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1 le of glr-3 gene that encodes a kainate-type glutamate receptor.
2 AT5 to serve functionally as an "inhibitory" glutamate receptor.
3 is independent of signaling by metabotropic glutamate receptors.
4 urons, presynaptic ribbons, and postsynaptic glutamate receptors.
5 l synaptic inputs and expression of specific glutamate receptors.
6 rface levels and synaptic clustering of AMPA glutamate receptors.
7 e cells (mGCs) through group II metabotropic glutamate receptors.
8 ropic and metabotropic GABA and metabotropic glutamate receptors.
9 GABA(A/B)-R in combination with metabotropic glutamate receptors.
10 enhanced the expression levels of AMPA-type glutamate receptors.
11 uctural plasticity induced through different glutamate receptors.
12 titive/fast off-rate antagonist of NMDA-type glutamate receptors.
13 , presynaptic release sites and postsynaptic glutamate receptors.
14 roxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptors.
15 n via the activation of group I metabotropic glutamate receptors.
16 c or glutamatergic neurons) and postsynaptic glutamate receptors.
17 among which are the tyrosine kinase Fyn and glutamate receptors.
18 nd high affinity homomeric glycine activated glutamate receptors.
19 o the brain, or effects of KP metabolites on glutamate receptors.
20 able AMPA receptors and group I metabotropic glutamate receptors.
21 sion, modulating the postsynaptic ionotropic glutamate receptors.
22 tion and depression through effects on brain glutamate receptors.
25 we have illustrated the role of metabotropic glutamate receptor 1 (GRM1) in neoplastic transformation
30 ent mutations in the same gene (metabotropic glutamate receptor 1) from two independent natural short
32 ptic G protein-coupled receptor metabotropic glutamate receptor 2 (mGlu(2)) robustly inhibits glutama
34 tion and trafficking of class C metabotropic glutamate receptor 2 (mGluR2) through a mechanism that r
35 and light to control endogenous metabotropic glutamate receptor 2 (mGluR2), a Family C GPCR, in prima
38 s shows increased expression of metabotropic glutamate receptor 2 in THL synaptosomes of RGS4KO mice
44 steric modulators (NAMs) of the metabotropic glutamate receptor 5 (mGlu(5)) hold great promise for th
45 increases signaling through the metabotropic glutamate receptor 5 (mGlu5) receptor within the BNST in
46 res to investigate the role for metabotropic glutamate receptor 5 (mGlu5) signaling within the BNST i
47 l dopamine D(2/3) receptors and metabotropic glutamate receptor 5 (mGluR5) and assessed decision maki
51 tic glutamate, which stimulates metabotropic glutamate receptor 5 (mGluR5) on a small population of i
52 mental expression of astroglial metabotropic glutamate receptor 5 (mGluR5), a major receptor in media
56 uivalent PKC regulatory site in metabotropic glutamate receptor 5 (Ser-839) aligns not with CaS(T888)
59 receptors, P2Y1 ATP receptors, metabotropic glutamate receptor 5, and TRP channels did not prevent t
60 glutamatergic transmission, the metabotropic glutamate receptor 6 and voltage-dependent calcium chann
61 bioavailable and CNS-penetrant metabotropic glutamate receptor 7 (mGlu(7)) negative allosteric modul
62 presynaptic components: mGluR7 (metabotropic glutamate receptor 7) and GluK2-KARs (kainate receptors
66 uscular junction, inhibition of postsynaptic glutamate receptors activates retrograde signaling that
67 ntersecting, signaling pathways that involve glutamate receptor activation in striatal neurons, as we
68 nner, with postsynaptic Group 1 metabotropic glutamate receptor activation triggering long-lasting pl
70 This study sought to further characterize glutamate receptor adaptations in NAc core during metham
72 oxazolepropionic acid (AMPA)-type ionotropic glutamate receptors (AMPA receptors) predetermines respo
74 -methyl-4-isoxazolepropionic acid(AMPA)-type glutamate receptors (AMPARs) are the predominant excitat
76 oxy-5-methyl-4-isoxazolepropionic acid)-type glutamate receptors (AMPARs) in the adult R59X hippocamp
81 sity protein-95 (PSD-95) localizes AMPA-type glutamate receptors (AMPARs) to postsynaptic sites of gl
82 is largely mediated by AMPA-type ionotropic glutamate receptors (AMPARs), which are activated by the
88 some of these spines are immunopositive for glutamate receptor and postsynaptic density proteins (vi
89 eural signalling (specifically an ionotropic glutamate receptor and two regucalcins), and overall our
90 connected with genetic variants of synaptic glutamate receptors and associated PDZ-binding proteins.
91 rexins and postsynaptic AMPA-type ionotropic glutamate receptors and induced the formation of excitat
92 h g-protein coupled GABA(B) and metabotropic glutamate receptors and involved an increase in postsyna
94 NA editing sites in genes encoding AMPA-type glutamate receptors and postsynaptic density proteins we
95 nding gating across the family of ionotropic glutamate receptors and the role of AMPA receptors in ex
96 en shown to directly inhibit AMPA receptors (glutamate receptors), and to change cell energetics thro
97 rgeting multiple ionotropic and metabotropic glutamate receptors, and intracellular cascades involved
98 es attribute an important role to ionotropic glutamate receptors, and it has been suggested that NMDA
99 with a glutamate receptor antibody, and the glutamate receptor antagonist 6-cyano-7-nitroquinoxaline
101 parametric analysis revealed that a group of glutamate receptor antagonists enhances branching and ne
102 used iontophoresis to eject small amounts of glutamate receptor antagonists, aiming to perturb, but n
103 e contact sites have immunoreactivity with a glutamate receptor antibody, and the glutamate receptor
111 everted by blockade of neuronal activity and glutamate receptors, as well as disruption of BDNF-TrkB
112 um channels to a trans-synaptic complex with glutamate receptors at the visual system's first synapse
113 ect can be mimicked by blockade of NMDA-type glutamate receptors but not voltage-gated calcium channe
115 itical for the synaptic trafficking of other glutamate receptors, but we found that its binding to PS
116 epatocyte growth factor receptor (hMET) into glutamate receptors by replacing their extracellular bin
117 D-related genes, ionotropic and metabotropic glutamate receptors, cholinergic enzymes and receptors,
120 findings reveal that calcium signalling via glutamate receptors controls the structure of the endoso
124 owed that activation of group I metabotropic glutamate receptors enhanced spontaneous glutamate relea
125 hyper-methylation and led to the recovery of glutamate receptor expression and excitatory synaptic fu
126 evations and Western blots reveal ionotropic glutamate receptor expression prior to immunocytochemica
128 ta (GluD) receptors belong to the ionotropic glutamate receptor family, yet they don't bind glutamate
129 c compartment of mutant NMJs include reduced glutamate receptor field size, and altered glutamate rec
130 binding profiles for these newly identified glutamate receptors, for example, kainate receptors on w
131 ary and sufficient to up-regulate ionotropic glutamate receptors from a pool of different receptors e
132 ines regulation of neuronal excitability via glutamate receptor function and neuroinflammation via ot
134 ogical manipulations of Group 1 metabotropic glutamate receptors (G1 mGluRs) demonstrated that G1 mGl
135 esponsiveness and the link between PMCA2 and glutamate receptors, GABA receptors (GABARs), and glutam
136 exosome-secreted miRNAs in the regulation of glutamate receptor gene expression and their relevance f
138 yer-wise transcriptional changes in multiple glutamate receptor genes and strong upregulation of gene
139 tease 46 (USP-46) removes ubiquitin from the glutamate receptor GLR-1 and regulates its trafficking a
145 owing that FMRP couples Group I metabotropic glutamate receptor (GpI mGluR) signaling to protein tran
146 c transmission is mediated by the ionotropic glutamate receptor homolog cation channel, delta glutama
147 ry synapses is determined by the presence of glutamate receptors (i.e. AMPA, NMDA, and kainate recept
154 ween Wnt receptors, activation of ionotropic glutamate receptors (iGluRs), and localized calcium tran
157 role of synaptic trafficking of AMPA-type of glutamate receptors in HSP, Mecp2 KO neurons have lower
158 several full-length structures of ionotropic glutamate receptors in putative desensitized states were
160 trol the trafficking of group I metabotropic glutamate receptors in the central nervous system have n
164 elf-administration of cocaine increases AMPA glutamate receptors in the VTA, and this effect enhances
165 Excitatory neurotransmission meditated by glutamate receptors including N-methyl-D-aspartate recep
166 at helped unravel the key role of ionotropic glutamate receptors, including the kainate receptor, in
168 al measures to demonstrate that metabotropic glutamate receptor-induced sensitization of TRPA1 nocice
169 the GluA2 subunit of the AMPAR and requires glutamate receptor interacting protein 1 (GRIP1) interac
170 76 is necessary for synaptic accumulation of glutamate receptor interacting protein 1 (GRIP1), a cruc
173 ing in identification of numerous eukaryotic glutamate receptor ion channels in the animal kingdom of
176 s of ligand binding, and that the biology of glutamate receptors is more complex than first anticipat
177 bition of the NMDA subtype of the ionotropic glutamate receptors is well characterized, the mechanism
178 o-agonist of the N-methyl-D-aspartate (NMDA) glutamate receptor, is potentially effective as a depres
179 ptic development, kainate-type of ionotropic glutamate receptors (KARs) are highly expressed in the B
180 in synaptic scaffolding proteins, studies of glutamate receptor levels and function are limited.
181 namics simulations of the GluA2 AMPA subtype glutamate receptor ligand-binding domain (LBD) dimers to
182 R2 and excitatory light-activated ionotropic glutamate receptor LiGluR yielded a distribution of expr
184 activates Ca(2+)-containing ion currents via GLUTAMATE RECEPTOR-LIKE (GLR) channels in root protoplas
185 of 1.0-cm stem sections from mutants lacking GLUTAMATE RECEPTOR-LIKE 3.5 or the mutants deficient in
186 tion of both GLR3.3 and GLR3.6, which encode glutamate receptor-like proteins (GLRs), or constitutive
187 ting membrane potential, type-1 metabotropic glutamate receptors locally enhance Ca(2+) influx mediat
191 N-methyl-d-aspartate (NMDA)-type ionotropic glutamate receptors mediate excitatory neurotransmission
192 isoxazole propionic acid)-subtype ionotropic glutamate receptors mediate fast excitatory neurotransmi
194 on reduced inhibitory GABA(A) and excitatory glutamate receptor-mediated synaptic transmission in the
195 f research have shown how phosphorylation of glutamate receptors mediates protein binding and recepto
196 te release and reversal behavior require the glutamate receptor MGL-2/mGluR5, expressed in RIM and ot
197 ons through a G protein-coupled metabotropic glutamate receptor, MGL-1, to release local search.
199 anslation downstream of group I metabotropic glutamate receptors (mGlu1/5) is a core pathophysiology
201 its distribution overlaps with metabotropic glutamate receptor (mGluR) 5 in regional brain circuitri
204 steady state and in response to metabotropic glutamate receptor (mGluR) stimulation, but the proteins
205 ation of one particular GPCR, a metabotropic glutamate receptor (mGluR), can reduce cone synaptic tra
208 onist activation of the group I metabotropic glutamate receptor mGluR1 increases the strength of this
210 on requires the activity of the metabotropic glutamate receptor, mGluR1, which is known to couple wit
211 signals are mediated by type-1 metabotropic glutamate receptors (mGluR1s) when the CF input is delay
213 Stimulation of the postsynaptic metabotropic glutamate receptor mGluR5 triggers retrograde signaling
214 alization of beta-DG with dystrophin and the glutamate receptor mGluR6 is disrupted, and the post-syn
215 execution, EAAC1 limits group I metabotropic glutamate receptor (mGluRI) activation, facilitates D1 d
216 that EAAC1 limits activation of metabotropic glutamate receptors (mGluRIs) in the striatum and, by do
217 he class C GPCRs, which include metabotropic glutamate receptors (mGluRs) and gamma-aminobutyric acid
221 e two distinct release modes by metabotropic glutamate receptors (mGluRs) constitutes critical suppor
231 ocalization of the N-methyl-D-aspartate type glutamate receptor (NMDAR) to dendritic spines is essent
232 pression regulates N-methyl-D-aspartate-type glutamate receptor (NMDAR)-dependent long-term potentiat
233 al synaptic responses, mediated by NMDA-type glutamate receptor (NMDARs) activation, form the cellula
237 Contributions of N-methyl-D-aspartate-type glutamate receptors (NMDARs) to cDCS-mediated plasticity
240 FF bipolar cells, and the novel metabotropic glutamate receptors of ON bipolar-cell dendrites, are bo
241 Here, we report that chronic blockade of glutamate receptors of the AMPA and NMDA types in hippoc
243 d by blockade of N-methyl-D-aspartate (NMDA) glutamate receptors, our experiments demonstrate that at
244 bserve that antagonism of NMDA and AMPA type glutamate receptors protects neurons from condition medi
245 portant in memory-related processes, such as glutamate receptor recycling, we also identified altered
247 ols highlighted canonical pathways involving glutamate receptor signaling and glutathione-mediated de
248 toxicity in AD, suggesting that targeting of glutamate receptor signaling may be a promising approach
250 harmacological specificity that metabotropic glutamate receptor signaling triggers opening of GluD2.
252 sis revealed that messenger RNAs involved in glutamate receptor signalling are enriched as miR-27a-3p
254 ine exposure, we identified the metabotropic glutamate receptor subtype 4 (mGluR4) as a promising pha
255 e discovered that expression of metabotropic glutamate receptor subtype 5 (mGluR5) in the VMH is regu
256 sruptive have been proposed and metabotropic glutamate receptor subtype 5 (mGluR5) represents one suc
258 of N-methyl-d-aspartate receptor (NMDAR), a glutamate receptor subtype and is involved in NMDAR-medi
259 e assessed the role of group II metabotropic glutamate receptor subtypes 2 (mGlu(2)) and 3 (mGlu(3))
260 Non-selective antagonists of metabotropic glutamate receptor subtypes 2 (mGlu(2)) and 3 (mGlu(3))
261 The identification of AMPA, kainate and NMDA glutamate receptor subtypes by Watkins and colleagues un
262 ortex depend on synaptic mobilization of the glutamate receptor subunit A1 (GluA1) mediated by GR-PO(
263 CANCE STATEMENT We report novel roles of the glutamate receptor subunit GluA3 in synaptic transmissio
264 beta, serotonin receptors (Htr1a, Htr2a) and glutamate receptor subunit Grin2b, were modified in the
265 deficiency in muscles specifically increased glutamate receptor subunit IIA (GluRIIA) level and the f
267 e (R59X), to investigate changes in synaptic glutamate receptor subunits and functional consequences.
268 gatively controls the synaptic levels of the glutamate receptor subunits GluRIIA, GluRIIC, and GluRII
269 o the understanding of the biology driven by glutamate receptors such as GRIK5 (also referred to as G
270 thyl-d-aspartate receptors in the ionotropic glutamate receptor superfamily have been targeted for th
271 ARs) constitute a subclass of the ionotropic glutamate receptor superfamily, which functions as gluta
274 Rs) are a subtype of postsynaptic ionotropic glutamate receptors that function as molecular coinciden
275 ess kainate receptors (KARs), a subfamily of glutamate receptors that modulate neurite outgrowth and
276 s the remodeling of the ionotropic AMPA-type glutamate receptors that underlie fast excitatory synapt
277 (TARPs), which mediate binding of AMPA-type glutamate receptors to PSD-95, was increased in young Sy
278 s a coordinated synthesis and trafficking of glutamate receptors to the cell surface that facilitate
279 tion of protein synthesis and trafficking of glutamate receptors to the cell surface, where they are
280 ctive excitatory synapses by recruiting AMPA glutamate receptors to the postsynaptic cell surface.
281 that sAPPalpha facilitated LTP via regulated glutamate receptor trafficking and de novo protein synth
282 esults highlight the diversity of ionotropic glutamate receptor trafficking rules at a single type of
284 gest that disrupted epigenetic regulation of glutamate receptor transcription underlies the synaptic
285 ory neurotransmitter in the CNS, but not all glutamate receptors transmit fast excitatory signals at
286 mulation of a dimeric GPCR, the metabotropic glutamate receptor type 1 (mGluR1), by two entirely diff
287 textual fear learning induced a metabotropic glutamate receptor type 1 (mGluR1)-mediated late long-te
289 strocytes through activation of metabotropic glutamate receptor type 5 (mGluR5) signaling and that th
291 , we determined the average quantity of each glutamate receptor type, their nanoscale organization, a
292 ignaling through ionotropic and metabotropic glutamate receptors, ultimately resulting in synaptic dy
294 itically modified by glycosylation including glutamate receptors, voltage-gated calcium channels, the
296 -223, an exosome-secreted miRNA that targets glutamate receptors, was increased at the mature miRNA l
297 s involved in neuronal signalling (including glutamate receptors), which was reversed by EHMT1/2 inhi
298 tors (KARs) consist of a class of ionotropic glutamate receptors, which exert diverse pre- and postsy
299 hippocampus proper, also express ionotropic glutamate receptors, which might provide additional sodi
300 A receptors are ionotropic calcium-permeable glutamate receptors with a voltage-dependence mediated b