate-gated chloride channels similar to ivermectin.

99 NMDA receptors (NMDARs) are glutamate-gated ion channels that mediate fast excitator

100 Glutamate (GLU) and gamma-aminobutyric acid (GABA) are t

101 tional magnetic resonance imaging (fMRI) and glutamate (Glu) concentration with magnetic resonance sp

102 t and mediates a critical salt bridge with a glutamate (Glu130) of alphaC helix, which is conserved a

103 t magnetic resonance spectroscopy to measure glutamate, glutamate+glutamine (Glx), and GABA levels in

104 resonance spectroscopy to measure glutamate, glutamate+glutamine (Glx), and GABA levels in dorsal ant

105 esonance spectroscopy of N-acetyl compounds, glutamate+glutamine, creatine+phosphocreatine, and choli

106 Abnormal levels of N-acetyl compounds, glutamate+glutamine, creatine+phosphocreatine, or cholin

107 We used the method to monitor glutamate, glutamine, gamma-aminobutyric acid and lactat

108 other data supporting a central imbalance of glutamate-glutamine cycling in depression, our results s

109 h control subjects, CHR individuals had high glutamate/glutamine and elevated focal cerebral blood vo

110 atal functional network deficits and reduced glutamate/glutamine ratio in the striatum of HD mice.

111 Hence, glutamine plus glutamate (Glx) and other metabolites were examined with

112 first 2 weeks, and mitigated alterations of glutamate, glycerophospholipids, and carnitine levels in

113 We hypothesize that excreting glutamate helps the cell to increase the nucleotide synt

114 However, we noted significant changes in glutamate homeostasis in the NA core of cocaine + alcoho

115 Using fluorescent glutamate imaging, we show that awake mice carrying a fa

116 By combining electron microscopy with glutamate immunogold labeling, we identified decreased i

117 onance spectroscopy ((1)H-MRS) investigating glutamate in DLPFC.

118 altered reward circuitry and increased brain glutamate in relation with symptoms of anhedonia.

119 To date, there is no systematic overview of glutamate in the dorsolateral prefrontal cortex (DLPFC)

120 Genetically encoded fluorescent glutamate indicators (iGluSnFRs) enable neurotransmitter

121 Both imaging of glutamate-induced calcium elevations and Western blots r

122 DNQX, by blocking excitatory AMPA glutamate inputs, is hypothesized to produce relative in

123 s suggest that tyramine, in interaction with glutamate, is involved in centrally mediated behavioral,

124 zed by the presence of a conserved aspartate-glutamate-leucine-leucine-alanine motif) competitively i

125 In particular, extracellular glutamate levels are tightly controlled by the astrocyti

126 (DG), CA3, and CA1 hippocampal extracellular glutamate levels in 2-4, 6-8, and 18-20 month-old male A

127 ts with a schizophrenia diagnosis had higher glutamate levels in thalamus (p = .01), but Glx levels i

128 ia and psychotic disorder, whereas increased glutamate levels in thalamus seem to be implicated in sc

129 results suggest that an increase in striatal glutamate levels may underlie acute cannabis-induced psy

130 rtly mitigated by replenishing extracellular glutamate levels, indicating a defect linked with decrea

131 esicular Na(+)/H(+) exchanger, and regulated glutamate loading as a function of the level of vesicle

132 o-switch" within delta-catenin, subject to a glutamate-mediated signaling pathway, that assists in ba

133 Functional validation supported a role for glutamate metabolism and glutamate oxaloacetate transami

134 We hypothesized that disrupted glutamate metabolism in pregenual anterior cingulate cor

135 ffects using dual-probe in vivo dopamine and glutamate microdialysis in nucleus accumbens and medial

136 tudy assessed orally administered monosodium glutamate (MSG) as a potential means of reducing kidney

137 Brain glutamate must be tightly controlled during hyperglycemi

138 five gamma-glutamyl amino acids, beta-citryl-glutamate, N-acetyl-aspartyl-glutamate, and ophthalmate-

139 l function proteins that function as coupled glutamate/Na(+)/H(+)/K(+) transporters and as anion-sele

140 The neurotransmitter N-acetyl-aspartyl-glutamate (NAAG) is the selective endogenous agonist of

141 this, we used optogenetics to stimulate VTA glutamate neurons in which tyrosine hydroxylase (TH), an

142 nd negative valence encoding in its GABA and glutamate neurons that influence both approach and avoid

143 e to gamma-aminobutyric acid (GABA), DA, and glutamate neurons within three sub-regions: the parabrac

144 -positive allosteric modulator (PAM) reduced glutamate neurotransmission in the BLA slices from panic

145 Glutamate neurotransmission is a prioritized target for

146 synaptic Panx1 in suppression of facilitated glutamate neurotransmission.SIGNIFICANCE STATEMENT The p

147 fluencing sensory signaling, as spillover of glutamate onto nearby glycinergic synapses would permit

148 mmunoreactive (ir) neurons express vesicular glutamate or GABA transporters.

149 magnetic resonance spectroscopy OR MRS) AND (glutamate OR glut* OR GLX) AND (schizophrenia OR psychos

150 ed decreases in cocaine-induced dopamine and glutamate outflow 4 weeks after VU0364572 treatment, wit

151 upported a role for glutamate metabolism and glutamate oxaloacetate transaminase 1 (GOT1)-dependent r

152 az(KD) mitochondria, but an up-regulation of glutamate oxidation supported respiration rates approxim

153 Mutants in other proline-glutamate (PE)/PPE clusters, responsive to magnesium and

154 agents with either one or two lysine-ureido-glutamate pharmacophores.

155 lly, R-(+)-EU-1180-453 was found to increase glutamate potency 2-fold, increase the response to maxim

156 statin (Sst) or parvalbumin (Pvalb), but not glutamate principle neurons in the medial prefrontal cor

157 We have developed a caged glutamate probe that is inert toward these receptors at

158 2-(13)C]pyruvate and hyperpolarized [1-(13)C]glutamate produced from [1-(13)C]alpha-ketoglutarate wer

159 with these results, hyperpolarized [5-(13)C]glutamate produced from [2-(13)C]pyruvate and hyperpolar

160 s demonstrate that suppression of either the glutamate racemase or epimerase activity of DapF comprom

161 and that Amph itself modulated postsynaptic glutamate receptor (GluRII) localization.

162 Metabotropic glutamate receptor (mGluR) 5 exhibits promising therapeu

163 highlight the important role of metabotropic glutamate receptor 1 in modulating sleep duration.

164 ent mutations in the same gene (metabotropic glutamate receptor 1) from two independent natural short

165 tion and trafficking of class C metabotropic glutamate receptor 2 (mGluR2) through a mechanism that r

166 Two metabotropic glutamate receptor 2/3 (mGluR2/3) agonists (pomaglumetad

167 l dopamine D(2/3) receptors and metabotropic glutamate receptor 5 (mGluR5) and assessed decision maki

168 or nonhyperbolic relationships (metabotropic glutamate receptor 5 and calcium-sensing receptor).

169 ot require postsynaptic Group 1 metabotropic glutamate receptor activation.

170 with a glutamate receptor antibody, and the glutamate receptor antagonist 6-cyano-7-nitroquinoxaline

171 e contact sites have immunoreactivity with a glutamate receptor antibody, and the glutamate receptor

172 evations and Western blots reveal ionotropic glutamate receptor expression prior to immunocytochemica

173 ines regulation of neuronal excitability via glutamate receptor function and neuroinflammation via ot

174 exosome-secreted miRNAs in the regulation of glutamate receptor gene expression and their relevance f

175 Here we show that glutamate receptor interacting protein 1 (GRIP1), an AMP

176 beta, serotonin receptors (Htr1a, Htr2a) and glutamate receptor subunit Grin2b, were modified in the

177 deficiency in muscles specifically increased glutamate receptor subunit IIA (GluRIIA) level and the f

178 thyl-d-aspartate receptors in the ionotropic glutamate receptor superfamily have been targeted for th

179 strocytes through activation of metabotropic glutamate receptor type 5 (mGluR5) signaling and that th

180 Arabidopsis thaliana glutamate receptor-like (GLR) channels are amino acid-ga

181 activates Ca(2+)-containing ion currents via GLUTAMATE RECEPTOR-LIKE (GLR) channels in root protoplas

182 on reduced inhibitory GABA(A) and excitatory glutamate receptor-mediated synaptic transmission in the

183 AT5 to serve functionally as an "inhibitory" glutamate receptor.

184 Presynaptic glutamate receptors (GluRs) modulate neurotransmitter re

185 ptic development, kainate-type of ionotropic glutamate receptors (KARs) are highly expressed in the B

186 e two distinct release modes by metabotropic glutamate receptors (mGluRs) constitutes critical suppor

187 Group I metabotropic glutamate receptors (mGluRs) play important roles in var

188 Calcium signalling through NMDA-type glutamate receptors (NMDARs) plays a key role in synapti

189 of leptin is mediated by the NMDA subtype of glutamate receptors (NMDARs).

190 Signals from peripheral glutamate receptors converge onto TRPV1, leading to mech

191 owed that activation of group I metabotropic glutamate receptors enhanced spontaneous glutamate relea

192 several full-length structures of ionotropic glutamate receptors in putative desensitized states were

193 Blockade of ionotropic glutamate receptors in the DMH, or brain transection ros

194 re protein synthesis and plasticity of GluA1 glutamate receptors in the mPFC.

195 istry enables covalent labeling of AMPA-type glutamate receptors in the same brain regions.

196 bition of the NMDA subtype of the ionotropic glutamate receptors is well characterized, the mechanism

197 f research have shown how phosphorylation of glutamate receptors mediates protein binding and recepto

198 FF bipolar cells, and the novel metabotropic glutamate receptors of ON bipolar-cell dendrites, are bo

199 es attribute an important role to ionotropic glutamate receptors, and it has been suggested that NMDA

200 binding profiles for these newly identified glutamate receptors, for example, kainate receptors on w

201 itically modified by glycosylation including glutamate receptors, voltage-gated calcium channels, the

202 uctural plasticity induced through different glutamate receptors.

203 , presynaptic release sites and postsynaptic glutamate receptors.

204 among which are the tyrosine kinase Fyn and glutamate receptors.

205 nd high affinity homomeric glycine activated glutamate receptors.

206 tion and depression through effects on brain glutamate receptors.

207 uN1 is more closed when bound to glycine and glutamate relative to what is observed in the presence o

208 fied both gamma-aminobutyric acid (GABA) and glutamate release and phospho-cFos expression in the NAc

209 BDNF-evoked glutamate release and synapsin phosphorylation was atten

210 napse and their respective activation during glutamate release are still unclear.

211 ercalated cells, we found that inhibition of glutamate release by a submaximal concentration of enkep

212 KV1.3 channel-dependent signaling stimulates glutamate release from Th17 cells upon direct cell-cell

213 However, CA1 evoked glutamate release in AbetaPP/PS1 mice was elevated at 2-

214 pic glutamate receptors enhanced spontaneous glutamate release in an auditory brainstem nucleus, whil

215 current at -60 mV and increased spontaneous glutamate release in MNTB neurons.

216 luR5 signaling is under the tight control of glutamate release machinery mediated through vesicular g

217 hese lamina terminalis AT1aR neurons induced glutamate release onto magnocellular neurons and was suf

218 Using inhibition of glutamate release onto the intercalated cells of the amy

219 hort-term plasticity because of an increased glutamate release that results from an anomalous contrib

220 the BLA and tonically activated to regulate glutamate release via a G-protein-dependent mechanism.

221 ith action-potential-independent spontaneous glutamate release, suggesting plumes are a consequence o

222 ues is accompanied by a rapid suppression of glutamate release.

223 myloid-beta (Abeta)(42), elicits presynaptic glutamate release.

224 on NMDAR function and disinhibition-mediated glutamate release.

225 ve can be associated with ~50% inhibition of glutamate release.

226 ransporter (VGlut) and increased spontaneous glutamate release.

227 g a morphologic explanation for the enhanced glutamate release.

228 This, together with glutamate released from damaged phloem, activates GLRs,

229 o the latter, they did not recover after the glutamate removal.

230 In this mutant, the protonation state of a glutamate residue (E120) in the pH sensor is sensitive t

231 idue on TM2, and replacing lysine 319 with a glutamate residue converts PAC to a cation-selective cha

232 ling a metal-binding site consisting of four glutamate residues close to the symmetry axis.

233 for deacetylated cell wall, and usage of two glutamate residues for catalysis.

234 strate the catalytic role of two interacting glutamate residues of TSP1, located in a cleft between t

235 1 and GluN2 subunits, which bind glycine and glutamate, respectively, to activate their ion channels.

236 e same as wild-type as a result of increased glutamate reuptake, producing faster decay kinetics.

237 leotide polymorphism (SNP) signal across the glutamate-rich 3 (ERICH3) gene that was nearly genome-wi

238 1-L5) were synthesized using the lysine-urea-glutamate scaffold, and PSMA inhibition constants were d

239 To test this hypothesis, a glutamate selective microelectrode array (MEA) was used

240 dendritic imaging with a genetically-encoded glutamate sensor in awake monkeys, and map the excitator

241 Optical glutamate sensors combined with patch-clamp and 3D molec

242 with deprotonated Ci1 or removal of the Ci1 glutamate side chain, the hydrogen-bonded system is less

243 bunits in biological systems responsible for glutamate signaling.

244 into the potential utility of adenosine- and glutamate-signaling as novel therapeutic targets to trea

245 astroglial glutamate transporters, boosting glutamate spillover and NMDA-receptor-mediated inter-syn

246 eurons from deficits in basal-stimulated and glutamate-stimulated respiration, effects requiring beta

247 nic alcohol use has important effects on the glutamate system.

248 -fold more sensitive to the toxic effects of glutamate than the MTT assay.

249 ght be linked with cytosolic pool of D and L-glutamate, thereby coupling protein and cell envelope sy

250 CR in order to find the relative quantity of glutamate to gamma-aminobutyric acid (GABA), DA, and glu

251 Applying glutamate to outside-out patches containing a single NMD

252 e dependent on GLS to maintain intracellular glutamate to prevent the amino acid deprivation response

253 ificity of PARP1 and PARP2 from aspartate or glutamate to serine(9,10).

254 Sustained application of glutamate to skeletal myotomes in vivo is necessary and

255 ssion of mutant ASIC1a bearing truncation or glutamate-to-alanine substitutions at distal NT causes c

256 tamate concentration and glutamate turnover (glutamate-to-glutamine ratio) in the putamen in patients

257 Using voltage and extracellular glutamate transient recording over widespread regions of

258 ing two approaches: (1) increased excitatory glutamate transmission at mossy fibers (MF)-CA3 synapses

259 , which plays a role in fine-tuning synaptic glutamate transmission.

260 ated in SLC7A11A, a gene involved in cystine/glutamate transport and the biosynthesis of glutathione,

261 ed the accumulation of presynaptic vesicular glutamate transporter (VGlut) and increased spontaneous

262 the adult, healthy brain expresses vesicular glutamate transporter 2 (VGluT2) and thus releases gluta

263 tive to previous expression of the vesicular glutamate transporter 2 (Vglut2) gene, coupled with immu

264 the VP [VP neurons expressing the vesicular glutamate transporter 2 (VP(VGluT2))], whose activation

265 s in the PVH co-localized with the vesicular glutamate transporter 2.

266 K neurons is composed of transient vesicular glutamate transporter 3 (tVGLUT3) neurons, which convey

267 ociated with reduced placental glutamine and glutamate transporter activity and expression, and propo

268 esis and suggest that abnormal glutamine and glutamate transporter activity is part of the spectrum o

269 EAAT5 acts as a slow glutamate transporter and also as glutamate-gated chlori

270 show reduced levels of one such client, the glutamate transporter EAAT1.

271 els are tightly controlled by the astrocytic glutamate transporter EAAT2, influencing synaptic functi

272 a brain tumor stem cells with low astrocytic glutamate transporter expression are dependent on GLS to

273 While glutamate transporter expression is reduced in numerous

274 ining, we assessed surface expression of the glutamate transporter GLT-1 and glutamate efflux in the

275 e fluorescence imaging of the archaeal model glutamate transporter homologue Glt(Ph) from Pyrococcus

276 Molecular identification of vesicular glutamate transporter three and cholecystokinin expressi

277 eurotrophic factors, BDNF and IGF-1, and the glutamate transporter, GLT-1 after ischemic brain damage

278 In addition, GltS was identified as a glutamate transporter.

279 release machinery mediated through vesicular glutamate transporters (VGLUTs) that ultimately dictate

280 By limiting spillover, glutamate transporters are believed to prevent excessive

281 n thus prompts spatial retreat of astroglial glutamate transporters, boosting glutamate spillover and

282 proteins, synapsin 1, unique microRNAs, and glutamate transporters.

283 t) is the primary target of these mDAP and l-glutamate treatments.

284 ant reduction in glutamate concentration and glutamate turnover (glutamate-to-glutamine ratio) in the

285 Glutamate typically stimulates burst firing subsequent t

286 Focal glutamate uncaging confirms MNTB neurons as a source of

287 Here, using two-photon glutamate uncaging to induce plasticity at individual de

288 eporter gene assays, RNA-Seq, and two-photon glutamate uncaging with calcium imaging, we show that kn

289 synapse currents, evaluated using two-photon glutamate uncaging.

290 which they display impaired phagocytosis and glutamate uptake and fail to support neuronal maturation

291 lass of EAAT2 inhibitors that were tested in glutamate uptake and whole-cell electrophysiology assays

292 on channels from ratios of anion currents by glutamate uptake currents.

293 vitro, including trophic support of neurons, glutamate uptake, and phagocytosis.

294 P (EGFP) in neurons expressing the vesicular glutamate (vGLUT2) or GABA transporter (vGAT), then dete

295 higher levels of medial prefrontal cortical glutamate were associated with negatively experienced eg

296 ego dissolution, lower levels in hippocampal glutamate were associated with positively experienced eg

297 imaging, and biosensor-mediated measures of glutamate were conducted with MAOIs in wild-type and TAA

298 Rs with near-complete efficiency relative to glutamate when attached to receptors via a range of orth

299 Inflammation is associated with increased glutamate, whereas the antioxidant glutathione may prote

300 /kg) induced region-dependent alterations in glutamate, which predicted distortions in the subjective