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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 is responsible for the majority of glutamate uptak
6                                              GLT-1 promoter activity in the adult CNS is almost compl
7                                              GLT-1, GLAST, and EAAC1 are high-affinity, Na(+)-depende
8                                              GLT-1, the major glutamate transporter in the adult brai
9                                              GLT-1-like immunoreactivity localized to the inner capsu
10 the function of the glutamate transporter 1 (GLT-1) and system xC- (Sxc) in the nucleus accumbens cor
11  been attributed to glutamate transporter 1 (GLT-1) and xCT (a catalytic subunit of Sxc)/Sxc upregula
12 sporter (GLAST) and glutamate transporter 1 (GLT-1) are reduced.
13 ion and function of glutamate transporter 1 (GLT-1) in rat astrocytes, an effect that was mediated by
14 d increase in glial glutamate transporter 1 (GLT-1) mRNA expression and the phosphorylation of cAMP-r
15 lation of the glial glutamate transporter 1 (GLT-1) on astrocytes and to reduce peri-ischemic extrace
16 duced expression of glutamate transporter-1 (GLT-1) and occurs concurrent with tau inclusion patholog
17 sporter (GLAST) and glutamate transporter-1 (GLT-1) are the most abundant subtypes and are essential
18                     Glutamate transporter-1 (GLT-1) is expressed predominantly in astroglial cells an
19                     Glutamate transporter-1 (GLT-1) is the main glutamate transporter in the central
20 sporter (GLAST) and glutamate transporter-1 (GLT-1), which are essential for the maintenance of low e
21 cytic expression of glutamate transporter-1 (GLT-1), which would prevent excitotoxic-induced neuronal
22  a reduction in the glutamate transporter-1 (GLT-1).
23 luorescent protein [glutamate transporter-1 (GLT-1)] reporter transgenic mice.
24                 The glutamate transporter-1 [GLT-1 (excitatory amino acid transporter 2)] subtype of
25 tified that after mutation to alanine (6L/6A GLT-1) prevented export of GLT-1 from the endoplasmic re
26 T-1; however, it did induce trafficking of a GLT-1 chimera containing the carboxyl-terminal domain of
27 on of both GluA1 and GluA2 without affecting GLT-1 expression while GLT-1 knockdown had no effect.
28 regulates GLAST expression without affecting GLT-1, as demonstrated in vitro by treatment with JAK in
29                                     Although GLT-1 is sensitive to inhibition by dihydrokainate in he
30 o glutamate transporters, GLAST (EAAT-1) and GLT-1 (EAAT-2), were studied by immunohistochemistry and
31 ported lower anion permeability of EAAC1 and GLT-1 compared with that of GLAST.
32  cultures that express the GLAST (EAAT1) and GLT-1 (EAAT2) transporter subtypes.
33                                    GLAST and GLT-1 are localized primarily in astrocytes, whereas EAA
34 have been identified in rat brain; GLAST and GLT-1 are primarily astrocytic, whereas EAAC1 and EAAT4
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 ing the expression and function of GLAST and GLT-1 in their native cell type.
42 t the glial glutamate transporters GLAST and GLT-1 limit the activation of Purkinje cell AMPA recepto
43 nsport in cultures expressing both GLAST and GLT-1, suggesting a weaker effect at GLT-1 than at GLAST
44 ressed the two glial transporters, GLAST and GLT-1, while none of the cultures expressed the neuronal
45 - to 4-times increase in levels of GLAST and GLT-1-mRNA expression both before and after scratch inju
46 rter EAAC1 in basal layer keratinocytes, and GLT-1, a related transporter, was expressed suprabasally
47           While upregulation of both xCT and GLT-1 are essential to the ability of ceftriaxone to att
48  the antibiotic ceftriaxone restores xCT and GLT-1 expression following cocaine self-administration a
49 ort important and distinct roles for xCT and GLT-1 in the actions of ceftriaxone and add to a body of
50 ses the probability that mitochondria appose GLT-1 particles within astrocyte processes, without chan
51                    In conclusion, astrocytic GLT-1 performs critical functions required for normal we
52      However, the contribution of astrocytic GLT-1 to glutamate uptake into synaptosomes is less than
53 to neuron-dependent regulation of astrocytic GLT-1 transcription.
54 nist of GPR30, and GPR30 siRNA on astrocytic GLT-1 expression, as well as glutamate uptake in rat pri
55               The effect of TX on astrocytic GLT-1 was attenuated by the inhibition of PKA, the upstr
56 ght, and seizures suggesting that astrocytic GLT-1 is of major importance.
57 AST and GLT-1, suggesting a weaker effect at GLT-1 than at GLAST.
58 egion of DNA surrounding the GLT-1 gene (BAC GLT-1 eGFP mice) were used to assess the role of nuclear
59      Transduction of astrocytes from the BAC GLT-1 eGFP mice with dominant-negative inhibitors of NF-
60 everal recombinant chimeric proteins between GLT-1 and EAAC1 transporter subtypes were generated to i
61 allel fibres, knocking out GLAST or blocking GLT-1 in the absence of GLAST greatly prolonged and enha
62              Knocking out GLAST, or blocking GLT-1 in the absence of GLAST, prolonged the EPSC when m
63 lencing GPR30 reduced the expression of both GLT-1 and TGF-alpha and abrogated the G1-induced increas
64 at ceftriaxone restores the function of both GLT-1 and xCT (glutamate reuptake and export, respective
65 unocytochemical staining indicates that both GLT-1 and GLAST protein are expressed in the tanycyte po
66 uent Western blotting demonstrated that both GLT-1 and GLAST were present at the cell surface.
67 lf of those observed in cortical tissue, but GLT-1 protein was present at very low levels compared wi
68 l accumulation of glutamate by GLAST than by GLT-1 cannot be used to explain the high glutamate conce
69 ures of neurons and astrocytes did not cause GLT-1 protein to increase further.
70 tate or glutamate killed the neurons, caused GLT-1 protein to decrease, and caused GLAST protein to i
71                   We generated a conditional GLT-1 knock-out mouse to uncover cell-type-specific func
72 does not alter levels of ALDH1L1, connexins, GLT-1 or binding partners of DISC1 and SR, LIS1 or PICK1
73                                  Spinal cord GLT-1 promoter reporter, protein density, and physiology
74                       In astrocyte cultures, GLT-1 expression parallels differentiation induced by cA
75              Tsc1 cKO mice exhibit decreased GLT-1 and GLAST protein expression.
76 , and disrupts glutamate reuptake (decreased GLT-1 and GLAST mRNA).
77 e (PMA) quickly and preferentially decreases GLT-1 localization on the process membrane, leading to d
78 idney (a tissue that expresses no detectable GLT-1).
79  we used an antisense strategy to knock down GLT-1 or xCT in the nucleus accumbens core and examined
80 from animal and human tissue: GLAST (EAAT1), GLT-1 (EAAT2), EAAC1 (EAAT3), EAAT4, and EAAT5.
81 high-affinity glutamate transporter 1 (EAAT2/GLT-1) in the nucleus accumbens (NAc).
82        The glutamate transporter gene, EAAT2/GLT-1, is induced by epidermal growth factor (EGF) and d
83 ination of this serine did not impair either GLT-1 ubiquitination or endocytosis in response to phorb
84 ons and astrocytes that endogenously express GLT-1 and C6 glioma cells transfected with GLT-1.
85 bserved in astrocyte cultures that expressed GLT-1.
86 from human embryonic kidney cells expressing GLT-1 transporters.
87 nsport of 2 Na+ (rather than of 3 Na+ as for GLT-1).
88 port by GLAST was found to be driven, as for GLT-1, by the cotransport of 3 Na+ and 1 H+ and the coun
89 mal, control and MS white matter, except for GLT-1, which showed low-level expression around active M
90                          A kinetic model for GLT-1 was developed to simulate the behavior of both com
91 le immunohistochemical staining patterns for GLT-1 were obtained with antibodies directed against bot
92 and that under certain conditions functional GLT-1 protein can be expressed in brain neurons.
93 ntified, named EAAT1-5 in humans, and GLAST, GLT-1, EAAC1, EAAT4, and EAAT5 in rodents, respectively.
94 n (glutaminase), glutamate transport (GLAST, GLT-1 and EAAT-1), glutamate metabolism (glutamate dehyd
95  electrogenic glutamate transporters, GLAST, GLT-1, and EAAC-1, was quantitated by the reverse transc
96 of its 31 amino acid residues from the glial GLT-1 transporter was individually mutated to cysteine.
97         Effects on mRNA expression of glial (GLT-1, GLAST) and neuronal (EAAC1) glutamate transporter
98  evaluated the functional role of the glial (GLT-1) and neuronal (EAAC1) glutamate transporters in me
99       Using double-label immunofluorescence, GLT-1 was shown to colocalize with the mitochondrial mat
100 corporation of (32)P into immunoprecipitable GLT-1, mutation of serine 486 did not reduce this signal
101 odeling, to modulate CRS-mediated changes in GLT-1 and GLT-1b expression.
102           The study suggests that changes in GLT-1 levels that occur with pathology or experimental m
103  treatment elicits a significant decrease in GLT-1 activity that is prevented by preexposure to eithe
104 endocytosis, and the concomitant decrease in GLT-1 activity triggered by PKC activation.
105  PKC with phorbol ester caused a decrease in GLT-1 cell surface expression.
106 PPF restored the cocaine-induced decrease in GLT-1 in the accumbens core; then, using an antisense st
107 to attenuate manganese-induced impairment in GLT-1 protein expression and glutamate uptake.
108 nerve transection resulted in an increase in GLT-1 compared with the control eye (P = 0.01, paired t-
109 ceptor suppressed the G1-induced increase in GLT-1 expression.
110 pha and abrogated the G1-induced increase in GLT-1 expression.
111         Moreover, the G1-induced increase in GLT-1 protein expression was abolished by a protein kina
112            The magnitude of the reduction in GLT-1 correlated significantly with mean IOP in the glau
113 emistry also confirmed a marked reduction in GLT-1 immunoreactivity in the cortex and hippocampus.
114                                Reductions in GLT-1 and GLAST may increase the potential for glutamate
115                                Reductions in GLT-1 expression were also observed in corticobasal dege
116  protein approximately 2-fold, and increased GLT-1 protein >/=8-20-fold.
117 ed expression of eGFP or GLT-1 and increased GLT-1-mediated transport activity.
118                                CRS increased GLT-1 mRNA expression in the dentate gyrus and CA3 regio
119                                 G1 increased GLT-1 protein and mRNA levels, subject to regulation by
120 ytes with a semipermeable membrane increased GLT-1 protein, indicating that the effect of neurons was
121 ramatic change in cell morphology, increased GLT-1 and GLAST mRNA levels approximately 5-fold, increa
122               CRS more selectively increased GLT-1 protein levels in the subregion where dendritic re
123 monstrate that activation of GPR30 increases GLT-1 expression via multiple pathways, suggesting that
124 ds 475-517) that is required for PKC-induced GLT-1 redistribution.
125 egative form of dynamin prevents PMA-induced GLT-1 internalization and cluster formation.
126 r mutant completely abolished the TX-induced GLT-1 promoter activity.
127                    Following focal ischemia, GLT-1 mRNA expression was decreased significantly in the
128                       At the cellular level, GLT-1 immunoreactivity did not entirely cover astrocyte
129 ate the mTOR cascade, acquire CD44, and lose GLT-1.
130     We have found that TNF-alpha can mediate GLT-1 downregulation.
131                   Using wild-type and mutant GLT-1 promoter reporter constructs, we found that NF-kap
132                                    Intra-NAc GLT-1 knockdown also prevented ceftriaxone from attenuat
133 cient mice infected with NSV exhibit neither GLT-1 downregulation nor neuronal death of brainstem and
134 n expected, and the contribution of neuronal GLT-1 to synaptosomal glutamate uptake is greater than e
135  of dihydrokainate, suggesting that neuronal GLT-1 is capable of participating in the clearance of sy
136 e-labeling experiments suggest that neuronal GLT-1 protein is primarily localized to the dendrites of
137 tamate escape into the surrounding neuropil, GLT-1 preserves the spatial specificity of synaptic sign
138                      Finally, GLAST, but not GLT-1, is expressed by specific layers of the meninges,
139 hysiological conditions approximately 35% of GLT-1 transporters function as buffers, releasing glutam
140 not functional unless amino acids 475-517 of GLT-1 were also present.
141            Here, we identified serine 520 of GLT-1 as the primary target for PKC-dependent phosphoryl
142 tes resulted in loss of approximately 80% of GLT-1 protein and of glutamate uptake activity that coul
143 eras containing the first 446 amino acids of GLT-1 were not functional unless amino acids 475-517 of
144 ther, these studies suggest that blockade of GLT-1 in the CEA is sufficient to induce both anhedonia
145 ly, we demonstrated that central blockade of GLT-1 induces anhedonia and c-Fos expression in the PFC.
146 t the initially proposed characterization of GLT-1 as a purely glial transporter is too simplistic an
147                            The clustering of GLT-1 at astrocyte endfeet indicates that it might serve
148 l and juvenile animals, discrete clusters of GLT-1 were also detected at perivascular endfeet.
149 a containing the carboxyl-terminal domain of GLT-1; however, it did induce trafficking of a GLT-1 chi
150 nt and to estimate the capture efficiency of GLT-1.
151                               Elimination of GLT-1 from astrocytes resulted in loss of approximately
152 n reported that the regulated endocytosis of GLT-1 depends on its ubiquitination triggered by protein
153 to alanine (6L/6A GLT-1) prevented export of GLT-1 from the endoplasmic reticulum (ER) to the plasma
154 used antisense to decrease the expression of GLT-1 and xCT (a catalytic subunit of Sxc) to determine
155                                Expression of GLT-1 correlates with astrocyte maturation in vivo and i
156                      Transient expression of GLT-1 immunoreactivity along axonal pathways was observe
157 le secreted by neurons induces expression of GLT-1 in astrocytes.
158             EGF also increased expression of GLT-1 in spinal cord organotypic cultures.
159 ed upon its ability to restore expression of GLT-1 in the nucleus accumbens.
160 rain early in development when expression of GLT-1 is low.
161                     Astrocytic expression of GLT-1 is regulated during development, by neuronal activ
162 g growth factor-alpha] induced expression of GLT-1 protein in cultured astrocytes.
163 the effect of neurons on glial expression of GLT-1 protein, but the addition of dbcAMP to mixed cultu
164 gh neurons activate astrocytic expression of GLT-1, the mechanisms involved have not been identified.
165 ytes with neurons also induced expression of GLT-1, which colocalized with the glial specific marker,
166 ut converging pathways mediate expression of GLT-1.
167 truct was sufficient to induce expression of GLT-1.
168 Nedd4-2 phosphorylation and the formation of GLT-1.Nedd4-2 complexes, whereas siRNA knockdown of Nedd
169 s membrane, leading to de novo generation of GLT-1 clusters along the process shaft.
170               PCR and immunoprecipitation of GLT-1 revealed that ceftriaxone does not upregulate GLT-
171  neuron-conditioned medium, the induction of GLT-1 by neuron-conditioned medium was completely abolis
172                             The induction of GLT-1 in both EGF- and dibutyryl-cAMP-treated astrocytes
173                                 Induction of GLT-1 protein was accompanied by an increase in mRNA and
174 nal cultures contribute to this induction of GLT-1, but little is known about the signaling pathways
175                      Selective inhibition of GLT-1 [for glutamate transporter; EAAT2 (for excitatory
176 lts support the idea that enhanced levels of GLT-1 in transgenic mice are responsible for reducing H/
177 in contrast to the exclusive localization of GLT-1 to astrocytes in the adult CNS.
178       Expression analysis revealed a loss of GLT-1 as well as qualitative changes in GLAST (glutamate
179 st that greater oxidative stress and loss of GLT-1 function selectively in CA1 astrocytes is central
180 is additional mutation rescued maturation of GLT-1 essentially excludes the possibility that the 6L/6
181 atment, suggesting that the morphogenesis of GLT-1 clusters is highly dependent on the actin network.
182 mmunoreactive inclusions and preservation of GLT-1 transporter expression.
183 processes, without changing the proximity of GLT-1 particles to VGLUT1.
184  abolish the PKC-dependent redistribution of GLT-1.
185 d for the subtype-specific redistribution of GLT-1.
186 oblastoma patients also display reduction of GLT-1 and mislocalization of GLAST.
187 sms that mediate TX-induced up-regulation of GLT-1 (EAAT2 in humans), we investigated its effect on G
188 tance of these clusters in the regulation of GLT-1 activity in the presence or absence of neurons.
189                           Down regulation of GLT-1 in these brain areas may impair normal clearance o
190 e differential and subregional regulation of GLT-1 isoforms in neuronal and glial compartments in the
191 t in cellular localization and regulation of GLT-1.
192 endent ubiquitination and down-regulation of GLT-1.
193                       The functional role of GLT-1 in dorsal wall tanycytes remains to be explored.
194 cover cell-type-specific functional roles of GLT-1.
195                    Overall, these studies of GLT-1 and GLAST promoter activity, protein expression, a
196 les mum(-)(3)), 100 times lower than that of GLT-1.
197                              Upregulation of GLT-1 expression in astrocytes with ceftriaxone protecte
198                          The upregulation of GLT-1 induced by transplanted NPCs was found to rely on
199                              Upregulation of GLT-1 was completed only at postnatal days (P) P20-25 an
200 we proposed that GPR30 mediates E2 action on GLT-1 expression.
201 T2 in humans), we investigated its effect on GLT-1 at the transcriptional level.
202 studies demonstrate a novel effect of PKC on GLT-1 activity and define a unique carboxyl-terminal dom
203             In addition, the effect of TX on GLT-1 promoter activity was abolished by the inhibition
204 a complete abrogation of the effect of TX on GLT-1 promoter activity.
205 Chimeras consisting of domains from EAAC1 or GLT-1 were used to investigate structural motifs involve
206 appaB subunits induced expression of eGFP or GLT-1 and increased GLT-1-mediated transport activity.
207 ng the glial glutamate transporters GLAST or GLT-1, the ischaemia-evoked AD current was indistinguish
208 hexokinase-1 overlapped with mitochondria or GLT-1, strongly suggesting that GLT-1, mitochondria, and
209  Na(+) and glutamate that resembles original GLT-1/EAAT2 in all tested functional aspects.
210  the distal end of C6 glioma cell processes, GLT-1 clusters undergo rapid morphological changes in bo
211 te the ability of endogenous and recombinant GLT-1 to form clusters in astrocytic processes and chara
212                                      Reduced GLT-1 expression was associated with a progressive decre
213 function, reactive astrocytosis, and reduced GLT-1 transporter expression in WT animals.
214  analysis demonstrated significantly reduced GLT-1 in glaucomatous eyes compared with control eyes at
215 F during the first week after stroke reduced GLT-1 upregulation as well as long-term behavioral recov
216  synaptically released glutamate by reducing GLT-1 surface expression in mouse astrocytes and that th
217  of PKA but that neurons and dbcAMP regulate GLT-1 protein through convergent pathways.
218 icated in astrocyte differentiation regulate GLT-1 expression.
219   This suggests that neurons do not regulate GLT-1 by activation of PKA but that neurons and dbcAMP r
220 er, our findings establish that TX regulates GLT-1 via the CREB and NF-kappaB pathways.
221  applications were occluded by the selective GLT-1 inhibitor dihydrokainate.
222 ingly, a high percentage of variably spliced GLT-1 mRNAs lacking parts of this domain are found in th
223       Furthermore, we have identified strong GLT-1 mRNA labeling in a population of tanycytes situate
224                        In the present study, GLT-1 immunoaffinity isolates were prepared from rat cor
225 DAR 1]) and a glutamate transporter subtype [GLT-1] within the leech CNS using mono- and polyclonal a
226 ced hippocampal slices, fluorescently tagged GLT-1 puncta overlapped with fluorescently tagged mitoch
227 ther adult brain areas at a lower level than GLT-1, and is present throughout the brain early in deve
228 s expressed GLAST in greater proportion than GLT-1.
229 anxiety and depression, we hypothesized that GLT-1 blockade in the CEA would induce symptoms of anhed
230 PFC in regulating mood, we hypothesized that GLT-1 blockade in the PFC alone would be sufficient to i
231                  These results indicate that GLT-1 endocytosis is independent of its phosphorylation
232           Together, these data indicate that GLT-1 trafficking and cluster formation in glial cell pr
233 th previous results, these studies show that GLT-1 cocompartmentalizes with Na(+)/K(+) ATPase, glycol
234                   These studies suggest that GLT-1 and GLAST protein are regulated independently in a
235 domain are found in the CNS, suggesting that GLT-1 expression may be regulated during assembly.
236 ochondria or GLT-1, strongly suggesting that GLT-1, mitochondria, and the first step in glycolysis ar
237                     This study suggests that GLT-1, but not EAAC1, knockdown exacerbates the neuronal
238  when GLT-1 was deleted in neurons, both the GLT-1 protein and glutamate uptake activity that could b
239                             Furthermore, the GLT-1-expressing tanycytes represent a population of tan
240                         We microinjected the GLT-1 inhibitor, dihydrokainic acid (DHK), into the CEA
241                         We microinjected the GLT-1 inhibitor, dihydrokainic acid (DHK), into the PFC
242 racterized two retinal EAATs from mouse, the GLT-1/EAAT2 splice variant GLT-1c, and EAAT5.
243                          Inactivation of the GLT-1 gene was achieved in either neurons or astrocytes
244 appaB) in neuron-dependent activation of the GLT-1 promoter.
245 d p50 to the NF-kappaB binding domain of the GLT-1 promoter.
246 st both the N terminal and C terminal of the GLT-1 protein.
247  cell surface expression and activity of the GLT-1 subtype of glutamate transporter were examined in
248 ibute to posttranslational processing of the GLT-1 subtype of glutamate transporter.
249 analyses revealed a robust expression of the GLT-1 transporter protein in the SON, which was diminish
250 , -583/-282/-251) or CRE (-308) sites on the GLT-1 promoter led to significant repression of the prom
251 g a very large region of DNA surrounding the GLT-1 gene (BAC GLT-1 eGFP mice) were used to assess the
252 d uptake to dihydrokainate suggests that the GLT-1 (glutamate transporter-1) subtype primarily mediat
253 ing protein (CREB) and recruited CREB to the GLT-1 promoter consensus site.
254 -kappaB p50 and NF-kappaB p65 binding to the GLT-1 promoter.
255 ohistochemistry using specific antibodies to GLT-1 and GLAST.
256 otential signaling pathways linking GPR30 to GLT-1.
257 activity for the third glutamate transporter GLT-1 (EAAT2), a putatively glial transporter, in microc
258 sion of the astroglial glutamate transporter GLT-1 (N-acetylcysteine and ceftriaxone) can decrease me
259 mber 2), also known as glutamate transporter GLT-1 and excitatory amino acid transporter EAAT2.
260 regulation of the glia glutamate transporter GLT-1 and the recently identified GLT isoform, GLT-1b, i
261 sion of the astrocytic glutamate transporter GLT-1 and to attenuated changes in dendrite morphology,
262 vels of the astrocytic glutamate transporter GLT-1 but normal expression levels of another glial glut
263 utamate uptake via the glutamate transporter GLT-1 in rat glial cells.
264 al inhibition of glial glutamate transporter GLT-1 induced the similar Kv2.1 dephosphorylation, where
265              The glial glutamate transporter GLT-1 may be the predominant Na(+)-dependent glutamate t
266 or GFAP, S100beta, and glutamate transporter GLT-1 within a few hours of reperfusion, but without ast
267 inhibitor of the glial glutamate transporter GLT-1, did not block the increase in glutamate uptake.
268 sense strategy against glutamate transporter GLT-1, we found that restored transporter expression was
269 ade of the astrocytic glutamate transporter (GLT-1) induces anhedonia and c-Fos expression in areas t
270 m the synapse via the glutamate transporter (GLT-1).
271 airment of astrocytic glutamate transporter (GLT-1; EAAT2) function is associated with multiple neuro
272 specific inhibitor of the glial transporter, GLT-1.
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 n expression of glutamate (Glu) transporters GLT-1 and GLAST and attenuated Glu uptake (p < 0.01).
279 A and protein for the glutamate transporters GLT-1 and GLAST in unique tanycyte populations of the th
280 pression of the glial glutamate transporters GLT-1 and GLAST was studied in primary cultures derived
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 ective dominant-negative effect on wild-type GLT-1 expression and formed coimmunoprecipitable complex
285                                       Unlike GLT-1 expression, which increases in parallel with circu
286 e not blocked by PKA antagonists, but unlike GLT-1, the addition of dbcAMP to mixed cultures of neuro
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                         As was observed with GLT-1, the increases in GLAST protein observed in cocult
301 s GLT-1 and C6 glioma cells transfected with GLT-1.

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