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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
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
14 s high levels of pS6 and demonstrate altered GluR subunit composition, resembling those of normal imm
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
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 levels of AMPA receptor subunits GluR-1 and GluR-4 are rapidly decreased in cultured rat hippocampal
24 fluenced by the degree of brain maturity and GluR subtype stimulation, independent of the severity of
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
31 most strongly concentration dependent of any GluR subtype and, except for low Ca(2+) concentrations,
34 ts its cytoskeletal association, attenuating GluR endocytosis and affecting the efficacy of synaptic
38 ule and putative microglia labeled with both GluR 5/6/7 and GluR 2/3 but not NMDAR 1 subunit antisera
39 ) = 33% of that of AnTx) that was blocked by GluR antagonists, supporting a model in which alpha7 nAC
40 retardation 1 (dfmr1) null mutants, A-class GluRs accumulate and B-class GluRs are lost, whereas tot
41 ts, there is an additive increase in A-class GluRs, and a similar additive impact on B-class GluRs, t
42 utants, A-class GluRs accumulate and B-class GluRs are lost, whereas total GluR levels do not change,
47 ted, including the glutamate receptor Dflop (GluR-Dflop) subunit of AMPA receptors and members of the
48 entially regulate the abundance of different GluR subclasses in a convergent mechanism within individ
49 the extensive distribution of the different GluR subunit mRNAs strengthen the view that glutamate is
52 tion training session, when conducted during GluR subunit overexpression, attenuates stress-induced r
55 l relationships between GluR0 and eukaryotic GluRs, we propose that a prokaryotic GluR was the precur
59 mRNAs suggests that many neurons can express GluR channels that belong to different families, which w
60 Cryostat-sectioned tissue revealed extensive GluR 5/6/7-like immunoreactivity throughout the neuropil
65 nsistent with previous reports of a role for GluR-A-dependent plasticity in hippocampus-dependent, sp
69 ice lacking the AMPA receptor subunit GluR1 (GluR-A) have deficits in hippocampal CA3-CA1 long-term p
72 es powerful new evidence linking hippocampal GluR-A-dependent synaptic plasticity to rapid, flexible
73 s, and IRAK/pelle kinase specifically impair GluR levels, assayed immunohistochemically and electroph
74 demonstrates cell-specific abnormalities in GluR expression that may contribute to seizure pathogene
78 ress lower pS6 levels and display changes in GluR subunit expression that are distinct from the patte
79 These results imply that the SWM deficit in GluR-A-/- mice is not due to increased susceptibility to
80 are consistent with pore-forming domains in GluR and K+ channels having a similar structure but inve
83 lexible spatial working memory impairment in GluR-A(-/-) mice, which might also underlie their mild d
86 mologous substitutions of the conserved R in GluR-B(o), GluR-A(i) and the kainate receptor GluR-6 sub
87 our results indicate that the M3 segment in GluR does not contain a glycine gating hinge and suggest
89 mined the functional role of the Q/R site in GluR-delta 2(Lc) by replacing glutamine with arginine.
90 expression of GFP-tagged GluR-A subunits in GluR-A-deficient mice rescues SWM, paralleling its rescu
91 , and subcellular distribution of ionotropic GluR subunits within the primary afferent and local syna
93 vation of glomerular mAChRs, with ionotropic GluRs and nAChRs blocked, increased IPSCs in MTCs and ET
95 wo negative residues C-terminal to M3 in KAR GluR-6(Q) subunits had no effect on Ca2+ permeability.
97 found in association with other full-length GluRs in the mouse brain and cultured primary neurons.
100 studies using tasks such as the water maze, GluR-A(-/-) mice were unimpaired during acquisition of t
102 ttermate controls in the type 1 metabotropic GluR (mGluR1), mGluR2, mGluR3, but not the mGluR5 subtyp
107 ptor, the AMPA, kainate and the metabotropic GluRs may be targets for the development of rapidly acti
109 ls of GluR-delta2 with the Lurcher mutation (GluR-delta 2(Lc)) expressed in human embryonic kidney 29
111 pose that the M3 segments in two neighboring GluR subunits are kinked within SYTANLAAF in opposite di
114 ntrastriatal injections of non-NMDA and NMDA GluR agonists were compared to apoptosis, as established
115 that rodent OLs also express functional NMDA GluRs (NMDARs), and overactivation of these receptors ca
119 pport our previous report that nonfunctional GluRs are retained intracellularly by a functional check
121 residues in the GluR3B region define a novel GluR subunit-specific agonist binding site and impart su
122 bstitutions of the conserved R in GluR-B(o), GluR-A(i) and the kainate receptor GluR-6 subunits produ
124 iption-polymerase chain reaction analyses of GluR-B RNA from dissected regions of rat brain showed si
126 y signaling in the brain and are composed of GluR principal subunits and transmembrane AMPA receptor
129 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
133 ernatively spliced flip and flop isoforms of GluR-B RNA varied among the choroid plexus, cortex, hipp
135 and L-type Ca channel mRNAs, high levels of GluR-2 versus GluR-1, and a high ratio of NMDAR-2A to NM
137 bstitution of the only two glycines in M3 of GluR-A with alanines produced channels with gating prope
140 by differential spatio-temporal patterns of GluR expression, by alternative RNA splicing and editing
142 ivo, and implicates AP2 in the regulation of GluR trafficking at an early step in the secretory pathw
147 on is determined by the cytoplasmic tails of GluR subunits, and in heteromeric receptors, GluR1 acts
148 ng/scaffold proteins functioning upstream of GluR localization are also grossly reduced or mislocaliz
149 athrin adaptor in promoting the abundance of GluRs at synapses in vivo, and implicates AP2 in the reg
150 vated glutamate, the excessive activation of GluRs causes internalization of pathologic levels of Ca(
155 tetramers and that the gating mechanisms of GluRs and potassium channels have some essential feature
156 rain is a consequence of a reduced number of GluRs in cell membranes transplanted from the AD brain.
157 units, the cytoplasmic to synaptic ratios of GluRs were measured within thalamo-amygdaloid spines.
160 uRA overexpression causes the exact opposite GluR phenotype to the dfmr1 null, confirming postsynapti
162 reating GluR3salpha) co-assembled with other GluR subunits and decreased receptor function in Xenopus
163 amed state and that modulation of peripheral GluRs reduces pain behaviors and nociceptor activity.
164 cological agents that will target peripheral GluRs, offering novel approaches to treatment of pain of
170 fusion of outside-out patches containing rat GluR-A or GluR6 subunits excised from transfected human
171 vidly and selectively binds to AMPA receptor GluR subunits and also binds to the AMPA receptor cluste
173 luR-B(o), GluR-A(i) and the kainate receptor GluR-6 subunits produced comparable but less visible eff
174 tor A (GluR-A) subunit of the AMPA receptor (GluR-A-/- mice) display normal spatial reference memory
177 e, we show that subunits glutamate receptor (GluR) 5 and GluR6 play distinct roles in kainate-induced
178 ist, bind selectively to glutamate receptor (GluR) 5 but not to the KA2 KAR subunit, we used molecula
180 and metabotropic (mGluR) glutamate receptor (GluR) activation and K+ depolarization was examined in c
181 gnals include changes in glutamate receptor (GluR) activation, changes in firing rate, or changes in
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
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
197 calization of ionotropic glutamate receptor (GluR) subunits was examined with light and electron micr
198 nto LA spines expressing glutamate receptor (GluR) subunits, but the GluR subunit distribution at the
201 rebellar neuromodulators glutamate receptor (GluR)-6, kainate-preferring glutamate receptor subunit-2
202 orking memory deficit in glutamate receptor (GluR)-A (GluR1) AMPA receptor subunit knockout mice.
203 in (ABP) and the related glutamate receptor (GluR)-interacting protein (GRIP), two multi-PDZ proteins
206 quantitatively analyzed glutamate receptor (GluR)1, GluR2/3, and GluR4 AMPA subunit immunoreactivity
207 er relative abundance of glutamate receptor (GluR)2 transcript and much lower levels of GluR2 immunor
208 ncoding the B subunit of glutamate receptor (GluR-B) has two functionally important editing sites (Q/
209 mutations in the orphan glutamate receptor, GluR delta2, a gene selectively expressed in Purkinje ne
211 cid (NMDA) and non-NMDA glutamate receptors (GluR) results in a spectrum of morphologically distinct
212 now studied the properties of Glu receptors (GluRs) from the cerebral cortices of AD and non-AD brain
214 (OLs) express non-NMDA glutamate receptors (GluRs) and are susceptible to GluR-mediated excitotoxici
216 tropic and metabotropic glutamate receptors (GluRs) are based on an azobenzene photoswitch that is op
217 have demonstrated that glutamate receptors (GluRs) are concentrated at postsynaptic sites in vivo an
220 the CNS kainate subtype glutamate receptors (GluRs) are likely to be heteromeric assemblies containin
223 lepropionic acid (AMPA) glutamate receptors (GluRs) from postsynaptic elements has been proposed as a
225 al studies of models of glutamate receptors (GluRs) have been limited to monomeric models of the liga
226 undance of postsynaptic glutamate receptors (GluRs) in Drosophila neuromuscular junctions is controll
229 g subtype of ionotropic glutamate receptors (GluRs) is a hetero-oligomeric ion channel assembled from
230 As the trafficking of glutamate receptors (GluRs) is thought to underlie some forms of synaptic pla
232 ediated by cell surface glutamate receptors (GluRs) of the AMPA subtype has been demonstrated as one
233 group III metabotropic glutamate receptors (GluRs) play in modulating transmission at the striatopal
236 ic acid (AMPA) class of glutamate receptors (GluRs) with different calcium permeabilities has been pr
237 rts Ca2+ influx through glutamate receptors (GluRs) with single-impulse and single-bouton resolution.
238 a subunit of ionotropic glutamate receptors (GluRs) with unknown natural ligands and channel properti
239 stimulating ionotropic glutamate receptors (GluRs) within the nucleus accumbens core or shell would
240 mM kynurenate (Kyn) for glutamate receptors (GluRs), and 100 microM Cd2+ for all chemical synapses) w
241 itization of ionotropic glutamate receptors (GluRs), specifically the AMPA receptor subtype, shapes t
243 n mutants lacking GLR-1 glutamate receptors (GluRs); however, mutations eliminating the egl-3 PC2 res
245 onic mutant synapses exhibit greatly reduced GluR function, and a corresponding loss of localized Glu
248 ty of this residue varies between respective GluR subunits, this suggested that this residue may be i
249 munocytochemistry to localize AMPA selective GluR 2/3 subunits (GluR2/3) and NMDA receptor subunit 1
250 LPFC of females with MDD, with more specific GluR alterations in the suicides and in the male groups.
253 geted mice lacking the AMPA receptor subunit GluR-A (also called GluR1 encoded by the gene Gria1,) ha
254 ckout mice lacking the AMPA receptor subunit GluR-A (GluR1), wild-type controls, mice with cytotoxic
257 report that levels of AMPA receptor subunits GluR-1 and GluR-4 are rapidly decreased in cultured rat
258 localize glutamate receptor (GluR) subunits (GluR 5/6/7, GluR 2/3 and N-methyl-D-aspartate receptor 1
259 g the AMPA-type glutamate receptor subunits (GluRs) 1 and 2 are localized to dendrites of hippocampal
260 on of AMPA-type glutamate receptor subunits (GluRs) in the nucleus accumbens (NAc), a key component o
265 forebrain-localized expression of GFP-tagged GluR-A subunits in GluR-A-deficient mice rescues SWM, pa
268 n channels have a similar architecture, that GluRs are tetramers and that the gating mechanisms of Gl
270 to their performance during acquisition, the GluR-A(-/-) mice displayed a mild deficit during reversa
271 f the membrane electric potential across the GluR channel pore, we recorded from alpha-amino-3-hydrox
272 glutamate receptor (GluR) subunits, but the GluR subunit distribution at the synapse and within the
274 ning M2 and M3 cysteine substitutions in the GluR-A subunit and measured the voltage dependence of th
277 docytic adaptor, we found that levels of the GluR GLR-1 are decreased at synapses in the ventral nerv
279 t while the differential distribution of the GluR subtypes may reflect distinct roles for their invol
280 assessed the hypothesis that deletion of the GluR-1 subtype of the alpha-amino-3-hydroxy-5-methyl-4-i
281 ture adjacent to the R/G editing site of the GluR-B pre-mRNA supports deamination of the R/G adenosin
282 different ionic conditions revealed that the GluR channel was equally permeable to Cs+ and Na+ but re
287 eralized disruption of the regulation of the GluRs in the DLPFC of females with MDD, with more specif
288 d GCaMP3 to detect Ca(2+) influx through the GluRs revealed little spatial overlap between synapses p
289 d rat RED1, were analyzed in vitro for their GluR B subunit (GluR-B) RNA editing site selectivity.
292 ggest that Ca2+ signaling pathways linked to GluR activation and membrane depolarization may be impor
293 t ethanol modulates Ca2+ signaling linked to GluR activation in a receptor subtype specific manner, a
296 te and B-class GluRs are lost, whereas total GluR levels do not change, resulting in a striking chang
297 es and that within these spines, the various GluRs are differentially distributed between synaptic an
298 channel mRNAs, high levels of GluR-2 versus GluR-1, and a high ratio of NMDAR-2A to NMDAR-2B mRNA.
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