ライフサイエンスコーパス: excitatory amino acid

1 ysiological and pathological effects of this excitatory amino acid.

2 omes when PC-12 cells were incubated without excitatory amino acid.

3 the neuronal damage produced by infusion of excitatory amino acids.

4 release of or the postsynaptic responses to excitatory amino acids.

5 Excitatory amino acids acting at non-NMDA receptors cont

6 InsP(6) did not affect spontaneous EPSCs or excitatory amino acid-activated currents in neurons lack

7 injection of N-methyl-D-aspartate (NMDA), an excitatory amino acid agonist, elicits reproducible foca

8 nse feeding response, feeding is elicited by excitatory amino acid agonists administered into the lat

9 The present study examined whether excitatory amino acid agonists elicited feeding followin

10 We examined whether injections of the excitatory amino acid AMPA are rewarding when injected i

11 Excitatory amino acids and glucocorticoids have key role

12 produce hyperalgesia through the release of excitatory amino acids and in part by the activation of

13 Besides glucocorticoids, excitatory amino acids and N-methyl-D-aspartate (NMDA) r

14 by a cascade involving the spinal release of excitatory amino acids and prostaglandins.

15 non-NMDA receptors, to subsequent release of excitatory amino acids and thus may attenuate transmissi

16 Glutamate is a key excitatory amino acid, and metabolism and neural sensing

17 Furthermore, microinjection of an excitatory amino acid antagonist into the ACC during con

18 administration of DA with the broad spectrum excitatory amino acid antagonist kynurenic acid inhibite

19 Finally, microinfusion of the excitatory amino acid antagonist, kynurenic acid, into t

20 Broad spectrum excitatory amino acid antagonists (kyurenic acid) or sel

21 These results raise the prospect that excitatory amino acid antagonists for neuronal NO syntha

22 Excitatory amino acid antagonists, NBQX (2, 3-dihydroxy-

23 After bath application of either an excitatory amino acid (AP-5 or CNQX) and a nicotinic cho

24 Anatomical studies indicate that excitatory amino acids are contained in VP inputs from t

25 ansporters for monoamines, GABA, glycine and excitatory amino acids are homologous to two sizable fam

26 The extracellular levels of excitatory amino acids are kept low by the action of the

27 Excess excitatory amino acids can provoke neuronal death in the

28 Transmembrane glutamate transport by the excitatory amino acid carrier (EAAC1) is coupled to the

29 The glutamate transporter excitatory amino acid carrier 1 (EAAC1) catalyzes the co

30 cells appearing as neurons, whereas neuronal excitatory amino acid carrier 1 (EAAC1) dissipated.

31 The neuronal transporter excitatory amino acid carrier 1 (EAAC1) is enriched in p

32 model system that endogenously expresses the excitatory amino acid carrier 1 (EAAC1) subtype of neuro

33 The sodium-dependent glutamate transporter, excitatory amino acid carrier 1 (EAAC1), has been implic

34 alysis showed that neuronal cultures express excitatory amino acid carrier 1 (EAAC1), shown previousl

35 pinal expression of a glutamate transporter, excitatory amino acid carrier 1 (EAAC1), was also quanti

36 sporter) but no measurable changes in EAAC1 (excitatory amino acid carrier 1) in spinal cord of end-s

37 In brain, EAAC1 (excitatory amino acid carrier 1) is the primary neuronal

38 ld-type glutamate transporter subtype EAAC1 (excitatory amino acid carrier 1) through photo-release f

39 The neuronal glutamate transporter, EAAC1 (excitatory amino acid carrier 1), undergoes rapid regula

40 e previously recognized neuronal transporter excitatory amino acid carrier 1.

41 The excitatory amino acid carrier EAAC1 belongs to a family

42 Forward glutamate transport by the excitatory amino acid carrier EAAC1 is coupled to the in

43 Glutamate transport by the excitatory amino acid carrier EAAC1 is known to be rever

44 also express a glutamate transporter, termed excitatory amino acid carrier-1 (EAAC1), but the physiol

45 previously shown was attributable to EAAC1 (excitatory amino acid carrier-1), a neuronal glutamate t

46 t neuronal glutamate transporter, EAAC1 (for excitatory amino acid carrier-1), is localized to the de

47 of the neuronal glutamate transporter EAAC1 (excitatory amino acid carrier-1).

48 -aspartate transporter; EAAT1) or EAAC1 (for excitatory amino acid carrier; EAAT3).

49 Excitatory amino-acid carrier 1 (EAAC1) is a high-affini

50 Released excitatory amino acids contribute significantly to secon

51 s indicate that during hypoglycemia, central excitatory amino acids contribute to the modulation of t

52 apped systematically using injections of the excitatory amino acid DL-homocysteic acid (DLH; 5-20 mM,

53 nosine as did injury, evidence that elevated excitatory amino acids do not elicit an appreciable frac

54 beta-estradiol (17betaE2) on spontaneous and excitatory amino acid (EAA) induced nucleus tractus soli

55 eely behaving females, three infusions of an excitatory amino acid (EAA) mixture applied at the same

56 However, the ability of these same excitatory amino acid (EAA) receptor antagonists to modu

57 ansmission can typically be blocked by using excitatory amino acid (EAA) receptor antagonists.

58 administration of kynurenate, a non-specific excitatory amino acid (EAA) receptor subtype antagonist,

59 have established that both NMDA and non-NMDA excitatory amino acid (EAA) receptor subtypes are involv

60 The NMDA receptor, an excitatory amino acid (EAA) receptor, appears to be invo

61 y was to examine the interaction of GABA and excitatory amino acid (EAA) receptors in the basolateral

62 The activation of excitatory amino acid (EAA) receptors within the central

63 the hypothesis that selective antagonism of excitatory amino acid (EAA) receptors within the ventral

64 thways on intracellular Ca(2+) accumulation, excitatory amino acid (EAA) release and neuronal death.

65 Excessive excitatory amino acid (EAA) release in cerebral ischemia

66 Excitatory amino acid (EAA) transmission in the rostral

67 of the basal ganglia motor system, sends an excitatory amino acid (EAA)-containing projection to the

68 We tested the hypothesis that excitatory amino acid (EAA)-mediated transmission plays

69 In brain and retina, stimulation with excitatory amino acids (EAA) can generate nitric oxide (

70 oderate hypothermia decreases the release of excitatory amino acids (EAA) from brain tissue of animal

71 se of small organic osmolytes, including the excitatory amino acids (EAA) glutamate and aspartate, vi

72 ers are the primary mechanism for removal of excitatory amino acids (EAAs) from the extracellular spa

73 riety of small organic anions, including the excitatory amino acids (EAAs) glutamate and aspartate.

74 We examined the role of excitatory amino acids (EAAs) in activation of noradrene

75 We examined the role of excitatory amino acids (EAAs) in the activation of midbr

76 her concentrations (e.g., 50 microM NMDA) of excitatory amino acids (EAAs) into the AP elicited an in

77 In anesthetized rats, microinjections of excitatory amino acids (EAAs) into the nucleus tractus s

78 Extracellular excitatory amino acids (EAAs) were detected from the sam

79 communicating information to the LC include excitatory amino acids (EAAs), corticotropin-releasing f

80 There is also considerable release of excitatory amino acids following SCI.

81 s not neuroprotective by blocking release of excitatory amino acids following SCI.

82 Isolation of a neurotoxic, excitatory amino acid from zonal geranium establishes th

83 ilure in brain ion homeostasis and efflux of excitatory amino acids from nerve cells.

84 Several neurotransmitters, including excitatory amino acids, GABA, and substance P, are invol

85 ng this system, multiple applications of the excitatory amino acid glutamate (10 nM-1 mM) elicited re

86 Rats received vehicle or the excitatory amino acid glutamate (25, 50, or 100 nmol/0.5

87 component of the senile plaques, and of the excitatory amino acid glutamate are both believed to be

88 The excitatory amino acid glutamate has been implicated in t

89 as suggested a neurotransmitter role for the excitatory amino acid glutamate in the leech central ner

90 The excitatory amino acid glutamate mediates transmission at

91 a condition exacerbated by liberation of the excitatory amino acid glutamate.

92 epidermal signaling pathway mediated by the excitatory amino acid glutamate.

93 using very high concentrations (1 mM) of the excitatory amino acids glutamate (Glu) and homocysteine

94 imulated by transsynaptic inputs provided by excitatory amino acids (glutamate) and at least one pept

95 ered domoic acid, a structural analog of the excitatory amino acids glutamic acid and kainic acid, ha

96 the possibility that motoneurons release an excitatory amino acid in addition to acetylcholine and t

97 It is known that glutamate (Glu), the major excitatory amino acid in the central nervous system, can

98 erefore examined the influence of endogenous excitatory amino acids in substantia nigra on stress-ind

99 The former two are major excitatory amino acids in the brain, and the last one ha

100 bral microdialysis to monitor the outputs of excitatory amino acids in the entopeduncular nucleus (EP

101 cused on the plasticity of channels gated by excitatory amino acids, including their acclaimed role i

102 Excitatory amino acids induce both acute membrane depola

103 ity is a process in which glutamate or other excitatory amino acids induce neuronal cell death.

104 -septal/preoptic area, their net response to excitatory amino acids is likely to be more complicated,

105 rexpression of TRF2 or administration of the excitatory amino acid kainic acid.

106 glial activation, possibly by cytokines and excitatory amino acids may play a role in the initiation

107 Excitatory amino acids may promote microtubular proteoly

108 t hippocampus, in which adrenal steroids and excitatory amino acids mediate a reversible remodeling o

109 Excitatory amino acids mediate this atrophy together wit

110 place aversion (CPA) in rats, we found that excitatory amino acid microinjection into the ACC during

111 protein kinase inhibitor staurosporine, the excitatory amino acid N-methyl-D-aspartate (NMDA), or a

112 In addition, alterations in excitatory amino acid neurotransmission in the basal gan

113 utamate receptors are important mediators of excitatory amino acid neurotransmission in the striatum.

114 by corticosterone (CORT) acting, in part, on excitatory amino acid neurotransmission.

115 The excitatory amino acid neurotransmitter glutamate partici

116 nd hydrolysis of NAAG yields the more potent excitatory amino acid neurotransmitter glutamate.

117 acid (NMDA), which mimics the action of the excitatory amino acid neurotransmitter glutamic acid, re

118 eostatic balance of the major inhibitory and excitatory amino acid neurotransmitter systems of gamma-

119 The balance between inhibitory and excitatory amino acid neurotransmitters contributes to t

120 tors - cytokines for the immune response and excitatory amino acid neurotransmitters for the hippocam

121 Both markers for inhibitory and excitatory amino acid neurotransmitters were found in va

122 ATP concentrations, decreased the release of excitatory amino acid neurotransmitters, and decreased t

123 s to the ultrastructural localization of the excitatory amino acid neurotransmitters, glutamate and a

124 death also can result from excess release of excitatory amino acid neurotransmitters, such as glutama

125 ed that altered brain energy metabolites and excitatory amino acids occurred during cerebral ischemia

126 enesis can be driven by activation of spinal excitatory amino acid or 5-HT receptors and that concomi

127 gh intraocular pressure, ischemia, excessive excitatory amino acids, or toxic products resulting from

128 mechanisms of neurodegeneration that involve excitatory amino acid pathways.

129 Excitatory amino acids play a key role in both adaptive

130 Excitatory amino acids play a key role in stress-induced

131 Domoic acid (DA), an excitatory amino acid produced by diatoms belonging to t

132 ral substrates that interact at the level of excitatory amino acid receptor activation and subsequent

133 ections (50 nl) of smaller concentrations of excitatory amino acid receptor agonists (e.g., NMDA, KA

134 Bilateral injections of the broad-spectrum excitatory amino acid receptor antagonist kynurenate (Ky

135 Tissue levels of the endogenous excitatory amino acid receptor antagonist kynurenic acid

136 Excitatory amino acid receptor antagonists 2-amino-5-pho

137 Studies utilizing excitatory amino acid receptor antagonists have been inc

138 upport the potential efficacy of competitive excitatory amino acid receptor antagonists in the treatm

139 5HT1F and 5HT1D receptor agonists, glutamate excitatory amino acid receptor antagonists, nitric oxide

140 was to determine if a change in brain tissue excitatory amino acid receptor binding occurs during pre

141 results suggest that d-amphetamine increases excitatory amino acid receptor function temporarily by r

142 ccinate (ABHS), a neurosteroid that inhibits excitatory amino acid receptor function, in a rabbit rev

143 The effects of prolonged ethanol exposure on excitatory amino acid receptor stimulated nitric oxide (

144 The postnatal development of excitatory amino acid receptor types including kainate,

145 targeted the N-methyl-D-aspartic acid (NMDA) excitatory amino acid receptor with an AAV-delivered ant

146 Excitatory amino acid receptor-dependent increases in de

147 e presence of important interactions between excitatory amino acid receptors and mu-opioid receptors

148 sult in activation of central nervous system excitatory amino acid receptors and subsequent intracell

149 developmental changes in the distribution of excitatory amino acid receptors in the chicken's auditor

150 nuation), or by prior blockade of ionotropic excitatory amino acid receptors in the commNTS with kynu

151 ere used to determine if the distribution of excitatory amino acid receptors in the owl's auditory br

152 Although pharmacologic modulation of excitatory amino acid receptors is well studied, minimal

153 njection of L-S-nitrosocysteine, blockade of excitatory amino acid receptors with kynurenic acid inhi

154 teroids, which act as negative modulators of excitatory amino acid receptors, may improve behavioral

155 onal interactions between opiate ligands and excitatory amino acid receptors, the ultrastructural loc

156 After activation of excitatory amino acid receptors, there is an influx of c

157 5)H(7)N(3)O(5)), a known but rare agonist of excitatory amino acid receptors.

158 aintenance of tolerance to diazepam, whereas excitatory amino acid-related processes (presumably via

159 show that P2X7 receptors provide a route for excitatory amino acid release from astrocytes.

160 Excess excitatory amino acid release is involved in pathways as

161 conclude that whilst inhibition of cortical excitatory amino acid release may contribute to the anti

162 is considerable support for an influence of excitatory amino acids released from corticofugal neuron

163 ought to mediate the postsynaptic effects of excitatory amino acids released from primary afferent te

164 ted vagal terminal calcium influx, while the excitatory amino acid reuptake inhibitor d,l-threo-beta-

165 to an ischemic event is the rapid release of excitatory amino acid's followed by the activation of th

166 ely via activation of PKA and enhancement of excitatory amino acid secretion.

167 ellular uptake and reduce cells apoptosis of excitatory amino acid stimulated PC-12 cells.

168 One factor involves excitatory amino acid stimulation of N-methyl-D-aspartat

169 al bushy cells, appears to be mediated by an excitatory amino acid such as glutamate, which acts at a

170 These data suggest that excitatory amino acids such as glutamate act on NMDA rec

171 ission can be activated by either opioids or excitatory amino acids such as N-methyl D-aspartate (NMD

172 that was evoked by iontophoretic ejection of excitatory amino acids, such as glutamate, was depressed

173 -PKA pathway modulates both tonic and phasic excitatory amino acid synaptic transmission and excitabi

174 ht to determine whether TACE is required for excitatory amino acids to activate the TGFalpha-erbB1 si

175 in neurological disorders in which excessive excitatory amino acid transmission is pathogenic.

176 widespread use of glutamate as the principal excitatory amino acid transmitter.

177 The stimulation of astroglial excitatory amino acid transport by amyloid protein precu

178 Astrocytic glutamate transporter excitatory amino acid transporter (EAAT) 1, also known a

179 asure conformational changes in the neuronal excitatory amino acid transporter (EAAT) 3 glutamate tra

180 transmission is terminated by members of the excitatory amino acid transporter (EAAT) family of prote

181 junction of three identical subunits in the excitatory amino acid transporter (EAAT) family.

182 stem slices, we show that application of the excitatory amino acid transporter (EAAT) substrate d-asp

183 ed levels of both the glutamate transporter, excitatory amino acid transporter (EAAT)-1, and the glut

184 Excitatory amino acid transporter (EAAT)-2 is one of the

185 H2O2, inhibit the function of an astrocytic excitatory amino acid transporter (EAAT1).

186 brain betaIII spectrin binds directly to the excitatory amino acid transporter (EAAT4), the glutamate

187 Glutamate transporters (excitatory amino acid transporter (EAATs)) are critical

188 cDNAs encoding five distinct salamander excitatory amino acid transporter (sEAAT) subtypes were

189 triggered astrocytic glutamate transport via excitatory amino acid transporter 1 (Eaat1), and blockin

190 ength-sensitive (M/L) cone opsin, rod opsin, excitatory amino acid transporter 1 (EAAT1), glutamate s

191 rthermore, expression of mRNA and protein of excitatory amino acid transporter 1 (GLAST), which is a

192 oning of the glutamate-aspartate transporter/excitatory amino acid transporter 1 (GLAST/EAAT1) in EAE

193 substitutions in the helical hairpin HP2 of excitatory amino acid transporter 1 form intersubunit di

194 by glutamate-aspartate transporters (GLAST) (excitatory amino acid transporter 1) because they were w

195 he glutamate-aspartate transporter (GLAST or excitatory amino acid transporter 1), vesicular glutamat

196 nown glutamate transporters, genderblind and excitatory amino acid transporter 1, in blood cells affe

197 main 10, a highly hydrophobic segment in the excitatory amino acid transporter 1, react readily when

198 ependent glutamate transport and loss of the excitatory amino acid transporter 2 (EAAT2) .

199 and expression of the glutamate transporter excitatory amino acid transporter 2 (EAAT2) in LPS-treat

200 KEY POINTS: Excitatory amino acid transporter 2 (EAAT2) is present o

201 Abeta also caused a significant reduction in excitatory amino acid transporter 2 (EAAT2) protein leve

202 with FcgammaRs triggers coendocytosis of the excitatory amino acid transporter 2 (EAAT2).

203 important glutamate transporters, especially excitatory amino acid transporter 2 (EAAT2, rodent analo

204 acid transporter 2, increased expression of excitatory amino acid transporter 2 repressor ying yang

205 e, an antagonist of glutamate transporter-1 (excitatory amino acid transporter 2) and were absent fro

206 nt astroglial L-glutamate transporter EAAT2 (excitatory amino acid transporter 2) does not contribute

207 EAAT2 (excitatory amino acid transporter 2) is a high affinity,

208 the astroglial glutamate transporter EAAT2 (excitatory amino acid transporter 2) protein in motor co

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

210 ipolar cells were labeled with antibodies to excitatory amino acid transporter 2, and they also made

211 trocytes significantly lowered expression of excitatory amino acid transporter 2, increased expressio

212 f AMPH-dependent trafficking of the neuronal excitatory amino acid transporter 3 (EAAT3) blocks poten

213 The glutamate transporter excitatory amino acid transporter 3 (EAAT3) is polarized

214 cysteine is then taken up by neurons through excitatory amino acid transporter 3 [EAAT3; also termed

215 se 1, metabotropic glutamate receptor 1, and excitatory amino acid transporter 3) were validated by W

216 STC) mediated by the PC-specific transporter excitatory amino acid transporter 4 (EAAT4).

217 zebrin II) and phosphofructokinase C and the excitatory amino acid transporter 4 (EAAT4).

218 (vesicular glutamate transporter 1), EAAT5 (excitatory amino acid transporter 5), and VAMP2 (vesicle

219 antly increase after bath application of the excitatory amino acid transporter blocker DL-threo-beta-

220 episodic ataxia (EA6) have mutations of the excitatory amino acid transporter EAAT1 (also known as G

221 The kinetic properties of the excitatory amino acid transporter EAAT2 were studied usi

222 lso known as glutamate transporter GLT-1 and excitatory amino acid transporter EAAT2.

223 The Na(+)-dependent high-affinity excitatory amino acid transporter EAAT3 (EAAC1) facilita

224 The excitatory amino acid transporter EAAT4 is expressed pre

225 In Xenopus laevis oocytes expressing the excitatory amino acid transporter EAAT4, physiologically

226 Secondary transporters in the excitatory amino acid transporter family terminate gluta

227 it of EAAC1, as well as other members of the excitatory amino acid transporter family.

228 a also caused an NFAT-dependent reduction in excitatory amino acid transporter levels, indicating a p

229 olesterol-rich microdomains is important for excitatory amino acid transporter localization and funct

230 esses the uptake of glutamate by the type 2A excitatory amino acid transporter on photoreceptors.

231 t class of selective inhibitors of the human excitatory amino acid transporter subtype 1 (EAAT1) and

232 ing of a small compound library at the three excitatory amino acid transporter subtypes 1-3 (EAAT1-3)

233 ized their pharmacological properties at the excitatory amino acid transporter subtypes EAAT1, EAAT2,

234 ation with riboprobes specific for the human excitatory amino acid transporter transcripts EAAT1, EAA

235 EAAT3 (excitatory amino acid transporter type 3, the neuron-spe

236 g via mu-opioid receptors, morphine inhibits excitatory amino acid transporter type 3-mediated cystei

237 m showing characteristics of members of the "excitatory amino acid transporter" (EAAT) family.

238 GLT-1 [for glutamate transporter; EAAT2 (for excitatory amino acid transporter)] with dihydrokainate

239 transporter, it stimulates endocytosis of an excitatory amino acid transporter, EAAT3, in dopamine ne

240 ere it colocalized with the sodium-dependent excitatory amino acid transporter, EAAT3.

241 g and functional characterization of a human excitatory amino acid transporter, EAAT5, expressed prim

242 tissue microarray analyses showed decreased excitatory amino acid transporter-2 (EAAT-2) expression

243 Excitatory amino acid transporter-2 (EAAT2) is a major g

244 ion of ENT1 reduced the expression of type 2 excitatory amino-acid transporter (EAAT2) and the astroc

245 low immunostaining for glutamine synthetase, excitatory amino-acid transporter 1 (EAAT1), and EAAT2.

246 rters such as glial glutamate transporter 1 (excitatory amino-acid transporter 2).

247 reases in extracellular glutamate through an excitatory amino-acid transporter to cause excitotoxicit

248 The glutamate (excitatory amino acid) transporter 2 (EAAT2; Slc1a2) has

249 r family 1A (SLC1A), which also includes the excitatory amino acid transporters (EAATs) and the proka

250 Excitatory amino acid transporters (EAATs) are a class o

251 Excitatory amino acid transporters (EAATs) are abundantl

252 Excitatory amino acid transporters (EAATs) are crucial f

253 Excitatory amino acid transporters (EAATs) are crucial i

254 Excitatory amino acid transporters (EAATs) are essential

255 In the mammalian central nervous system, excitatory amino acid transporters (EAATs) are responsib

256 Excitatory amino acid transporters (EAATs) are responsib

257 Excitatory amino acid transporters (EAATs) are the prima

258 Excitatory amino acid transporters (EAATs) buffer and re

259 Excitatory amino acid transporters (EAATs) control the g

260 duct synaptic transmission and activation of excitatory amino acid transporters (EAATs) for transmitt

261 Excitatory amino acid transporters (EAATs) function as b

262 However, blocking excitatory amino acid transporters (EAATs) generates bea

263 L-glutamate from the extracellular space by excitatory amino acid transporters (EAATs) has been post

264 at synapses is sequestered by the action of excitatory amino acid transporters (EAATs) in glia and p

265 embrane Na(+)/Ca(2+) exchanger (NCX) and the excitatory amino acid transporters (EAATs) in Glu uptake

266 In the CNS, excitatory amino acid transporters (EAATs) localized to

267 Excitatory amino acid transporters (EAATs) located on ne

268 y have enabled a deeper understanding of how excitatory amino acid transporters (EAATs) mediate chlor

269 The excitatory amino acid transporters (EAATs) play essentia

270 Excitatory amino acid transporters (EAATs) remove glutam

271 Excitatory amino acid transporters (EAATs) terminate glu

272 Excitatory amino acid transporters (EAATs) terminate sig

273 Excitatory amino acid transporters (EAATs) use sodium an

274 Glutamate transporters, also referred to as excitatory amino acid transporters (EAATs), are membrane

275 -function studies of mammalian and bacterial excitatory amino acid transporters (EAATs), as well as t

276 mate in nerve synapses is carried out by the excitatory amino acid transporters (EAATs), involving th

277 ties was previously reported for the related excitatory amino acid transporters (EAATs), suggesting t

278 cules of the glutamate synapse, specifically excitatory amino acid transporters (EAATs), whose normal

279 rders, pursuit of the transport proteins--or excitatory amino acid transporters (EAATs)--toward a sim

280 centration occurs in part through astrocytic excitatory amino acid transporters (EAATs).

281 a family of glutamate transporters known as "excitatory amino acid transporters (EAATs)." Here we clo

282 tic glutamate in the cerebral cortex are the excitatory amino acid transporters 1-3 (EAAT1-3).

283 rimarily achieved by glutamate transporters (excitatory amino acid transporters 1-5, EAATs1-5) locate

284 Blockade of excitatory amino acid transporters or vesicular glutamat

285 Excitatory amino acid transporters remove synaptically r

286 nsporters, which also includes the mammalian excitatory amino acid transporters that take up the neur

287 Glutamate transporters (excitatory amino acid transporters, EAAT) play an import

288 o includes the human glutamate transporters (excitatory amino acid transporters, EAATs) and the proka

289 Glutamate transporters (also called excitatory amino acid transporters, EAATs) bind extracel

290 th synaptic regions in neuropil, and express excitatory amino acid transporters, which are presumably

291 or the "elevator" mechanism in the mammalian excitatory amino acid transporters.

292 vated anion currents and both phases involve excitatory amino acid transporters.

293 e insights into structural features of human excitatory amino acid transporters.

294 nd Na(+)-dependent glutamate cotransporters (excitatory amino acid transporters; EAATs) exist exclusi

295 Excitatory amino-acid transporters (EAATs) bind and tran

296 matergic synapse is tightly regulated by the excitatory amino-acid transporters (EAATs).

297 in extracellular glutamate were mediated by excitatory amino-acid transporters, the reverse dialysis

298 ion by cAMP was potentiated by inhibitors of excitatory amino acid uptake, suggesting a role for extr

299 re 4% in vitro, and detection limits for the excitatory amino acids were approximately 60 nM.

300 ctly suggest that kappa-opioid receptors and excitatory amino acids within the LC mediate withdrawal