ライフサイエンスコーパス: GLT-1

1 GLT-1 (EAAT2) mediates the bulk of this activity in fore

2 GLT-1 (EAAT2; slc1a2) is the major glutamate transporter

3 GLT-1 and GLAST were significantly reduced in an experim

4 GLT-1 exhibited a laminar expression pattern from P10-15

5 GLT-1 expressed in neurons appears to be required to pro

6 GLT-1 is responsible for the majority of glutamate uptak

7 GLT-1 is the major glutamate transporter, and most GLT-1

8 GLT-1 loss drives aberrant repetitive locomotory reversa

9 GLT-1 promoter activity in the adult CNS is almost compl

10 GLT-1, the major glutamate transporter in the adult brai

11 GLT-1-like immunoreactivity localized to the inner capsu

12 the function of the glutamate transporter 1 (GLT-1) and system xC- (Sxc) in the nucleus accumbens cor

13 been attributed to glutamate transporter 1 (GLT-1) and xCT (a catalytic subunit of Sxc)/Sxc upregula

14 sporter (GLAST) and glutamate transporter 1 (GLT-1) are reduced.

15 ion and function of glutamate transporter 1 (GLT-1) in rat astrocytes, an effect that was mediated by

16 d increase in glial glutamate transporter 1 (GLT-1) mRNA expression and the phosphorylation of cAMP-r

17 lation of the glial glutamate transporter 1 (GLT-1) on astrocytes and to reduce peri-ischemic extrace

18 duced expression of glutamate transporter-1 (GLT-1) and occurs concurrent with tau inclusion patholog

19 sporter (GLAST) and glutamate transporter-1 (GLT-1) are the most abundant subtypes and are essential

20 Glutamate transporter-1 (GLT-1) is expressed predominantly in astroglial cells an

21 Glutamate transporter-1 (GLT-1) is the main glutamate transporter in the central

22 sporter (GLAST) and glutamate transporter-1 (GLT-1), which are essential for the maintenance of low e

23 cytic expression of glutamate transporter-1 (GLT-1), which would prevent excitotoxic-induced neuronal

24 a reduction in the glutamate transporter-1 (GLT-1).

25 luorescent protein [glutamate transporter-1 (GLT-1)] reporter transgenic mice.

26 maintained by glutamate transporter type-1 (GLT-1), which plays a vital role in clearing the release

27 The glutamate transporter-1 [GLT-1 (excitatory amino acid transporter 2)] subtype of

28 tified that after mutation to alanine (6L/6A GLT-1) prevented export of GLT-1 from the endoplasmic re

29 T-1; however, it did induce trafficking of a GLT-1 chimera containing the carboxyl-terminal domain of

30 on of both GluA1 and GluA2 without affecting GLT-1 expression while GLT-1 knockdown had no effect.

31 regulates GLAST expression without affecting GLT-1, as demonstrated in vitro by treatment with JAK in

32 o glutamate transporters, GLAST (EAAT-1) and GLT-1 (EAAT-2), were studied by immunohistochemistry and

33 cultures that express the GLAST (EAAT1) and GLT-1 (EAAT2) transporter subtypes.

34 GLAST and GLT-1 are localized primarily in astrocytes, whereas EAA

35 The glial glutamate transporters GLAST and GLT-1 are primarily responsible for the removal of gluta

36 Thus, GLAST and GLT-1 curtail the EPSC produced by a single stimulus onl

37 study compares the distribution of GLAST and GLT-1 expression in the circumventricular organs of the

38 kable subcellular heterogeneity of GLAST and GLT-1 expression in the developing hippocampus.

39 bral cortex also displayed reduced GLAST and GLT-1 expression.

40 subcellular expression profile of GLAST and GLT-1 in the developing postnatal mouse hippocampus by u

41 t the glial glutamate transporters GLAST and GLT-1 limit the activation of Purkinje cell AMPA recepto

42 udies have shown that Mn repressed GLAST and GLT-1 via activation of transcription factor Yin Yang 1

43 ressed the two glial transporters, GLAST and GLT-1, while none of the cultures expressed the neuronal

44 histochemistry to assess YY1, TH, GLAST, and GLT-1 levels.

45 rter EAAC1 in basal layer keratinocytes, and GLT-1, a related transporter, was expressed suprabasally

46 While upregulation of both xCT and GLT-1 are essential to the ability of ceftriaxone to att

47 the antibiotic ceftriaxone restores xCT and GLT-1 expression following cocaine self-administration a

48 ort important and distinct roles for xCT and GLT-1 in the actions of ceftriaxone and add to a body of

49 ses the probability that mitochondria appose GLT-1 particles within astrocyte processes, without chan

50 In conclusion, astrocytic GLT-1 performs critical functions required for normal we

51 However, the contribution of astrocytic GLT-1 to glutamate uptake into synaptosomes is less than

52 to neuron-dependent regulation of astrocytic GLT-1 transcription.

53 nist of GPR30, and GPR30 siRNA on astrocytic GLT-1 expression, as well as glutamate uptake in rat pri

54 The effect of TX on astrocytic GLT-1 was attenuated by the inhibition of PKA, the upstr

55 ght, and seizures suggesting that astrocytic GLT-1 is of major importance.

56 egion of DNA surrounding the GLT-1 gene (BAC GLT-1 eGFP mice) were used to assess the role of nuclear

57 Transduction of astrocytes from the BAC GLT-1 eGFP mice with dominant-negative inhibitors of NF-

58 everal recombinant chimeric proteins between GLT-1 and EAAC1 transporter subtypes were generated to i

59 allel fibres, knocking out GLAST or blocking GLT-1 in the absence of GLAST greatly prolonged and enha

60 Knocking out GLAST, or blocking GLT-1 in the absence of GLAST, prolonged the EPSC when m

61 lencing GPR30 reduced the expression of both GLT-1 and TGF-alpha and abrogated the G1-induced increas

62 at ceftriaxone restores the function of both GLT-1 and xCT (glutamate reuptake and export, respective

63 unocytochemical staining indicates that both GLT-1 and GLAST protein are expressed in the tanycyte po

64 uent Western blotting demonstrated that both GLT-1 and GLAST were present at the cell surface.

65 lf of those observed in cortical tissue, but GLT-1 protein was present at very low levels compared wi

66 l accumulation of glutamate by GLAST than by GLT-1 cannot be used to explain the high glutamate conce

67 We generated a conditional GLT-1 knock-out mouse to uncover cell-type-specific func

68 does not alter levels of ALDH1L1, connexins, GLT-1 or binding partners of DISC1 and SR, LIS1 or PICK1

69 Spinal cord GLT-1 promoter reporter, protein density, and physiology

70 In astrocyte cultures, GLT-1 expression parallels differentiation induced by cA

71 Tsc1 cKO mice exhibit decreased GLT-1 and GLAST protein expression.

72 , and disrupts glutamate reuptake (decreased GLT-1 and GLAST mRNA).

73 e (PMA) quickly and preferentially decreases GLT-1 localization on the process membrane, leading to d

74 idney (a tissue that expresses no detectable GLT-1).

75 we used an antisense strategy to knock down GLT-1 or xCT in the nucleus accumbens core and examined

76 from animal and human tissue: GLAST (EAAT1), GLT-1 (EAAT2), EAAC1 (EAAT3), EAAT4, and EAAT5.

77 high-affinity glutamate transporter 1 (EAAT2/GLT-1) in the nucleus accumbens (NAc).

78 The glutamate transporter gene, EAAT2/GLT-1, is induced by epidermal growth factor (EGF) and d

79 ination of this serine did not impair either GLT-1 ubiquitination or endocytosis in response to phorb

80 ons and astrocytes that endogenously express GLT-1 and C6 glioma cells transfected with GLT-1.

81 from human embryonic kidney cells expressing GLT-1 transporters.

82 nsport of 2 Na+ (rather than of 3 Na+ as for GLT-1).

83 port by GLAST was found to be driven, as for GLT-1, by the cotransport of 3 Na+ and 1 H+ and the coun

84 mal, control and MS white matter, except for GLT-1, which showed low-level expression around active M

85 A kinetic model for GLT-1 was developed to simulate the behavior of both com

86 le immunohistochemical staining patterns for GLT-1 were obtained with antibodies directed against bot

87 ntified, named EAAT1-5 in humans, and GLAST, GLT-1, EAAC1, EAAT4, and EAAT5 in rodents, respectively.

88 n (glutaminase), glutamate transport (GLAST, GLT-1 and EAAT-1), glutamate metabolism (glutamate dehyd

89 least in part, by reducing astrocytic GLAST/GLT-1.

90 y, attenuating Mn-induced reduction in GLAST/GLT-1 expression in murine substantia nigra (SN).

91 attenuated the Mn-induced decrease in GLAST/GLT-1 mRNA/protein levels in midbrain.

92 rders associated with dysregulation of GLAST/GLT-1.

93 of its 31 amino acid residues from the glial GLT-1 transporter was individually mutated to cysteine.

94 Effects on mRNA expression of glial (GLT-1, GLAST) and neuronal (EAAC1) glutamate transporter

95 evaluated the functional role of the glial (GLT-1) and neuronal (EAAC1) glutamate transporters in me

96 Using double-label immunofluorescence, GLT-1 was shown to colocalize with the mitochondrial mat

97 corporation of (32)P into immunoprecipitable GLT-1, mutation of serine 486 did not reduce this signal

98 odeling, to modulate CRS-mediated changes in GLT-1 and GLT-1b expression.

99 treatment elicits a significant decrease in GLT-1 activity that is prevented by preexposure to eithe

100 endocytosis, and the concomitant decrease in GLT-1 activity triggered by PKC activation.

101 PKC with phorbol ester caused a decrease in GLT-1 cell surface expression.

102 PPF restored the cocaine-induced decrease in GLT-1 in the accumbens core; then, using an antisense st

103 to attenuate manganese-induced impairment in GLT-1 protein expression and glutamate uptake.

104 nerve transection resulted in an increase in GLT-1 compared with the control eye (P = 0.01, paired t-

105 ceptor suppressed the G1-induced increase in GLT-1 expression.

106 pha and abrogated the G1-induced increase in GLT-1 expression.

107 Moreover, the G1-induced increase in GLT-1 protein expression was abolished by a protein kina

108 The magnitude of the reduction in GLT-1 correlated significantly with mean IOP in the glau

109 emistry also confirmed a marked reduction in GLT-1 immunoreactivity in the cortex and hippocampus.

110 Reductions in GLT-1 and GLAST may increase the potential for glutamate

111 Reductions in GLT-1 expression were also observed in corticobasal dege

112 protein approximately 2-fold, and increased GLT-1 protein >/=8-20-fold.

113 ed expression of eGFP or GLT-1 and increased GLT-1-mediated transport activity.

114 CRS increased GLT-1 mRNA expression in the dentate gyrus and CA3 regio

115 G1 increased GLT-1 protein and mRNA levels, subject to regulation by

116 ramatic change in cell morphology, increased GLT-1 and GLAST mRNA levels approximately 5-fold, increa

117 CRS more selectively increased GLT-1 protein levels in the subregion where dendritic re

118 monstrate that activation of GPR30 increases GLT-1 expression via multiple pathways, suggesting that

119 ds 475-517) that is required for PKC-induced GLT-1 redistribution.

120 egative form of dynamin prevents PMA-induced GLT-1 internalization and cluster formation.

121 r mutant completely abolished the TX-induced GLT-1 promoter activity.

122 Following focal ischemia, GLT-1 mRNA expression was decreased significantly in the

123 At the cellular level, GLT-1 immunoreactivity did not entirely cover astrocyte

124 ate the mTOR cascade, acquire CD44, and lose GLT-1.

125 We have found that TNF-alpha can mediate GLT-1 downregulation.

126 is the major glutamate transporter, and most GLT-1 is expressed in astrocytes.

127 Using wild-type and mutant GLT-1 promoter reporter constructs, we found that NF-kap

128 Intra-NAc GLT-1 knockdown also prevented ceftriaxone from attenuat

129 cient mice infected with NSV exhibit neither GLT-1 downregulation nor neuronal death of brainstem and

130 We generated a conditional neuronal GLT-1 KO using synapsin 1-Cre (synGLT-1 KO) to elucidate

131 n expected, and the contribution of neuronal GLT-1 to synaptosomal glutamate uptake is greater than e

132 ion by synaptic mitochondria in the neuronal GLT-1 KO.

133 tamate escape into the surrounding neuropil, GLT-1 preserves the spatial specificity of synaptic sign

134 Finally, GLAST, but not GLT-1, is expressed by specific layers of the meninges,

135 hysiological conditions approximately 35% of GLT-1 transporters function as buffers, releasing glutam

136 not functional unless amino acids 475-517 of GLT-1 were also present.

137 Here, we identified serine 520 of GLT-1 as the primary target for PKC-dependent phosphoryl

138 tes resulted in loss of approximately 80% of GLT-1 protein and of glutamate uptake activity that coul

139 eras containing the first 446 amino acids of GLT-1 were not functional unless amino acids 475-517 of

140 ther, these studies suggest that blockade of GLT-1 in the CEA is sufficient to induce both anhedonia

141 ly, we demonstrated that central blockade of GLT-1 induces anhedonia and c-Fos expression in the PFC.

142 The clustering of GLT-1 at astrocyte endfeet indicates that it might serve

143 l and juvenile animals, discrete clusters of GLT-1 were also detected at perivascular endfeet.

144 a containing the carboxyl-terminal domain of GLT-1; however, it did induce trafficking of a GLT-1 chi

145 nt and to estimate the capture efficiency of GLT-1.

146 Elimination of GLT-1 from astrocytes resulted in loss of approximately

147 n reported that the regulated endocytosis of GLT-1 depends on its ubiquitination triggered by protein

148 to alanine (6L/6A GLT-1) prevented export of GLT-1 from the endoplasmic reticulum (ER) to the plasma

149 used antisense to decrease the expression of GLT-1 and xCT (a catalytic subunit of Sxc) to determine

150 Expression of GLT-1 correlates with astrocyte maturation in vivo and i

151 le secreted by neurons induces expression of GLT-1 in astrocytes.

152 tigate the significance of the expression of GLT-1 in neurons.

153 EGF also increased expression of GLT-1 in spinal cord organotypic cultures.

154 ed upon its ability to restore expression of GLT-1 in the nucleus accumbens.

155 rain early in development when expression of GLT-1 is low.

156 Astrocytic expression of GLT-1 is regulated during development, by neuronal activ

157 g growth factor-alpha] induced expression of GLT-1 protein in cultured astrocytes.

158 gh neurons activate astrocytic expression of GLT-1, the mechanisms involved have not been identified.

159 ut converging pathways mediate expression of GLT-1.

160 truct was sufficient to induce expression of GLT-1.

161 Nedd4-2 phosphorylation and the formation of GLT-1.Nedd4-2 complexes, whereas siRNA knockdown of Nedd

162 The function of GLT-1 in axon terminals remains unknown.

163 KO) to elucidate the metabolic functions of GLT-1 expressed in neurons, here focusing on the cerebra

164 s membrane, leading to de novo generation of GLT-1 clusters along the process shaft.

165 PCR and immunoprecipitation of GLT-1 revealed that ceftriaxone does not upregulate GLT-

166 neuron-conditioned medium, the induction of GLT-1 by neuron-conditioned medium was completely abolis

167 The induction of GLT-1 in both EGF- and dibutyryl-cAMP-treated astrocytes

168 Induction of GLT-1 protein was accompanied by an increase in mRNA and

169 nal cultures contribute to this induction of GLT-1, but little is known about the signaling pathways

170 Selective inhibition of GLT-1 [for glutamate transporter; EAAT2 (for excitatory

171 mmunocytochemistry demonstrated knockdown of GLT-1 in the cerebral cortex in the synGLT-1 KO mice.

172 lts support the idea that enhanced levels of GLT-1 in transgenic mice are responsible for reducing H/

173 Expression analysis revealed a loss of GLT-1 as well as qualitative changes in GLAST (glutamate

174 st that greater oxidative stress and loss of GLT-1 function selectively in CA1 astrocytes is central

175 ollowing selective blockade of a majority of GLT-1, the brain's most abundant glutamate transporter.

176 is additional mutation rescued maturation of GLT-1 essentially excludes the possibility that the 6L/6

177 atment, suggesting that the morphogenesis of GLT-1 clusters is highly dependent on the actin network.

178 mmunoreactive inclusions and preservation of GLT-1 transporter expression.

179 processes, without changing the proximity of GLT-1 particles to VGLUT1.

180 abolish the PKC-dependent redistribution of GLT-1.

181 d for the subtype-specific redistribution of GLT-1.

182 oblastoma patients also display reduction of GLT-1 and mislocalization of GLAST.

183 sms that mediate TX-induced up-regulation of GLT-1 (EAAT2 in humans), we investigated its effect on G

184 tance of these clusters in the regulation of GLT-1 activity in the presence or absence of neurons.

185 Down regulation of GLT-1 in these brain areas may impair normal clearance o

186 e differential and subregional regulation of GLT-1 isoforms in neuronal and glial compartments in the

187 endent ubiquitination and down-regulation of GLT-1.

188 t in cellular localization and regulation of GLT-1.

189 The functional role of GLT-1 in dorsal wall tanycytes remains to be explored.

190 cover cell-type-specific functional roles of GLT-1.

191 Overall, these studies of GLT-1 and GLAST promoter activity, protein expression, a

192 les mum(-)(3)), 100 times lower than that of GLT-1.

193 Upregulation of GLT-1 expression in astrocytes with ceftriaxone protecte

194 The upregulation of GLT-1 induced by transplanted NPCs was found to rely on

195 Upregulation of GLT-1 was completed only at postnatal days (P) P20-25 an

196 we proposed that GPR30 mediates E2 action on GLT-1 expression.

197 T2 in humans), we investigated its effect on GLT-1 at the transcriptional level.

198 studies demonstrate a novel effect of PKC on GLT-1 activity and define a unique carboxyl-terminal dom

199 In addition, the effect of TX on GLT-1 promoter activity was abolished by the inhibition

200 a complete abrogation of the effect of TX on GLT-1 promoter activity.

201 Chimeras consisting of domains from EAAC1 or GLT-1 were used to investigate structural motifs involve

202 appaB subunits induced expression of eGFP or GLT-1 and increased GLT-1-mediated transport activity.

203 ng the glial glutamate transporters GLAST or GLT-1, the ischaemia-evoked AD current was indistinguish

204 hexokinase-1 overlapped with mitochondria or GLT-1, strongly suggesting that GLT-1, mitochondria, and

205 Na(+) and glutamate that resembles original GLT-1/EAAT2 in all tested functional aspects.

206 ng behavior with ceftriaxone (CEF), a potent GLT-1 upregulator.

207 the distal end of C6 glioma cell processes, GLT-1 clusters undergo rapid morphological changes in bo

208 te the ability of endogenous and recombinant GLT-1 to form clusters in astrocytic processes and chara

209 Reduced GLT-1 expression was associated with a progressive decre

210 function, reactive astrocytosis, and reduced GLT-1 transporter expression in WT animals.

211 analysis demonstrated significantly reduced GLT-1 in glaucomatous eyes compared with control eyes at

212 F during the first week after stroke reduced GLT-1 upregulation as well as long-term behavioral recov

213 synaptically released glutamate by reducing GLT-1 surface expression in mouse astrocytes and that th

214 icated in astrocyte differentiation regulate GLT-1 expression.

215 er, our findings establish that TX regulates GLT-1 via the CREB and NF-kappaB pathways.

216 ingly, a high percentage of variably spliced GLT-1 mRNAs lacking parts of this domain are found in th

217 Furthermore, we have identified strong GLT-1 mRNA labeling in a population of tanycytes situate

218 In the present study, GLT-1 immunoaffinity isolates were prepared from rat cor

219 DAR 1]) and a glutamate transporter subtype [GLT-1] within the leech CNS using mono- and polyclonal a

220 ing cocaine alone, such as increased surface GLT-1 expression and a lack of increase in glutamate eff

221 ced hippocampal slices, fluorescently tagged GLT-1 puncta overlapped with fluorescently tagged mitoch

222 ther adult brain areas at a lower level than GLT-1, and is present throughout the brain early in deve

223 s expressed GLAST in greater proportion than GLT-1.

224 anxiety and depression, we hypothesized that GLT-1 blockade in the CEA would induce symptoms of anhed

225 PFC in regulating mood, we hypothesized that GLT-1 blockade in the PFC alone would be sufficient to i

226 These results indicate that GLT-1 endocytosis is independent of its phosphorylation

227 Together, these data indicate that GLT-1 trafficking and cluster formation in glial cell pr

228 th previous results, these studies show that GLT-1 cocompartmentalizes with Na(+)/K(+) ATPase, glycol

229 These studies suggest that GLT-1 and GLAST protein are regulated independently in a

230 These data suggest that GLT-1 expressed in axon terminals may be important in ma

231 domain are found in the CNS, suggesting that GLT-1 expression may be regulated during assembly.

232 ochondria or GLT-1, strongly suggesting that GLT-1, mitochondria, and the first step in glycolysis ar

233 This study suggests that GLT-1, but not EAAC1, knockdown exacerbates the neuronal

234 when GLT-1 was deleted in neurons, both the GLT-1 protein and glutamate uptake activity that could b

235 Furthermore, the GLT-1-expressing tanycytes represent a population of tan

236 We microinjected the GLT-1 inhibitor, dihydrokainic acid (DHK), into the CEA

237 We microinjected the GLT-1 inhibitor, dihydrokainic acid (DHK), into the PFC

238 racterized two retinal EAATs from mouse, the GLT-1/EAAT2 splice variant GLT-1c, and EAAT5.

239 Inactivation of the GLT-1 gene was achieved in either neurons or astrocytes

240 appaB) in neuron-dependent activation of the GLT-1 promoter.

241 d p50 to the NF-kappaB binding domain of the GLT-1 promoter.

242 st both the N terminal and C terminal of the GLT-1 protein.

243 cell surface expression and activity of the GLT-1 subtype of glutamate transporter were examined in

244 ibute to posttranslational processing of the GLT-1 subtype of glutamate transporter.

245 analyses revealed a robust expression of the GLT-1 transporter protein in the SON, which was diminish

246 , -583/-282/-251) or CRE (-308) sites on the GLT-1 promoter led to significant repression of the prom

247 g a very large region of DNA surrounding the GLT-1 gene (BAC GLT-1 eGFP mice) were used to assess the

248 d uptake to dihydrokainate suggests that the GLT-1 (glutamate transporter-1) subtype primarily mediat

249 ing protein (CREB) and recruited CREB to the GLT-1 promoter consensus site.

250 -kappaB p50 and NF-kappaB p65 binding to the GLT-1 promoter.

251 ohistochemistry using specific antibodies to GLT-1 and GLAST.

252 otential signaling pathways linking GPR30 to GLT-1.

253 sion of the astroglial glutamate transporter GLT-1 (N-acetylcysteine and ceftriaxone) can decrease me

254 mber 2), also known as glutamate transporter GLT-1 and excitatory amino acid transporter EAAT2.

255 face expression of the glutamate transporter GLT-1 and glutamate efflux in the nucleus accumbens (NA)

256 regulation of the glia glutamate transporter GLT-1 and the recently identified GLT isoform, GLT-1b, i

257 sion of the astrocytic glutamate transporter GLT-1 and to attenuated changes in dendrite morphology,

258 vels of the astrocytic glutamate transporter GLT-1 but normal expression levels of another glial glut

259 utamate uptake via the glutamate transporter GLT-1 in rat glial cells.

260 al inhibition of glial glutamate transporter GLT-1 induced the similar Kv2.1 dephosphorylation, where

261 The glutamate transporter GLT-1 is highly expressed in astrocytes but also in neur

262 The glial glutamate transporter GLT-1 may be the predominant Na(+)-dependent glutamate t

263 or GFAP, S100beta, and glutamate transporter GLT-1 within a few hours of reperfusion, but without ast

264 inhibitor of the glial glutamate transporter GLT-1, did not block the increase in glutamate uptake.

265 sense strategy against glutamate transporter GLT-1, we found that restored transporter expression was

266 ng the conserved glial glutamate transporter GLT-1.

267 Loss of one glutamate transporter (GLT-1) from VTA astrocytes selectively blocks these avoi

268 ade of the astrocytic glutamate transporter (GLT-1) induces anhedonia and c-Fos expression in areas t

269 m the synapse via the glutamate transporter (GLT-1).

270 airment of astrocytic glutamate transporter (GLT-1; EAAT2) function is associated with multiple neuro

271 specific inhibitor of the glial transporter, GLT-1.

272 NF and IGF-1, and the glutamate transporter, GLT-1 after ischemic brain damage.

273 lization of the glial glutamate transporter, GLT-1, after transfection into C6 glioma cells.

274 of the most abundant glutamate transporter, GLT-1, predicts that a very low glutamate concentration,

275 l levels of the glial glutamate transporter, GLT-1, were higher in brains of transgenic as compared t

276 function of the major glutamate transporter, GLT-1.

277 ion of the astrocytic glutamate transporter, GLT-1.

278 ell as the astrocytic glutamate transporter, GLT-1.

279 n expression of glutamate (Glu) transporters GLT-1 and GLAST and attenuated Glu uptake (p < 0.01).

280 A and protein for the glutamate transporters GLT-1 and GLAST in unique tanycyte populations of the th

281 d that the astroglial glutamate transporters GLT-1 and GLAST, but not the neuronal transporter EAAC1,

282 ion of the astroglial glutamate transporters GLT-1 and GLAST.

283 blocking astroglial glutamate transporters (GLT-1) had no effect on reinstated sucrose seeking.

284 regulates astrocytic glutamate transporters, GLT-1 and GLAST, and dopaminergic function, including ty

285 ective dominant-negative effect on wild-type GLT-1 expression and formed coimmunoprecipitable complex

286 Unlike GLT-1 expression, which increases in parallel with circu

287 evealed that ceftriaxone does not upregulate GLT-1 and xCT through a transcriptional mechanism, and t

288 pse, nor is it clear whether the upregulated GLT-1 is functionally important for suppressing of drug

289 enuating reinstatement and from upregulating GLT-1 and resulted in increased surface expression of AM

290 In contrast, when GLT-1 was deleted in neurons, both the GLT-1 protein and

291 strema, GLAST is strongly expressed, whereas GLT-1 is faintly expressed or absent.

292 by pituicytes in the posterior lobe, whereas GLT-1 is expressed only by the astrocyte-like cells in t

293 rocytic cells near the pineal stalk, whereas GLT-1 is expressed by pinealocytes throughout the gland.

294 uA2 without affecting GLT-1 expression while GLT-1 knockdown had no effect.

295 ic extracellular glutamate in the NAc, while GLT-1 is responsible for the majority of glutamate uptak

296 ins have been identified that associate with GLT-1.

297 and increased mortality rate, compared with GLT-1 sense/random ODN-infused controls.

298 d formed coimmunoprecipitable complexes with GLT-1.

299 Transient MCAO in rats infused with GLT-1 antisense oligodeoxynucleotides (ODNs) led to incr

300 s GLT-1 and C6 glioma cells transfected with GLT-1.