ライフサイエンスコーパス: GluR

1 GluR-A-/- mice were hyperactive, displayed a subtle lack

2 GluR-based Ca2+ signals were uniform within a given conn

3 GluRs are permeable to Na+, K+ and Ca2+, are gated by gl

4 GluRs in taste cells might be presynaptic autoreceptors

5 PC2 restored nose touch sensitivity to glr-1 GluR mutants.

6 fic for glutamate receptor subtypes, GluR 1, GluR 2/3, and GluR 4.

7 tamate receptor (GluR) subunits (GluR 5/6/7, GluR 2/3 and N-methyl-D-aspartate receptor 1 [NMDAR 1])

8 ng pathway that leads to the activation of a GluR-A-dependent expression mechanism in a rapidly acqui

9 ified mice lacking the glutamate receptor A (GluR-A) subunit of the AMPA receptor (GluR-A-/- mice) di

10 ined with mice lacking glutamate receptor-A (GluR-A)-containing AMPA receptors, which support long-te

11 oocytes injected with AD membranes acquired GluRs that have essentially the same functional properti

12 In addition, GluR agonist treatment of cultured cortical neurons incr

13 nduced relapse to cocaine seeking even after GluR overexpression declines.

14 s high levels of pS6 and demonstrate altered GluR subunit composition, resembling those of normal imm

15 By contrast, endocytosis of rodent AMPA GluRs is apparently regulated by ubiquitination of assoc

16 FR1, ICAM-1, inducible NO synthase, and AMPA-GluR, all of which were altered in MRL/lpr mouse brains,

17 nt up-regulation of glutamate receptor (AMPA-GluR) expression in lupus brains, which was also validat

18 n range in recombinant NMDAR NR1-NR2A, AMPAR GluR-A(Q) and KAR GluR-6(Q) channels.

19 of a conserved asparagine (N) in M3 of AMPAR GluR-B(Q) channels strongly attenuated Ca2+ permeability

20 s in the pore-lining M3 segment of the AMPAR GluR-A subunit and various cysteine-reactive agents to s

21 e gephyrin, and modulates the synaptic AMPAR/GluR composition both in the PFC and the nucleus accumbe

22 levels of AMPA receptor subunits GluR-1 and GluR-4 are rapidly decreased in cultured rat hippocampal

23 ate receptor subtypes, GluR 1, GluR 2/3, and GluR 4.

24 e microglia labeled with both GluR 5/6/7 and GluR 2/3 but not NMDAR 1 subunit antisera.

25 is expressed at weak, GluR 6 at moderate and GluR 4 at high levels.

26 way downstream molecule phospho-S6 (pS6) and GluR subunits, and compared with control cortical tissue

27 tudy evaluated male and female wild-type and GluR-A-/- mice on a test battery that assessed sensorimo

28 missing link between potassium channels and GluRs, and we suggest that their ion channels have a sim

29 otentials recorded after blocking nAChRs and GluRs with DHbetaE plus Kyn, a small unidentified compon

30 most strongly concentration dependent of any GluR subtype and, except for low Ca(2+) concentrations,

31 Synthesis of many synaptic proteins, such as GluR and PSD-95, is under local control.

32 food reward is NR2A independent, as well as GluR-A independent.

33 ts its cytoskeletal association, attenuating GluR endocytosis and affecting the efficacy of synaptic

34 ss is understood about presynaptic auxiliary GluR subunits and their functions.

35 ed into a mimic of the glutamate receptor B (GluR B) mRNA R/G editing site.

36 senger RNA for glutamate receptor subunit B (GluR-B).

37 ule and putative microglia labeled with both GluR 5/6/7 and GluR 2/3 but not NMDAR 1 subunit antisera

38 ) = 33% of that of AnTx) that was blocked by GluR antagonists, supporting a model in which alpha7 nAC

39 retardation 1 (dfmr1) null mutants, A-class GluRs accumulate and B-class GluRs are lost, whereas tot

40 ts, there is an additive increase in A-class GluRs, and a similar additive impact on B-class GluRs, t

41 utants, A-class GluRs accumulate and B-class GluRs are lost, whereas total GluR levels do not change,

42 Rs, and a similar additive impact on B-class GluRs, toward normal levels in the double mutants.

43 In comparison, GluR-A AMPA receptors were much less sensitive.

44 Neuronal AMPA receptors comprise GluR subunits and transmembrane AMPA receptor regulatory

45 riptionally, outside the nucleus, to control GluR density.

46 entially regulate the abundance of different GluR subclasses in a convergent mechanism within individ

47 the extensive distribution of the different GluR subunit mRNAs strengthen the view that glutamate is

48 l is not structurally identical in different GluRs.

49 maintains the post-synaptic pathways driving GluR domain formation.

50 tion training session, when conducted during GluR subunit overexpression, attenuates stress-induced r

51 egulating synapses that contain a C. elegans GluR, GLR-1.

52 l relationships between GluR0 and eukaryotic GluRs, we propose that a prokaryotic GluR was the precur

53 ed in amino-acid sequence to both eukaryotic GluRs and potassium channels.

54 In contrast, eukaryotic GluRs have an additional transmembrane segment (M4), loc

55 aryotic GluR was the precursor to eukaryotic GluRs.

56 mRNAs suggests that many neurons can express GluR channels that belong to different families, which w

57 Cryostat-sectioned tissue revealed extensive GluR 5/6/7-like immunoreactivity throughout the neuropil

58 m Synechocystis PCC 6803, which is the first GluR found in a prokaryote.

59 For GluR-6(Q) channels, P(Ca)/P(Na) derived from P(f) measur

60 For GluR-A(Q) channels, P(Ca)/P(Na) derived from all three a

61 ET assays that detect cAMP as a read-out for GluR and GLP-1R activation.

62 ue face of the M4 helix that is required for GluR surface expression.

63 nsistent with previous reports of a role for GluR-A-dependent plasticity in hippocampus-dependent, sp

64 Arrays containing GABA A (GABAAR), GluR, NMDA receptor (NR) subunits, GAD65, the vesicular

65 In general, GluR 5/6/7-like immunofluorescence was both more intense

66 tein-coupled receptors (GPCRs) for glucagon (GluR) and glucagon-like peptide-1 (GLP-1R) are normally

67 are encoded by four genes designated GluR1 (GluR-A) through GluR4 (GluR-D).

68 ice lacking the AMPA receptor subunit GluR1 (GluR-A) have deficits in hippocampal CA3-CA1 long-term p

69 nes designated GluR1 (GluR-A) through GluR4 (GluR-D).

70 Hence, GluR-delta 2(Lc) channels are functionally similar to th

71 es powerful new evidence linking hippocampal GluR-A-dependent synaptic plasticity to rapid, flexible

72 s, and IRAK/pelle kinase specifically impair GluR levels, assayed immunohistochemically and electroph

73 demonstrates cell-specific abnormalities in GluR expression that may contribute to seizure pathogene

74 s to characterize the in vivo role of AP2 in GluR trafficking.

75 ot change, resulting in a striking change in GluR subclass ratio at individual synapses.

76 ern blotting was used to quantify changes in GluR subunit expression in tubers versus controls.

77 ress lower pS6 levels and display changes in GluR subunit expression that are distinct from the patte

78 These results imply that the SWM deficit in GluR-A-/- mice is not due to increased susceptibility to

79 are consistent with pore-forming domains in GluR and K+ channels having a similar structure but inve

80 basis for the distinct features of gating in GluR and K+ channels.

81 SWM was impaired in GluR-A-/- mice, both during testing with pseudotrial-uni

82 lexible spatial working memory impairment in GluR-A(-/-) mice, which might also underlie their mild d

83 omain interactions at the dimer interface in GluR channel function.

84 l and suggest a model of gating movements in GluR pore-forming domains.

85 mologous substitutions of the conserved R in GluR-B(o), GluR-A(i) and the kainate receptor GluR-6 sub

86 our results indicate that the M3 segment in GluR does not contain a glycine gating hinge and suggest

87 ied with the specific target editing site in GluR-B RNA.

88 mined the functional role of the Q/R site in GluR-delta 2(Lc) by replacing glutamine with arginine.

89 expression of GFP-tagged GluR-A subunits in GluR-A-deficient mice rescues SWM, paralleling its rescu

90 , and subcellular distribution of ionotropic GluR subunits within the primary afferent and local syna

91 ervation of the striatum, whereas ionotropic GluR antagonists had no effect.

92 vation of glomerular mAChRs, with ionotropic GluRs and nAChRs blocked, increased IPSCs in MTCs and ET

93 nant NMDAR NR1-NR2A, AMPAR GluR-A(Q) and KAR GluR-6(Q) channels.

94 wo negative residues C-terminal to M3 in KAR GluR-6(Q) subunits had no effect on Ca2+ permeability.

95 The receptors appear to lack GluR-2 subunits and may be Ca2+ permeable.

96 found in association with other full-length GluRs in the mouse brain and cultured primary neurons.

97 ction, and a corresponding loss of localized GluR domains.

98 described for transcripts encoding mammalian GluRs.

99 studies using tasks such as the water maze, GluR-A(-/-) mice were unimpaired during acquisition of t

100 Metabotropic GluR-induced suppression of I(D) was manifest in three a

101 ttermate controls in the type 1 metabotropic GluR (mGluR1), mGluR2, mGluR3, but not the mGluR5 subtyp

102 In contrast, group I metabotropic GluR signaling promotes microtubule-based trafficking of

103 action-potential generation, or metabotropic GluR activation.

104 clamshell lobes, reminiscent of metabotropic GluRs (mGluRs).

105 Here we report that metabotropic GluRs (mGluRs) are highly expressed in OL precursors but

106 ptor, the AMPA, kainate and the metabotropic GluRs may be targets for the development of rapidly acti

107 ls of GluR-delta2 with the Lurcher mutation (GluR-delta 2(Lc)) expressed in human embryonic kidney 29

108 Experimentally naive GluR-A-/- mice also exhibited chance performance during

109 pose that the M3 segments in two neighboring GluR subunits are kinked within SYTANLAAF in opposite di

110 Nevertheless, GluRs lack a glycine residue at a homologous structural

111 The insertion of new GluRs is accompanied by an increase in the frequency of

112 that rodent OLs also express functional NMDA GluRs (NMDARs), and overactivation of these receptors ca

113 n pericallosal white matter express non-NMDA GluRs at P7.

114 The finding that both NMDA and non-NMDA GluRs were involved in glutamate-induced excitotoxicity

115 was mediated through both NMDA and non-NMDA GluRs.

116 pport our previous report that nonfunctional GluRs are retained intracellularly by a functional check

117 outcome as the CS in wild-type (WT), but not GluR-1-super(-/-), mice.

118 residues in the GluR3B region define a novel GluR subunit-specific agonist binding site and impart su

119 bstitutions of the conserved R in GluR-B(o), GluR-A(i) and the kainate receptor GluR-6 subunits produ

120 Furthermore, systemic administration of GluR or GLP-1R agonists and antagonists at high doses ma

121 The amount of GluR 2/3 immunolabeling was similar for sound-stimulated

122 iption-polymerase chain reaction analyses of GluR-B RNA from dissected regions of rat brain showed si

123 Homo-oligomeric channels of GluR-delta2 with the Lurcher mutation (GluR-delta 2(Lc))

124 y signaling in the brain and are composed of GluR principal subunits and transmembrane AMPA receptor

125 tion in homomeric AMPA receptors composed of GluR-B(i) subunits.

126 , in part, by a differential distribution of GluR subunits.

127 ice-site variants to catalyze the editing of GluR-B pre-mRNA at the Q/R and R/G sites as well as an i

128 Enhanced expression of GluR 3, 4, and 6 and NR2B and 2C subunit mRNAs was noted

129 Differential expression of GluR, NR, and GABAAR mRNAs in tubers reflects cell-speci

130 ain ischemia develop depressed expression of GluR-B in CA1 hippocampal neurons.

131 ernatively spliced flip and flop isoforms of GluR-B RNA varied among the choroid plexus, cortex, hipp

132 and L-type Ca channel mRNAs, high levels of GluR-2 versus GluR-1, and a high ratio of NMDAR-2A to NM

133 sulted neurons expressed increased levels of GluR-D flop.

134 bstitution of the only two glycines in M3 of GluR-A with alanines produced channels with gating prope

135 Measurement of GluR-B pre-mRNA editing in vitro revealed different site

136 The electron microscopy of GluR 2/3 in the IC revealed immunoreaction products asso

137 by differential spatio-temporal patterns of GluR expression, by alternative RNA splicing and editing

138 The SWM performance of GluR-A-/- and wild-type mice was assessed during nonmatc

139 ivo, and implicates AP2 in the regulation of GluR trafficking at an early step in the secretory pathw

140 We evaluated the role of GluR-mediated OL excitotoxicity in hypoxic/ischemic whit

141 iciently edits both the Q/R and R/G sites of GluR-B RNA.

142 on is determined by the cytoplasmic tails of GluR subunits, and in heteromeric receptors, GluR1 acts

143 ng/scaffold proteins functioning upstream of GluR localization are also grossly reduced or mislocaliz

144 athrin adaptor in promoting the abundance of GluRs at synapses in vivo, and implicates AP2 in the reg

145 vated glutamate, the excessive activation of GluRs causes internalization of pathologic levels of Ca(

146 The function of GluRs in taste buds is not yet known, but the data sugge

147 fects the agonist-induced internalization of GluRs in cultured hippocampal neurons.

148 completely prevented the internalization of GluRs.

149 ist AMPA induced a robust internalization of GluRs.

150 tetramers and that the gating mechanisms of GluRs and potassium channels have some essential feature

151 ns are fundamental homeostatic modulators of GluRs on both sides of the synapse.

152 rain is a consequence of a reduced number of GluRs in cell membranes transplanted from the AD brain.

153 units, the cytoplasmic to synaptic ratios of GluRs were measured within thalamo-amygdaloid spines.

154 evoked transmission employ distinct sets of GluRs.

155 When expressed in Xenopus oocytes, GluR-WS was secreted and water-soluble; GluR1-M1 was dis

156 uRA overexpression causes the exact opposite GluR phenotype to the dfmr1 null, confirming postsynapti

157 As with other GluR molecules, labeling was usually confined to one of

158 reating GluR3salpha) co-assembled with other GluR subunits and decreased receptor function in Xenopus

159 amed state and that modulation of peripheral GluRs reduces pain behaviors and nociceptor activity.

160 cological agents that will target peripheral GluRs, offering novel approaches to treatment of pain of

161 Thus, the three Ca(2+)-permeable GluR subtypes showed unique patterns of Ca(2+) permeabil

162 e to the dfmr1 null, confirming postsynaptic GluR subtype-specific regulation.

163 lease in response to diminished postsynaptic GluR functionality, a process referred to as presynaptic

164 is, leads to large increases in postsynaptic GluR subunit messenger RNA and protein.

165 r the homeostatic modulation of postsynaptic GluRs in mammals, our data demonstrate that dSol-1 is re

166 iliary subunits associated with postsynaptic GluRs, far less is understood about presynaptic auxiliar

167 ophila neuromuscular junction, a presynaptic GluR, DKaiR1D, localizes near active zones and operates

168 or the homeostatic regulation of presynaptic GluRs.

169 aryotic GluRs, we propose that a prokaryotic GluR was the precursor to eukaryotic GluRs.

170 Like P-loop channels, prokaryotic GluR subunits (e.g. GluR0) have two transmembrane segmen

171 fusion of outside-out patches containing rat GluR-A or GluR6 subunits excised from transfected human

172 vidly and selectively binds to AMPA receptor GluR subunits and also binds to the AMPA receptor cluste

173 tribution of the M3 segment in AMPA receptor GluR-A subunits to channel structure and gating.

174 luR-B(o), GluR-A(i) and the kainate receptor GluR-6 subunits produced comparable but less visible eff

175 tor A (GluR-A) subunit of the AMPA receptor (GluR-A-/- mice) display normal spatial reference memory

176 pression of AMPA subtype glutamate receptor (GluR) 1 and GluR2 subunits.

177 ession of AMPARs lacking glutamate receptor (GluR) 2 in hippocampal synaptic fractions.

178 e, we show that subunits glutamate receptor (GluR) 5 and GluR6 play distinct roles in kainate-induced

179 ist, bind selectively to glutamate receptor (GluR) 5 but not to the KA2 KAR subunit, we used molecula

180 Regulation of glutamate receptor (GluR) abundance at synapses by clathrin-mediated endocyt

181 gnals include changes in glutamate receptor (GluR) activation, changes in firing rate, or changes in

182 The glutamate receptor (GluR) agonist-binding site consists of amino acid residu

183 The glutamate receptor (GluR) agonist-binding site consists of amino acid residu

184 alpha-conotoxin-ImI) and glutamate receptor (GluR) antagonists [kynurenic acid, 6,7-dinitroquinoxalin

185 nce of the use-dependent glutamate receptor (GluR) blocker philanthotoxin, indicated that spontaneous

186 us surround postsynaptic glutamate receptor (GluR) clusters at the Drosophila NMJ.

187 e with the post-synaptic glutamate receptor (GluR) domain.

188 Ionotropic glutamate receptor (GluR) expression and function is regulated through multi

189 Glutamate receptor (GluR) ion channels mediate fast synaptic transmission in

190 l-specific expression of glutamate receptor (GluR) mRNAs and polypeptide subunits in motor and somato

191 fluence of activation of glutamate receptor (GluR) on outward K(+) current in cultured neonate rat hi

192 dysplastic cells express glutamate receptor (GluR) patterns consistent with increased cortical networ

193 channels associated with glutamate receptor (GluR) subtypes, namely N-methyl-D-aspartate receptors (N

194 bunits, D1 preferred the glutamate receptor (GluR) subunit GluR4 flip (0.64 microM) over GluR4 flop (

195 y, we sought to localize glutamate receptor (GluR) subunits (GluR 5/6/7, GluR 2/3 and N-methyl-D-aspa

196 calization of ionotropic glutamate receptor (GluR) subunits was examined with light and electron micr

197 nto LA spines expressing glutamate receptor (GluR) subunits, but the GluR subunit distribution at the

198 ethyl-d-aspartate (NMDA) glutamate receptor (GluR), has rapid antidepressant efficacy.

199 ethyl-D-aspartate) class glutamate receptor (GluR), resulting in its removal from synapses.

200 rebellar neuromodulators glutamate receptor (GluR)-6, kainate-preferring glutamate receptor subunit-2

201 orking memory deficit in glutamate receptor (GluR)-A (GluR1) AMPA receptor subunit knockout mice.

202 in (ABP) and the related glutamate receptor (GluR)-interacting protein (GRIP), two multi-PDZ proteins

203 Glutamate receptor (GluR)-mediated neurotoxicity is implicated in a variety

204 subtypes of postsynaptic glutamate receptor (GluR).

205 quantitatively analyzed glutamate receptor (GluR)1, GluR2/3, and GluR4 AMPA subunit immunoreactivity

206 er relative abundance of glutamate receptor (GluR)2 transcript and much lower levels of GluR2 immunor

207 ncoding the B subunit of glutamate receptor (GluR-B) has two functionally important editing sites (Q/

208 mutations in the orphan glutamate receptor, GluR delta2, a gene selectively expressed in Purkinje ne

209 ggregation of AMPA-type glutamate receptors (GluR) at excitatory synapses.

210 now studied the properties of Glu receptors (GluRs) from the cerebral cortices of AD and non-AD brain

211 ell as the two types of glutamate receptors (GluRs) (AMPARs and NMDARs).

212 (OLs) express non-NMDA glutamate receptors (GluRs) and are susceptible to GluR-mediated excitotoxici

213 channels are ionotropic glutamate receptors (GluRs) and potassium channels.

214 tropic and metabotropic glutamate receptors (GluRs) are based on an azobenzene photoswitch that is op

215 Ionotropic glutamate receptors (GluRs) are ligand-gated ion channels with a modular stru

216 Ionotropic glutamate receptors (GluRs) are ligand-gated membrane channel proteins found

217 the CNS kainate subtype glutamate receptors (GluRs) are likely to be heteromeric assemblies containin

218 Glutamate receptors (GluRs) are localized in the periphery on nociceptive pri

219 Most AMPA-type glutamate receptors (GluRs) exhibit rapid and virtually complete desensitizat

220 lepropionic acid (AMPA) glutamate receptors (GluRs) from postsynaptic elements has been proposed as a

221 igand binding domain of glutamate receptors (GluRs) has 2-fold rotational symmetry.

222 al studies of models of glutamate receptors (GluRs) have been limited to monomeric models of the liga

223 undance of postsynaptic glutamate receptors (GluRs) in Drosophila neuromuscular junctions is controll

224 est for the presence of glutamate receptors (GluRs) in living isolated tissue preparations.

225 Analysis of glutamate receptors (GluRs) in symptomatic 12-week-old R6/2 mice revealed dec

226 g subtype of ionotropic glutamate receptors (GluRs) is a hetero-oligomeric ion channel assembled from

227 As the trafficking of glutamate receptors (GluRs) is thought to underlie some forms of synaptic pla

228 AMPA-type glutamate receptors (GluRs) mediate most excitatory signaling in the brain an

229 Presynaptic glutamate receptors (GluRs) modulate neurotransmitter release and are physiol

230 ediated by cell surface glutamate receptors (GluRs) of the AMPA subtype has been demonstrated as one

231 group III metabotropic glutamate receptors (GluRs) play in modulating transmission at the striatopal

232 AMPA-type glutamate receptors (GluRs) play major roles in excitatory synaptic transmiss

233 es of channel gating in glutamate receptors (GluRs) remain unknown.

234 ic acid (AMPA) class of glutamate receptors (GluRs) with different calcium permeabilities has been pr

235 rts Ca2+ influx through glutamate receptors (GluRs) with single-impulse and single-bouton resolution.

236 a subunit of ionotropic glutamate receptors (GluRs) with unknown natural ligands and channel properti

237 stimulating ionotropic glutamate receptors (GluRs) within the nucleus accumbens core or shell would

238 mM kynurenate (Kyn) for glutamate receptors (GluRs), and 100 microM Cd2+ for all chemical synapses) w

239 itization of ionotropic glutamate receptors (GluRs), specifically the AMPA receptor subtype, shapes t

240 cytosis of postsynaptic glutamate receptors (GluRs).

241 n mutants lacking GLR-1 glutamate receptors (GluRs); however, mutations eliminating the egl-3 PC2 res

242 Analogous to AMPA/kainate receptors, GluR-delta 2(Lc)(R) channels showed no voltage-dependent

243 onic mutant synapses exhibit greatly reduced GluR function, and a corresponding loss of localized Glu

244 y and specialization between closely related GluR subunits is accomplished.

245 Most of the de-repressed GluR protein, however, does not appear to be incorporate

246 ty of this residue varies between respective GluR subunits, this suggested that this residue may be i

247 munocytochemistry to localize AMPA selective GluR 2/3 subunits (GluR2/3) and NMDA receptor subunit 1

248 LPFC of females with MDD, with more specific GluR alterations in the suicides and in the male groups.

249 ally at the postsynaptic density, to specify GluR levels.

250 es specific for glutamate receptor subtypes, GluR 1, GluR 2/3, and GluR 4.

251 geted mice lacking the AMPA receptor subunit GluR-A (also called GluR1 encoded by the gene Gria1,) ha

252 ckout mice lacking the AMPA receptor subunit GluR-A (GluR1), wild-type controls, mice with cytotoxic

253 for the human glutamate receptor B subunit (GluR B).

254 report that levels of AMPA receptor subunits GluR-1 and GluR-4 are rapidly decreased in cultured rat

255 localize glutamate receptor (GluR) subunits (GluR 5/6/7, GluR 2/3 and N-methyl-D-aspartate receptor 1

256 g the AMPA-type glutamate receptor subunits (GluRs) 1 and 2 are localized to dendrites of hippocampal

257 on of AMPA-type glutamate receptor subunits (GluRs) in the nucleus accumbens (NAc), a key component o

258 ng of mammalian glutamate receptor subunits (GluRs).

259 Moreover, surface GluR 1 and synaptic GluR2/3 clusters were reduced by Sli

260 at this association is required for synaptic GluR internalization.

261 , resulting in an increase in total synaptic GluR content at individual synapses.

262 forebrain-localized expression of GFP-tagged GluR-A subunits in GluR-A-deficient mice rescues SWM, pa

263 s both more intense and more widespread than GluR 2/3-like immunolabeling.

264 The results support the hypothesis that GluR-1 deletion impairs the associative activation of a

265 n channels have a similar architecture, that GluRs are tetramers and that the gating mechanisms of Gl

266 These results demonstrate that GluRs in the nucleus accumbens core and shell influence

267 The GluR allosteric inhibitors LY2409021 and MK 0893 antagon

268 to their performance during acquisition, the GluR-A(-/-) mice displayed a mild deficit during reversa

269 f the membrane electric potential across the GluR channel pore, we recorded from alpha-amino-3-hydrox

270 ted a dual agonist action of glucagon at the GluR and GLP-1R.

271 eptide YY (PYY) acted as a triagonist at the GluR, GLP-1R, and neuropeptide Y2 receptor (NPY2R).

272 ]glucagon antagonized glucagon action at the GluR, while having minimal inhibitory action versus gluc

273 glutamate receptor (GluR) subunits, but the GluR subunit distribution at the synapse and within the

274 g disc, and are inhibited by EGTA and by the GluR inhibitor NASPM (1-naphthylacetyl spermine trihydro

275 ent are the major pore-lining domains in the GluR channel.

276 ning M2 and M3 cysteine substitutions in the GluR-A subunit and measured the voltage dependence of th

277 ences of mRNA through RNA editing, as in the GluR-B Q/R site.

278 ivation or desensitization properties of the GluR channels depended on membrane potential.

279 docytic adaptor, we found that levels of the GluR GLR-1 are decreased at synapses in the ventral nerv

280 The structure including the symmetry of the GluR ion channel remains undefined.

281 t while the differential distribution of the GluR subtypes may reflect distinct roles for their invol

282 assessed the hypothesis that deletion of the GluR-1 subtype of the alpha-amino-3-hydroxy-5-methyl-4-i

283 ture adjacent to the R/G editing site of the GluR-B pre-mRNA supports deamination of the R/G adenosin

284 triagonist strategy with which to target the GluR, GLP-1R, and NPY2R.

285 different ionic conditions revealed that the GluR channel was equally permeable to Cs+ and Na+ but re

286 nostaining of the IC was most dense with the GluR 2/3 antibody for both strains of animals.

287 Conformational changes within the GluR ligand binding domain were also monitored.

288 tembedding immunoelectron microscopy for the GluRs in adult rats.

289 eralized disruption of the regulation of the GluRs in the DLPFC of females with MDD, with more specif

290 d GCaMP3 to detect Ca(2+) influx through the GluRs revealed little spatial overlap between synapses p

291 Currents through GluR-delta 2(Lc) channels were also potentiated by extra

292 Thus GluR channels appear to be of the AMPA subtype and not t

293 3salpha imparts lateral membrane mobility to GluR complexes.

294 ate receptors (GluRs) and are susceptible to GluR-mediated excitotoxicity.

295 te and B-class GluRs are lost, whereas total GluR levels do not change, resulting in a striking chang

296 es and that within these spines, the various GluRs are differentially distributed between synaptic an

297 channel mRNAs, high levels of GluR-2 versus GluR-1, and a high ratio of NMDAR-2A to NMDAR-2B mRNA.

298 GluR3 is expressed at weak, GluR 6 at moderate and GluR 4 at high levels.

299 impetus to reevaluate prior studies in which GluR and GLP-1R agonists and antagonists were assumed no

300 was found for mEPSCs associating nAChRs with GluRs.