ライフサイエンスコーパス: glutamate

1 V) did not contrast the neurotoxic effect of glutamate.

2 ecrease the release of the neurotransmitter, glutamate.

3 ich the first step involves glycosylation on glutamate.

4 izes the gamma-carboxyl linked, branch point glutamate.

5 surprisingly rich effects on the kinetics of glutamate-activated currents, without any effect on asse

6 We demonstrated that glutamate acts through kainic acid receptors in the VMH

7 c circuit is conferred at the level of three glutamate afferents: dorsal raphe nucleus (DR), peduncul

8 nd also showed gating alterations, a reduced glutamate affinity associated with a strong decrease of

9 Gated by the neurotransmitter glutamate, AMPA receptors are critical for synaptic stre

10 njected (mice, intraocular) unimNPs with the glutamate analog N-methyl-d-aspartate (NMDA), which is e

11 ing INs displayed differential modulation by glutamate and 5-HT.

12 y catalyzing the synthesis of glutamine from glutamate and ammonia.

13 o examine the effect of age and diagnosis on glutamate and cerebral blood flow (rCBF) in adults with

14 Neurons co-storing glutamate and dopamine were found to project from the pr

15 rons include a subpopulation containing both glutamate and GABA (SuM(vgat/vglut2)) and another also e

16 We disclose compartmentalized corelease of glutamate and GABA and its differential plasticity from

17 spectroscopy in humans, to measure levels of glutamate and GABA in dACC.

18 The mossy fibers (MFs) corelease glutamate and GABA onto pyramidal cells of CA3 during de

19 It is well established that glutamate and GABA signal through both ionotropic and me

20 ng, optogenetics, and dual-color uncaging of glutamate and GABA, we demonstrate that plateau potentia

21 gnal mode, and that the neurons also release glutamate and gamma-aminobutyric acid as cotransmitters,

22 Fast glutamate and gamma-aminobutyric acid cotransmission con

23 in association with altered brain levels of glutamate and gamma-aminobutyric acid have been identifi

24 GABA and those of the combined resonances of glutamate and glutamine (Glx), were measured by 1H MRS i

25 al GABA levels and Glx (combined estimate of glutamate and glutamine) levels using magnetic resonance

26 and M705V caused a significant reduction in glutamate and glycine agonist potency, whilst D731N was

27 activated by the excitatory neurotransmitter glutamate and have well-characterized roles in the nervo

28 re reported to reduce spontaneous release of glutamate and it was proposed that there was conservatio

29 rget of rapamycin (mTOR) activation, loss of glutamate and potassium buffering capacity, loss of astr

30 MA preference/taking by lowering endogenous glutamate and/or Homer2 expression within this subregion

31 des the involvement of the major excitatory (glutamate) and inhibitory (gamma aminobutyric acid (GABA

32 N-methyl-d-aspartate (NMDA) receptors are glutamate- and glycine-gated channels that flux Na(+) an

33 dictate glutamine dependence via the cystine/glutamate antiporter xCT/SLC7A11.

34 Our observations can be explained if ACh and glutamate are released from common vesicles onto spatial

35 primary sequence of proteins and additional glutamates are then sequentially added via alpha-carboxy

36 Glutamate aspartate transporter levels were higher and g

37 , including the amino acid neurotransmitters glutamate, aspartate and taurine.

38 -1beta-dependent downregulation of the glial glutamate-aspartate transporter (GLAST), which causes an

39 While erasers for the MARylation of glutamate/aspartate and arginine have been identified, t

40 he LBD surface form pathways that facilitate glutamate binding by effectively reducing a three-dimens

41 Since the locked glutamate-binding clefts primarily contributes to recept

42 s I814T, D933N and N976S located between the glutamate-binding domain and C-terminus.

43 s comprise two glycine-binding GluN1 and two glutamate-binding GluN2 subunits (GluN2A-D).

44 spartate receptor (NMDAR) is controlled by a glutamate-binding site and a distinct, independently reg

45 Contrast analyses showed increased glutamate both in children with ASD and OCD compared wit

46 failed clearance and exaggerated release of glutamate by glial cells during immune activation leads

47 These simulations also reveal that glutamate can bind in an inverted conformation and also

48 1 is a potent hydroxamate-based inhibitor of glutamate carboxypeptidase II.

49 catalyze hydrolysis of alpha-carboxyl-linked glutamates, CCP5 uniquely metabolizes the gamma-carboxyl

50 We found that photoactivation of PPTg glutamate cell bodies could serve as a direct positive r

51 The faster glutamate clearance induced by PAR1 activation leads to

52 ort cells of the CNS and are responsible for glutamate clearance, metabolic support, response to inju

53 cific control over BA circuitry via 5-HT and glutamate co-release to inhibit the BA output.SIGNIFICAN

54 Maintenance of nTS glutamate concentration occurs in part through astrocyti

55 uals and was inversely correlated with serum glutamate concentration.

56 s is the first study to directly compare the glutamate concentrations across the two disorders with t

57 AAT3 internalization increases extracellular glutamate concentrations and activates GluN2B-containing

58 te, glutamine, and the sum of glutamine plus glutamate concentrations in vivo in patients with schizo

59 The response was transient and bimodal; glutamate concentrations that exceeded 250 microM failed

60 Importantly, EM2 and glutamate-containing varicosities appose spinal neurons

61 ival and transmission were unaffected, while glutamate cotransmission at phasic firing frequencies wa

62 s, is coupled with a rapid transient rise in glutamate cycling in the medial prefronal cortex (mPFC)

63 The glutamate/cystine antiporter solute carrier family 7 mem

64 setting caused by epigenetic upregulation of glutamate decarboxylase 1 (GAD1), a regulator of the GAB

65 ate transporters (vglut1, vglut2.1, vglut3), glutamate decarboxylases (gad1, gad2), and choline acety

66 From 2-step testing, all glutamate dehydrogenase (GDH)-positive specimens, regard

67 Here we report that a glutaminolytic enzyme, glutamate dehydrogenase 1 (GDH1), upregulated upon detac

68 K18], high mobility group box-1 [HMGB1], and glutamate dehydrogenase [GLDH]).

69 Targeting a glutamate-dependent metabolic pathway thus represents a

70 tion is associated with an abrupt shift from glutamate-dominant excitatory to GABA-dominant inhibitor

71 he release and extracellular accumulation of glutamate during PIDs is strongly curtailed in Ip3r2-def

72 tor alpha (mERalpha; during diestrus) versus glutamate (during proestrus), concomitant with the ebb a

73 may act as a phosphomimetic, with a Y102-to-glutamate (E) mutation, lost both activities.

74 Glutamate E153 on the E-loop and arginine R210 on the ad

75 Upon ring rotation, the protonated glutamate encounters the matrix channel and deprotonates

76 on in the intact rat, mimicking responses to glutamate excitation.

77 abundance of Bacteroides thetaiotaomicron, a glutamate-fermenting commensal, was markedly decreased i

78 which plays an antioxidant role by exporting glutamate for cystine.

79 ing: stimulatory, which requires a catalytic glutamate for most of the targets except for the matR tr

80 bens core (NAcore) and requires spillover of glutamate from prefrontal cortical afferents.

81 further show that the endogenous release of glutamate from the inner hair cells may increase the str

82 PSMA's carboxypeptidase activity releases glutamate from vitamin B9 and other glutamated substrate

83 dicts improvements in growth under increased glutamate:fumarate ratios.

84 separate proline dehydrogenase (PRODH) and l-glutamate-gamma-semialdehyde dehydrogenase active sites.

85 tion-state analogue inhibitor reveals that a glutamate gatekeeper and a sterically constricted active

86 ctroscopy to measure anterior cingulate (AC) glutamate (Glu) and glutamine (Gln) and arterial spin la

87 Lower and moderate levels of glutamate (Glu) in the right pACC significantly moderate

88 50% of OTR-expressing cells in the VTA were glutamate (GLU) neurons, as indicated by expression of m

89 pendent acid tolerance and contribute to the glutamate (Glu)-dependent acid resistance system in this

90 E STATEMENT Astrocytes spontaneously release glutamate (Glut) and other gliotransmitters (GTs) that c

91 , and dorsolateral prefrontal cortex (DLPFC) glutamate+glutamine (Glx) were measured using a clinicia

92 Glutamate, glutamine, and GABA were measured cortically

93 addressed this hypothesis by measuring GABA, glutamate, glutamine, and the sum of glutamine plus glut

94 n metabolites including the choline species, glutamate, glutathione, and GABA.

95 res for the three primary neurotransmitters (glutamate, glycine, and GABA) in the auditory brainstem

96 ion of orexin, neurotensin, and metabotropic glutamate Gq/11-linked receptors mimicked the effects of

97 rk with mGlu2 receptors to prime an enhanced glutamate homeostasis that promotes both pro-resilient a

98 ing dynamics, dynamic ion concentrations and glutamate homeostasis, neuronal and astroglial volume ch

99 confirm the role for nucleus accumbens (NAC) glutamate/Homer2 expression in MA preference/aversion.

100 ability to inflammatory molecules, disrupted glutamate homoeostasis, impaired action of antipsychotic

101 Here, we use a novel 7 Tesla MRI glutamate imaging technique (GluCEST) to estimate change

102 ated with increased activation and decreased glutamate in executive regions.

103 ptors activate cell signaling in response to glutamate in Schwann cells.

104 es the majority of nonsynaptic extracellular glutamate in the NAc, while GLT-1 is responsible for the

105 ally linked to the gamma-carboxyl group of a glutamate in the primary sequence of proteins and additi

106 brain and for the reuptake and recycling of glutamate in the synapse.

107 ivity, and sequential deletion of individual glutamates in GC-A-8E progressively increased the Km Dou

108 The glutamine/glutamate increase in the pgACC caused by ketamine at 24

109 lial cells during immune activation leads to glutamate increases and promotes aberrant extrasynaptic

110 ein expression at 24 h and protected against glutamate-induced cell death.

111 Glutamate-induced excitotoxicity, mediated by overstimul

112 firm overlap between ASD and OCD in terms of glutamate involvement.

113 A receptors, represent different subtypes of glutamate ion channels.

114 as a future guide to investigate the role of glutamate, ion concentrations, and dynamics cell volume

115 e matR transcript, and inhibitory, for which glutamate is dispensable.

116 Glutamate is loaded into synaptic vesicles via the vesic

117 ys in the inner plexiform layer (IPL), where glutamate is released from ON and OFF bipolar cell termi

118 Glutamate is the dominant excitatory neurotransmitter in

119 Since glutamate is the major monovalent anion in E. coli, thes

120 Only alanine, glutamate, isoleucine, and valine, but not leucine, were

121 6A1 indicated that CYP46A1 is activated by l-glutamate (l-Glu), l-aspartate, gamma-aminobutyric acid,

122 may induce switch in conformation similar to glutamate LBD locked state.

123 g technique (GluCEST) to estimate changes in glutamate levels across cortical and subcortical regions

124 r cingulate cortex (ACC) has shown decreased glutamate levels in patients with major depressive disor

125 y of SCN neurons by regulating extracellular glutamate levels.

126 slowly than predicted, and proline, glycine, glutamate, lysine and arginine, which were all consumed

127 Glutamate may function not only in a signaling role at a

128 led a significant effect of region, with the glutamate measure lowest in the primary visual cortex an

129 AT inhibitory peptide VIVIT reduced signs of glutamate-mediated hyperexcitability in 5xFAD mice, meas

130 ect, indicating that the interaction between glutamate-mediated synaptic activity and TrkB signaling

131 h periodontitis, and significantly decreased glutamate metabolism metal transport in oral cancer pati

132 on has been given to targeting mitochondrial glutamate metabolism to control neurotransmitter levels.

133 fied novel alterations in purine metabolism, glutamate metabolism, and the pentose phosphate pathway.

134 es for astrocyte processes, such as GABA and glutamate metabolism.

135 st that antagonists of group II metabotropic glutamate (mGlu) receptors (mGlu2 and mGlu3) reduce stre

136 Riluzole is a glutamate-modulating agent with neuroprotective properti

137 The glutamate modulator, riluzole, which was recently shown

138 hat activation of CB1Rs in VgluT2-expressing glutamate neurons produces aversive effects that might e

139 ndicate that inflammation and alterations in glutamate neurotransmission are two novel pathways to pa

140 studies during the last 20 years implicated glutamate neurotransmission in different brain regions i

141 role for pedunculopontine tegmental nucleus glutamate neurotransmission in modulating VTA dopamine n

142 synaptic gene expression and protein levels, glutamate neurotransmitter release, and, consequently, r

143 -type transport activity, when the catalytic glutamate of the canonical nucleotide binding site 2 was

144 found that 5-HT neurons co-release 5-HT and glutamate onto BA neurons in a cell-type-specific and fr

145 When glutamate or NMDA was injected directly into crush-injur

146 ase only in neurons producing acetylcholine, glutamate, or GABA.

147 Glutamate oxaloacetate transaminase enables anaplerotic

148 hese results demonstrate that ascending PPTg glutamate projections can drive motivated behavior, and

149 Glutamate promoted SC migration by a pathway that requir

150 ement is mirrored by the change of glutamine/glutamate ratio and if such effects show a regional and

151 n, and treatment was found for the glutamine/glutamate ratios (placebo, n=14; ketamine, n=12).

152 Regulation of AMPA-type glutamate receptor (AMPAR) number at synapses is a major

153 and GluD2 receptors form the GluD ionotropic glutamate receptor (iGluR) subfamily.

154 ation of one particular GPCR, a metabotropic glutamate receptor (mGluR), can reduce cone synaptic tra

155 receptors, specifically via the metabotropic glutamate receptor (mGluR).

156 execution, EAAC1 limits group I metabotropic glutamate receptor (mGluRI) activation, facilitates D1 d

157 Metabotropic glutamate receptor 1 (mGluR1) function in Purkinje neuro

158 The metabotropic glutamate receptor 1 (mGluR1) is abundantly expressed in

159 Phrenic motoneuron AMPA glutamate receptor 2 (GluR2) subunit mRNA expression dec

160 Here, we find that metabotropic glutamate receptor 2 (mGluR2) signaling, which acts on v

161 s observed biophysically on the metabotropic glutamate receptor 2 homodimer.

162 The metabotropic glutamate receptor 4 (mGluR4) is an emerging target for

163 Drugs targeting metabotropic glutamate receptor 5 (mGluR5) have therapeutic potential

164 outon enlargement, and increase postsynaptic glutamate receptor abundance.

165 We show the coexistence of time-locked, glutamate receptor and GABA receptor-mediated mono synap

166 GABA or glutamate receptor antagonists did not block the ethanol

167 reticulum, the postsynaptic density, and the glutamate receptor cluster.

168 d glutamate receptor field size, and altered glutamate receptor composition.

169 en 1 (EEA1), a protein involved in AMPA-type glutamate receptor endocytosis.

170 c compartment of mutant NMJs include reduced glutamate receptor field size, and altered glutamate rec

171 possibly via the modulation of postsynaptic glutamate receptor functionality.

172 namics simulations of the GluA2 AMPA subtype glutamate receptor ligand-binding domain (LBD) dimers to

173 R2 and excitatory light-activated ionotropic glutamate receptor LiGluR yielded a distribution of expr

174 onist activation of the group I metabotropic glutamate receptor mGluR1 increases the strength of this

175 We demonstrated previously that CeA glutamate receptor signaling mediates cisplatin-induced

176 rent site substitution (p.A636T) occurs in a glutamate receptor subunit, GRIA1.

177 The formin Delphilin binds the glutamate receptor, GluRdelta2, in dendritic spines of P

178 al measures to demonstrate that metabotropic glutamate receptor-induced sensitization of TRPA1 nocice

179 Glutamate-receptor signaling initiates the activity-depe

180 KEY POINTS: The AMPA-type ionotropic glutamate receptors (AMPARs) mediate the majority of exc

181 sity protein-95 (PSD-95) localizes AMPA-type glutamate receptors (AMPARs) to postsynaptic sites of gl

182 ssion is mediated by AMPA-subtype ionotropic glutamate receptors (AMPARs).

183 a*ss* receptors) as well as the two types of glutamate receptors (GluRs) (AMPARs and NMDARs).

184 ry synapses is determined by the presence of glutamate receptors (i.e. AMPA, NMDA, and kainate recept

185 anslation downstream of group I metabotropic glutamate receptors (mGlu1/5) is a core pathophysiology

186 that EAAC1 limits activation of metabotropic glutamate receptors (mGluRIs) in the striatum and, by do

187 Metabotropic glutamate receptors (mGluRs) are mandatory dimers playin

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

189 duced at excitatory synapses by metabotropic glutamate receptors (mGluRs).

190 create a family of light-gated metabotropic glutamate receptors (mGluRs).

191 Ionotropic glutamate receptors activate cell signaling in response

192 These results identified ionotropic glutamate receptors and NMDA-Rs, specifically, as potent

193 Ionotropic glutamate receptors are important for estradiol feedback

194 Ionotropic glutamate receptors are thought to play an essential rol

195 Glutamate receptors are well characterized channels that

196 um channels to a trans-synaptic complex with glutamate receptors at the visual system's first synapse

197 role of synaptic trafficking of AMPA-type of glutamate receptors in HSP, Mecp2 KO neurons have lower

198 Stimulating these glutamate receptors increases nitric oxide (NO) producti

199 At the same time, metabotropic glutamate receptors mediate 20-hydroxyeicosatetraenoic a

200 isoxazole propionic acid)-subtype ionotropic glutamate receptors mediate fast excitatory neurotransmi

201 NMDA receptors (NMDARs) are ionotropic glutamate receptors that are crucial for neuronal develo

202 Rs) are a subtype of postsynaptic ionotropic glutamate receptors that function as molecular coinciden

203 ess kainate receptors (KARs), a subfamily of glutamate receptors that modulate neurite outgrowth and

204 s the remodeling of the ionotropic AMPA-type glutamate receptors that underlie fast excitatory synapt

205 ctive excitatory synapses by recruiting AMPA glutamate receptors to the postsynaptic cell surface.

206 en shown to directly inhibit AMPA receptors (glutamate receptors), and to change cell energetics thro

207 rgeting multiple ionotropic and metabotropic glutamate receptors, and intracellular cascades involved

208 mature animals require MAGUKs for anchoring glutamate receptors, but are much more stable.

209 esponsiveness and the link between PMCA2 and glutamate receptors, GABA receptors (GABARs), and glutam

210 ignaling through ionotropic and metabotropic glutamate receptors, ultimately resulting in synaptic dy

211 tors (KARs) consist of a class of ionotropic glutamate receptors, which exert diverse pre- and postsy

212 titive/fast off-rate antagonist of NMDA-type glutamate receptors.

213 roxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptors.

214 n via the activation of group I metabotropic glutamate receptors.

215 c or glutamatergic neurons) and postsynaptic glutamate receptors.

216 Glutamate recognition by neurotransmitter receptors ofte

217 These results also associate glutamate recycling and sleep regulation, adding further

218 role of the cotransmission, we targeted the glutamate-recycling enzyme glutaminase (gene Gls1).

219 ansporter EAAT2's ability to scavenge excess glutamate, regulating synaptic transmission.

220 aptic voltage-gated Ca(2+) channel directing glutamate release (CaV1.4) with postsynaptic mGluR6 rece

221 fied alcohol-sensitive proteins that control glutamate release (e.g., SV2A, synaptogyrin-1) and posts

222 ther, I compile evidence regarding astrocyte glutamate release as well as astrocyte association with

223 Our results show that N-type VGCCs control glutamate release at a limited number of release sites t

224 ir cell development, and genes essential for glutamate release at hair cell ribbon synapses, suggesti

225 that modulate neurite outgrowth and regulate glutamate release at the DRG-dorsal horn synapse.

226 Here, by imaging light-driven glutamate release from more than 13,000 bipolar cell axo

227 tive to sound and only weakly depolarized by glutamate release from OHCs.

228 ed following selective genetic disruption of glutamate release from SuM(vglut2) neurons.

229 stimulation of 5-HT terminals did not evoke glutamate release onto BA principal neurons, but inhibit

230 afferents displayed a higher probability of glutamate release, although short-term synaptic plastici

231 e capacity of axonal D-type current to limit glutamate release, thus contributing to epileptogenesis.

232 ebbian activity, which increases Pr, and (2) glutamate release, which decreases Pr.

233 MDA receptors (NMDARs), and does not require glutamate release.

234 peptides, indicating a presynaptic action on glutamate release.

235 d in virtually complete absence of vesicular glutamate release.

236 Here we show that glutamate-releasing ARC neurons expressing oxytocin rece

237 Here we report that glutamate-releasing neurons of the supramammillary regio

238 mental evidence that protonation of Glu37, a glutamate residue embedded in a hydrophobic pocket of Hd

239 We have now identified a highly conserved glutamate residue in the transmembrane region of E. coli

240 al modification - polyglutamylation, where a glutamate residue is enzymatically linked to the gamma-c

241 of betaS fibril structures indicate that key glutamate residues (Glu-31 and Glu-61) in these domains

242 Exposed glutamate residues in CaM (Glu-11, Glu-14, Glu-84, and G

243 Arginine and Glutamate-Rich protein 1 (ARGLU1) is a protein whose fun

244 target of rapamycin (mTOR) kinase, promotes glutamate secretion, cystine uptake, and incorporation i

245 d via alpha-carboxyl-linkages to the growing glutamate side chain.

246 ng adeno-associated virus vectors normalized glutamate signaling dynamics, increased astrocytic gluta

247 models of HD show aberrant cortical-striatal glutamate signaling.

248 Hebbian plasticity is thought to require glutamate signalling.

249 - and postsynaptic spiking in the absence of glutamate signalling.

250 insight suggests that subunit selectivity of glutamate-site antagonists can be mediated by mechanisms

251 ypothesized that pharmacologically promoting glutamate spillover in the NAcore would mimic cocaine-in

252 510 reduced maximal velocity (Vmax), whereas glutamate substitutions had no effect or increased Vmax

253 releases glutamate from vitamin B9 and other glutamated substrates, which activate mGluR I.

254 ed mGluR5 internalization in response to the glutamate surge.

255 ediators related to the so-called tripartite glutamate synapse, including pre- and post-synaptic neur

256 iazo-5-oxo-l-norleucine (DON, 14) attenuates glutamate synthesis in HIV-infected microglia/macrophage

257 The p-aminobenzoyl-l-glutamate tail of THF remains weakly bound in a widened

258 Inhibition of the conversion of glutamate to alpha-ketoglutaric acid prevented the produ

259 d decarboxylase enzyme isoforms that convert glutamate to GABA.

260 Adding more glutamates to make GC-A-9E or GC-A-10E had little effect

261 The enhanced endogenous glutamate tone in RVH rats was not due to blunted glutam

262 studies indicate that an elevated endogenous glutamate tone results in an exacerbated activation of e

263 ion of ERalpha in kisspeptin cells decreased glutamate transmission to AVPV neurons and markedly incr

264 We found that excessive glutamate transmission upregulated mRNA expression of Fg

265 aired bSC dendritogenesis but also abolished glutamate transmission-induced dendritic overgrowth.

266 resembling the changes induced by excessive glutamate transmission.

267 +) binding to hEAAT1 as a novel mechanism of glutamate transport dysfunction in human disease.

268 was also associated with reduced astrocytic glutamate transport in the VMH.

269 ving aberrant CN/NFAT signaling and impaired glutamate transport.

270 ded into synaptic vesicles via the vesicular glutamate transporter (VGLUT), a mechanism conserved acr

271 eracidification is mediated by the vesicular glutamate transporter (VGLUT).

272 seeking while increasing the function of the glutamate transporter 1 (GLT-1) and system xC- (Sxc) in

273 g the tibial nerve (TN), and using Vesicular GLUtamate Transporter 1 (VGLUT1) and the 65 kDa isoform

274 ate transporter levels were higher and glial glutamate transporter 1 levels were lower in the DH of f

275 droxylase in periglomerular cells, vesicular glutamate transporter 1, a presynaptic protein, in mitra

276 N-->CeA CGRP projections coexpress vesicular glutamate transporter 2 (VGLUT2), providing evidence tha

277 glutamatergic neurons that express vesicular glutamate transporter 2 (VgluT2).

278 markers [neurofilament, NeuN, and vesicular glutamate transporter 2 (VGlut2)], and cultures exhibite

279 mate tone in RVH rats was not due to blunted glutamate transporter activity.

280 g debate on the contribution of the neuronal glutamate transporter EAAC1 to the onset of compulsive b

281 Riluzole is known to increase the glutamate transporter EAAT2's ability to scavenge excess

282 c vesicle machinery, including the vesicular glutamate transporter eat-4/VGLUT, induction of neuropep

283 ed to increased expression of the astrocytic glutamate transporter GLT-1 and to attenuated changes in

284 ate signaling dynamics, increased astrocytic glutamate transporter levels and alleviated multiple sig

285 ing in situ hybridization to label vesicular glutamate transporters (vglut1, vglut2.1, vglut3), gluta

286 mate receptors, GABA receptors (GABARs), and glutamate transporters that have been implicated in pain

287 smission due to their abundant expression of glutamate transporters.

288 n their MA preference/taking, to examine the glutamate underpinnings of MA abuse vulnerability.

289 , we examined whether PrP(c) participates in glutamate uptake and found that rPrP(c) decreased uptake

290 ake place in astrocyte systems that regulate glutamate uptake and release.

291 ar is whether PAR1 activation also regulates glutamate uptake in astrocytes and how this shapes excit

292 comprehensive model to elucidate the role of glutamate uptake in the dynamics of spreading depolariza

293 with AQP4: AQP4 internalization, attenuated glutamate uptake, intramyelinic edema, interleukin-6 rel

294 ile GLT-1 is responsible for the majority of glutamate uptake.

295 talyzes the two-step oxidation of proline to glutamate using separate proline dehydrogenase (PRODH) a

296 Decreased glutamate was also associated with reduced astrocytic gl

297 Glutamate, which is preferentially excluded from protein

298 pe was recapitulated by elevating endogenous glutamate within the NAC shell of mice and we reversed M

299 ons expressing the neurotransmitters GABA or glutamate within this circuit markedly reduced the capac

300 the flow of glucose carbons into lactate and glutamate without markedly increasing glucose-to-ribose