ライフサイエンスコーパス: AMPA receptor

1 te, providing the first view of an activated AMPA receptor.

2 decreased constitutive endocytosis of GluA1-AMPA receptor.

3 tate is the desensitized state of the intact AMPA receptor.

4 from Ca(2+)-impermeable to Ca(2+)-permeable AMPA receptors.

5 ate receptors (mGluRs) and Ca(2+) -permeable AMPA receptors.

6 h disordered regulation of calcium-permeable AMPA receptors.

7 inant rat GluA1-3, at GluK1-3, and at native AMPA receptors.

8 tors, it is necessary for the recruitment of AMPA receptors.

9 osed to be silent, but most are labelled for AMPA receptors.

10 he amino-terminal domains of GluA2 and GluA3 AMPA receptors.

11 presynaptic Ca(2+) channels and postsynaptic AMPA receptors.

12 rons via synaptic insertion of GluA2-lacking AMPA receptors.

13 in, a trafficking chaperone and modulator of AMPA receptors.

14 ed trans-synaptic regulation of postsynaptic AMPA receptors.

15 venting activity-driven membrane delivery of AMPA receptors.

16 hosphorylation of striatal GluA1 subunits of AMPA receptors.

17 uce postsynaptic AP firing in the absence of AMPA receptors.

18 reduced levels of membrane GluA1-containing AMPA receptors.

19 hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) receptors.

20 -hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors.

21 n both regions were dependent upon GABAA and AMPA receptor activation but NMDA receptor blockade decr

22 eurons in this area are primed for increased AMPA receptor activation upon withdrawal.

23 pothesized that IVH damages white matter via AMPA receptor activation, and that AMPA-kainate receptor

24 apses showed a decrease in calcium-permeable AMPA receptors after cocaine, but no change in the AMPA-

25 nd selective antagonists of Ca(2+)-permeable AMPA receptors also blocked the potentiation of AMPA-med

26 light responses in the sustained cells, the AMPA receptors also mediated a portion of the responses

27 perior olive (LSO) principal neurons receive AMPA receptor (AMPAR) - and NMDA receptor (NMDAR)-mediat

28 role during synapse development to regulate AMPA receptor (AMPAR) and PSD-95 content at excitatory s

29 The modulation of AMPA receptor (AMPAR) content at synapses is thought to

30 Previous studies tracking AMPA receptor (AMPAR) diffusion at synapses observed a l

31 elicit changes in synaptic efficacy through AMPA receptor (AMPAR) endocytosis.

32 aptic strength can result from modulation of AMPA receptor (AMPAR) function and trafficking to synapt

33 Regulation of AMPA receptor (AMPAR) function is a fundamental mechanis

34 AMPA receptor (AMPAR) function is modulated by auxiliary

35 Regulation of AMPA receptor (AMPAR) membrane trafficking is critical f

36 The number of AMPA receptor (AMPAR) miniature events was reduced by de

37 n this region by two forms of post-ischaemic AMPA receptor (AMPAR) plasticity - namely, anoxic long-t

38 ven effects measured in these mice depend on AMPA receptor (AMPAR) subunit GluA3.

39 An emerging model posits that the GluA2 AMPA receptor (AMPAR) subunit may be important for the b

40 tional responses are mediated in part by NAc AMPA receptor (AMPAR) transmission, and recent work show

41 gration in the LSO, so that 1 week later the AMPA receptor (AMPAR)-EPSC decay was slowed and mRNA for

42 otine selectively increased the amplitude of AMPA receptor (AMPAR)-mediated current and AMPA/NMDA rat

43 icient neurons exhibit significantly reduced AMPA receptor (AMPAR)-mediated currents and cell-surface

44 We pioneer the first description of AMPA receptor (AMPAR)-mediated currents in the PNS glia

45 Regulation of AMPA receptor (AMPAR)-mediated synaptic transmission is

46 w that cocaine self-administration generates AMPA receptor (AMPAR)-silent excitatory synapses within

47 inistration, we observed increased levels of AMPA receptor (AMPAR)-silent glutamatergic synapses in t

48 DAR)-mediated synaptic currents and decrease AMPA receptor (AMPAR)/NMDAR ratios in midbrain dopamine

49 ed synaptic accumulation of GluA2-containing AMPA receptors (AMPAR), but the receptor trafficking ste

50 re and used a patch-clamp technique to study AMPA-receptor (AMPAR)-mediated currents in SCs for the f

51 The amino-terminal domain (ATD) of AMPA receptors (AMPARs) accounts for approximately 50% o

52 AMPA receptors (AMPARs) are glutamate-gated cation chann

53 Most AMPA receptors (AMPARs) are heteromeric complexes of sub

54 AMPA receptors (AMPARs) are tetrameric ion channels that

55 AMPA receptors (AMPARs) are the major excitatory recepto

56 aintaining an optimal number of postsynaptic AMPA receptors (AMPARs) at each synapse of a given neuro

57 However, the degree to which NAc AMPA receptors (AMPARs) contribute to somatic and affect

58 Glutamatergic synapses rely on AMPA receptors (AMPARs) for fast synaptic transmission a

59 ctivation of two plasticity-related targets: AMPA receptors (AMPARs) for memory acquisition and short

60 e Thorase to regulate the internalization of AMPA receptors (AMPARs) in order to selectively manipula

61 s, the rapid endocytosis of GluA2-containing AMPA receptors (AMPARs) in response to NMDA receptor (NM

62 Activation of AMPA receptors (AMPARs) in the nucleus accumbens is nece

63 Dynamic trafficking of AMPA receptors (AMPARs) into and out of synapses plays a

64 Membrane trafficking of AMPA receptors (AMPARs) is critical for neuronal functio

65 amatergic synapses, high and low activity of AMPA receptors (AMPARs) is observed when pore-forming su

66 AMPA receptors (AMPARs) mediate fast excitatory neurotra

67 the core of LTP is the synaptic insertion of AMPA receptors (AMPARs) triggered by the NMDA receptor-d

68 I), which phosphorylates GluA1, a subunit of AMPA receptors (AMPARs), and promotes hippocampal long-t

69 e auxiliary subunits control the function of AMPA receptors (AMPARs), but the underlying mechanisms r

70 mission by promoting the removal of synaptic AMPA receptors (AMPARs), dendritic spine loss, and synap

71 he similarity between the LBDs of NMDARs and AMPA receptors (AMPARs), GluN2A PAMs with good selectivi

72 y the recruitment of additional postsynaptic AMPA receptors (AMPARs), sourced either from an intracel

73 the C-terminal domains (CTDs) of endogenous AMPA receptors (AMPARs), the principal mediators of fast

74 naptic plasticity, and synaptic targeting of AMPA receptors (AMPARs), which mediate the vast majority

75 g the activation of PKA and GluA1-containing AMPA receptors (AMPARs).

76 moting surface insertion and/or retention of AMPA receptors (AMPARs).

77 by increasing the abundance of postsynaptic AMPA receptors (AMPARs).

78 onductance, rapidly gating, GluA4-containing AMPA receptors (AMPARs).

79 t al. (2017) dissect the interaction between AMPA receptors and auxiliary (TARP) subunits, revealing

80 ved in the ubiquitination and degradation of AMPA receptors and cognition.

81 s processed differentially by starbursts via AMPA receptors and DSGCs via NMDA receptors.

82 requires co-activation of Ca(2+) -permeable AMPA receptors and group I metabotropic glutamate recept

83 h the binding of glutamate to the ionotropic AMPA receptors and metabotropic glutamate receptor 1 and

84 tic activation most sodium entry was through AMPA receptors and not through NMDA receptors or through

85 g to phosphorylation of serine S845 on GluA1 AMPA receptors and their trafficking to the plasma membr

86 -hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor and mammalian target of rapamycin (mTOR)

87 nds on Ca(2+) entry through Ca(2+)-permeable AMPA receptors, and has been labeled anti-Hebbian LTP.

88 A selective TARP gamma-8-dependent AMPA receptor antagonist (TDAA) is an innovative approac

89 irst time, the discovery of a noncompetitive AMPA receptor antagonist that is dependent on the presen

90 All effects of ketamine were abolished by AMPA receptor antagonists and mimicked by the AMPA-posit

91 gy, not previously seen for amino acid-based AMPA receptor antagonists, X-ray crystal structures of b

92 mpairment associated with non-TARP-dependent AMPA receptor antagonists.

93 Although efficacious, AMPA-receptor antagonists, including perampanel (Fycompa

94 ing the keywords autoimmune encephalitis and AMPA receptor antibodies until February 15, 2015.

95 Unitary EPSCs were small and brief (AMPA receptor, approximately 1 nS, approximately 1 ms; N

96 stsynaptic NMDA receptors are absent and the AMPA receptors are Ca(2+) -impermeable; postsynaptic vol

97 Gated by the neurotransmitter glutamate, AMPA receptors are critical for synaptic strength, and d

98 AMPA receptors are glutamate-gated cation channels assem

99 AMPA receptors are important for excitatory synaptic tra

100 he absence of GluN2B, the synaptic levels of AMPA receptors are increased and accompanied by decrease

101 due to activation of putative extrasynaptic AMPA receptors as their antagonism blocked DHK responses

102 NBQX mirrors the differential sensitivity of AMPA receptors associated with the transmembrane AMPA re

103 Ca(2+) permeable, making them distinct from AMPA receptors at most principal cell synapses.

104 nced relative expression of Ca(2+)-permeable AMPA receptors at muscle afferent synapses drives greate

105 is generally weaker than the association of AMPA receptor ATD dimers, but both show a general patter

106 Taking advantage of an AMPA receptor auxiliary protein, TARP gamma-8, which is

107 ity-dependent palmitoylation of the atypical AMPA receptor auxiliary transmembrane protein SynDIG1 re

108 ectron microscopy to solve the structures of AMPA receptor-auxiliary subunit complexes in the apo, an

109 diated by enhanced recycling of internalized AMPA receptors back to the postsynaptic membrane.

110 Hyperpolarizing current injection, but not AMPA receptor blockade, prevents synaptic stimulation fr

111 facilitated the phosphorylation of NMDA and AMPA receptors by protein kinase A.

112 by the receptor-specific antagonist AP-7 or AMPA receptors by the receptor-specific antagonist NBQX

113 gest that Ca(2+) influx via Ca(2+)-permeable AMPA receptors can elicit a rapid form of postsynaptic p

114 s previously overlooked site proximal to the AMPA receptor channel gate.

115 Ionic currents through AMPA receptor channels can be allosterically regulated v

116 We propose that the inhibitors stabilize the AMPA receptor closed state by acting as wedges between t

117 In mature neurons AMPA receptors cluster at excitatory synapses primarily

118 Glypican 4 induces release of the AMPA receptor clustering factor neuronal pentraxin 1 fro

119 Within the postsynaptic density, however, AMPA receptors coassemble with transmembrane AMPA recept

120 on the formation of the PLP-alphav integrin-AMPA receptor complex in vivo and whether complex format

121 We built structural models of TARP-AMPA receptor complexes for TARPs gamma2 and gamma8, com

122 emonstrate that EAAT4 loss, but not abnormal AMPA receptor composition, in young beta-III-/- mice und

123 s where it regulates spine morphogenesis and AMPA receptor confinement.

124 lectively antagonized recombinant and native AMPA receptors containing gamma-8, but not gamma-2 (cere

125 hat the high-open-probability gating mode of AMPA receptors containing the auxiliary subunit transmem

126 The rectification properties of such AMPA receptors contribute to the preferential induction

127 OFF bipolar cells, whereas both kainate and AMPA receptors contributed in the other cells.

128 riggers the upregulation of Ca(2+)-permeable AMPA receptor (CP-AMPAR) expression in RGCs of glaucomat

129 ntiation (LTP) and inserts calcium permeable AMPA receptor (CP-AMPAR) for variable periods.

130 imulates the expression of calcium-permeable AMPA receptors (CP-AMPAR) in RGCs, a response that does

131 Calcium-permeable AMPA receptors (CP-AMPARs) are an important group of rec

132 Calcium-permeable AMPA receptors (CP-AMPARs) contribute to various forms o

133 rogressive accumulation of calcium-permeable AMPA receptors (CP-AMPARs) in the nucleus accumbens (NAc

134 this regimen; furthermore, Ca(2+)-permeable AMPA receptors (CP-AMPARs) increase in the NAc core afte

135 this regimen; furthermore, Ca(2+)-permeable AMPA receptors (CP-AMPARs) increase in the NAc core afte

136 f GluA1 subunit-containing calcium-permeable AMPA receptors (CP-AMPARs) to synapses in subregions of

137 in the frequency of excitatory postsynaptic AMPA receptor currents in medium spiny projection neuron

138 wever, the potential for plasticity in their AMPA receptor currents remains largely unknown.

139 is occurs simultaneously with an increase in AMPA receptor currents, suggesting a high-to-low frequen

140 is occurs simultaneously with an increase in AMPA receptor currents, thus suggesting a high-to-low fr

141 rs and potent downregulation of NMDA but not AMPA receptor currents.

142 argazer (stg/stg) mice bearing a presynaptic AMPA receptor defect, but not homozygous tottering (tg/t

143 Drosophila kainate receptor DKaiR1D and the AMPA receptor DGluR1A revealed novel ligand selectivity

144 Surprisingly, the AMPA receptor DGluR1A shows weak activation by its names

145 We modeled AMPA receptor diffusion in synapses where the distributi

146 Consequently loss of RIN1 blocks surface AMPA receptor down-regulation evoked by chemically induc

147 )-sensors for Ca(2+)-dependent exocytosis of AMPA receptors during LTP, and thereby delineate a simpl

148 osomal sorting complex in the trafficking of AMPA receptors during NMDA-receptor-dependent LTP at mat

149 iments verified) that fast calcium-permeable AMPA receptors enable basket cells to respond rapidly, s

150 y of GluR2 to AP2 and subsequently decreases AMPA receptor endocytosis and recycling.

151 or antagonist (ifenprodil) or infusion of an AMPA receptor endocytosis inhibitor (GluA23Y) before rap

152 nections and is a key player in postsynaptic AMPA receptor endocytosis, providing multiple ways of ne

153 educed levels of EEA1, a protein involved in AMPA receptor endocytosis.

154 d reinstatement is mediated by regulation of AMPA-receptor endocytosis in the basolateral amygdala.

155 y fibre inputs to CbN cells generate unitary AMPA receptor EPSCs of approximately 1 nS that decay in

156 ring LTP-inducing stimulation, CCNY inhibits AMPA receptor exocytosis in dendritic spines.

157 , also blocked Ca(2+)-dependent postsynaptic AMPA receptor exocytosis, thereby abolishing LTP.

158 ough downstream PKC-dependent activation and AMPA receptor exocytosis, thus enhancing PV neuronal inh

159 We also observed antagonism of AMPA receptors expressed in hippocampal, but not cerebel

160 s associated with an increase in GluA1/GluA2 AMPA receptor expression and a decrease in GluN2B NMDA r

161 ory transmission and increases GluA2-lacking AMPA receptor expression in D1R-MSNs, while reducing sig

162 ncement of both associative taste memory and AMPA receptor expression in insular cortex.

163 glutamate levels as being a key mediator of AMPA receptor expression in the NAc.SIGNIFICANCE STATEME

164 mutations result in either reduced synaptic AMPA receptor expression or enhanced glutamatergic synap

165 of Kalirin is sufficient to enhance synaptic AMPA receptor expression, and that preventing CaMKII sig

166 ylation of the GluA1 (Thr840) subunit of the AMPA receptor following extinction training.

167 At synapses throughout the mammalian brain, AMPA receptors form complexes with auxiliary proteins, i

168 es in D2-type neurons via internalization of AMPA receptors from pre-existing synapses.

169 removal of high-conducting Ca(2+)-permeable AMPA receptors from synapses, resulting in synaptic depr

170 ss of GLUA1 protein in 5-HT neurons enhances AMPA receptor function and leads to multiple local molec

171 a hub for powerful allosteric modulation of AMPA receptor function that can be used for developing n

172 sed NMDA receptor function with no change in AMPA receptor function.

173 However, how TARPs modulate AMPA receptor gating remains poorly understood.

174 s for introduced mutations at this region on AMPA receptor gating.

175 ene decreased the synaptic expression of the AMPA receptor GluA2 and GluA3 subunits, but not the GluA

176 tors, consistent with an upregulation of the AMPA receptor GluA2 subunit and reduced Ca(2+) permeabil

177 c diet), have been shown to directly inhibit AMPA receptors (glutamate receptors), and to change cell

178 The GluA1 subunit of the AMPA receptor has been implicated in schizophrenia.

179 lts, and the fact that other subunits of the AMPA receptor have already been associated with neurodev

180 In the hippocampus, calcium-permeable AMPA receptors have been found in a restricted subset of

181 ydroxy-5-methylisoxazol-4-yl)propanoic acid (AMPA) receptors have been reported, no such ligands are

182 -induced IVH and evaluated the expression of AMPA receptors in autopsy samples from human preterm inf

183 notropic glutamate receptors and the role of AMPA receptors in excitatory neurotransmission.

184 me activator restored the synaptic levels of AMPA receptors in GluN2B(-/-) neurons and their endocyto

185 chemically induced LTP by detecting surface AMPA receptors in isolated synaptosomes: fluorescence an

186 ndent synaptic localization of GluA2 lacking AMPA receptors in NAc shell MSNs.

187 quired for the activity-dependent removal of AMPA receptors in rat hippocampal pyramidal neurons.

188 lyze the functional role of GLUA1-containing AMPA receptors in serotonergic neurons, we used the Cre-

189 (TDAA) is an innovative approach to modulate AMPA receptors in specific brain regions to potentially

190 esent study, we looked for calcium-permeable AMPA receptors in two distinct populations of neocortica

191 icity in vitro and homeostatic expression of AMPA receptors in vivo in response to chronic or repeate

192 tinct asymmetry: here, feed-forward drive at AMPA receptors increases in the presence of decreased NM

193 ces the interaction between neuroligin-3 and AMPA receptors, increases AMPA-receptor internalization

194 In vivo, arousal was linked to AMPA receptor-independent elevations of [K(+)]e concomit

195 eral functional link between neuroligins and AMPA receptors, indicate that both neuroligin-3 and -4 a

196 e receptors with systemic NBQX, or selective AMPA receptor inhibition by intramuscular perampanel res

197 , we show that this effect is through direct AMPA receptor inhibition, a target shared by a recently

198 The most potent and well-tolerated AMPA receptor inhibitors act via a noncompetitive mechan

199 ty-induced postsynaptic actin remodeling and AMPA receptor insertion.

200 onstrate a novel role for Parkin in synaptic AMPA receptor internalization and suggest a Parkin-depen

201 T3 accompanied chemical induction of LTD and AMPA receptor internalization.

202 n neuroligin-3 and AMPA receptors, increases AMPA-receptor internalization and decreases postsynaptic

203 Our data support a model where adding AMPA receptors is sufficient to activate synapses that h

204 ntrast, they were insensitive to blockers of AMPA receptors, L-type voltage-gated Ca(2+) channels, or

205 mplitudes, indicating an increase in surface AMPA receptor levels compared with wild-type neurons.

206 tic scaffolding protein controlling synaptic AMPA receptor levels, and thus the strength of excitator

207 required for maintaining proper cell-surface AMPA receptor levels.

208 r internalization and decreases postsynaptic AMPA-receptor levels.

209 AMPA receptors mediate fast excitatory neurotransmission

210 Whereas Ca(2+)-permeable AMPA receptors mediate input from rod bipolar cells to b

211 um-dependent increase in functional synaptic AMPA receptors, mediated by enhanced recycling of intern

212 ow that Parkin deficiency leads to decreased AMPA receptor-mediated activity due to disruption of the

213 mponent of the EPSC that is activated by the AMPA receptor-mediated depolarization of the spine and t

214 lesser extent by AMPA receptors, whereas an AMPA receptor-mediated excitation prevails in Group II m

215 for synaptic strength, and dysregulation of AMPA receptor-mediated signalling is linked to numerous

216 merised Abeta induces a rapid enhancement of AMPA receptor-mediated synaptic transmission (EPSC(A)) w

217 In addition, SALM5 regulates AMPA receptor-mediated synaptic transmission through mec

218 e largely extrasynaptic, without a change in AMPA-receptor-mediated responses.

219 ly, the R704C mutation unexpectedly elevated AMPA-receptor-mediated synaptic responses.

220 Pentraxin then accumulates AMPA receptors on the postsynaptic terminal forming func

221 molecular dynamics simulations to predict an AMPA receptor open state structure and rationalize the r

222 MPA receptor proteins increase the number of AMPA receptor openings that result from a single recepto

223 , reduce levels of synaptic or extrasynaptic AMPA receptors, or alter other AMPA receptor trafficking

224 hogenic variants in FRRS1L, which encodes an AMPA receptor outer-core protein.

225 diazine 1,1-dioxides and their evaluation as AMPA receptor positive allosteric modulators (AMPApams).

226 Type I transmembrane AMPA receptor proteins increase the number of AMPA recep

227 f the MAGUKs causes a transient reduction in AMPA receptor quantal size followed by synaptic consolid

228 postsynaptic bursting selectively depressed AMPA receptor (R) synaptic transmission, or silenced exc

229 vel mechanism in which mGluR signals release AMPA receptors rapidly from the ER and couple ER release

230 -independent mechanism that drives increased AMPA receptor recycling and LTP.

231 ntaining the auxiliary subunit transmembrane AMPA receptor regulatory protein gamma-2 makes a substan

232 receptors associated with the transmembrane AMPA receptor regulatory protein, gamma-2, gating in the

233 Transmembrane AMPA receptor regulatory proteins (TARPs) are a family o

234 AMPA receptors coassemble with transmembrane AMPA receptor regulatory proteins (TARPs), yielding a re

235 ccumulation or removal, respectively, of the AMPA-receptor regulatory scaffold protein A-kinase ancho

236 How Ca(2+) induces the recruitment of AMPA receptors remains unclear.

237 The insertion of AMPA receptors requires SNAP25-syntaxin1A/B-VAMP2 comple

238 g the localization of potassium channels and AMPA receptors, respectively.

239 PA, suggesting a paradoxical increase in VTA AMPA receptor responsiveness.

240 o-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) receptors, RNA editing and alternative splicing ge

241 ference in recovery time course is caused by AMPA receptor saturation, where partial refilling of the

242 , and imparted sensitivity to aniracetam, an AMPA receptor-selective positive modulator.

243 w that targeting a TARP auxiliary subunit of AMPA receptors selectively modulates neuronal excitabili

244 cluding neurotransmitter receptors (NMDA and AMPA receptors), signalling proteins that regulate the p

245 both drugs induced NMDA receptor-containing, AMPA receptor-silent excitatory synapses, albeit in dist

246 AMPA receptor stimulation of wild-type OPCs caused decre

247 creased cell-surface expression of the GluR2 AMPA receptor subunit and increased intracellular Ca(2+)

248 of glutamatergic transmission and changes in AMPA receptor subunit composition at 72 h postsurgery.

249 ely spliced, flip and flop variants of GluA1 AMPA receptor subunit exhibit no functional difference i

250 ranslated region of Gria1, which encodes the AMPA receptor subunit GluA1, to pull down miRNAs binding

251 a (15-fold), GluK1b (5-fold), as well as the AMPA receptor subunit GluA1i (5-fold).

252 et al. (2017) reveal a critical role for the AMPA receptor subunit GluA3 in cerebellar synaptic plast

253 pses on PV interneurons are dependent on the AMPA receptor subunit GluA4, which is regulated by presy

254 GRIA4 encodes an AMPA receptor subunit known as GluR4, which is found on

255 dala (BLA) revealed an increase in the GluA1 AMPA receptor subunit that correlated with SEFL.

256 howed enhanced ability to increase glutamate AMPA receptor subunits at the cell surface of wild type

257 resulted in increased surface expression of AMPA receptor subunits GluA1 and GluA2.

258 to extensive hydrophobic interfaces between AMPA receptor subunits in the ion channel.

259 (PSD) thickness and an upregulation of GluA3 AMPA receptor subunits on bushy cells.

260 oduces a paradoxical enhancement in membrane AMPA receptor subunits, AMPA responsiveness, and the mot

261 variants, and those variants, as in GluA2-4 AMPA receptor subunits, generally show different propert

262 pression increases the surface expression of AMPA receptor subunits, providing insight to the mechani

263 roximately 5 mum, along with GluA1 and GluA2 AMPA receptor subunits.

264 pathway and downstream events that result in AMPA receptor synaptic accumulation, spine enlargement,

265 ic proteasome is responsible for fine tuning AMPA receptor synaptic levels under basal conditions.

266 ands by exponential enrichment with a single AMPA receptor target (i.e. GluA1/2R) to isolate RNA apta

267 ion of GluA2, without affecting formation of AMPA receptor-TARP complexes.

268 conformational changes throughout the entire AMPA receptor that accompany activation and desensitizat

269 , interneuron glutamatergic synapses contain AMPA receptors that are GluA2-subunit lacking and Ca(2+)

270 sition distinct from that of the majority of AMPA receptors that dominate the horizontal cell postsyn

271 so leads to compensatory scaling of synaptic AMPA receptors that enhance the motivational for cocaine

272 te a simple mechanism for the recruitment of AMPA receptors that mediates LTP.

273 n the NMDAR activity-mediated trafficking of AMPA receptors that takes place during memory retrieval.

274 Surprisingly, adding more AMPA receptors to excitatory contacts had little effect

275 es to spines, enhances synaptic recycling of AMPA receptors to increase their surface expression and

276 t synapses became 'unsilenced' by recruiting AMPA receptors to strengthen excitatory inputs to D1-typ

277 -hydroxy-5-methyl-4-isoxazolepropionic acid, AMPA, receptors to the plasma membrane); conversely, the

278 important because it suggests that targeting AMPA receptor trafficking and activation could provide n

279 family of scaffolding proteins that regulate AMPA receptor trafficking and function.

280 that TFR functions as a regulator to control AMPA receptor trafficking efficiency and synaptic plasti

281 extrasynaptic AMPA receptors, or alter other AMPA receptor trafficking events.

282 ated with a reduction in retrieval-dependent AMPA receptor trafficking, as evidenced by a reduction i

283 ed expression levels of proteins involved in AMPA receptor trafficking, suggesting previously unident

284 IBRA signaling pathways, actin dynamics, and AMPA receptor trafficking.

285 ) of synaptic strength through inhibition of AMPA receptor trafficking.

286 ste memory through increase of glutamatergic AMPA receptor trafficking.

287 se, paired-pulse facilitation, and increased AMPA receptor transmission.

288 ts of CaMKII phosphorylation responsible for AMPA receptor up-regulation during LTP.

289 erference with NMDA receptor function blocks AMPA receptor upregulation, it also produces a paradoxic

290 R, LGI1, CASPR2, the GABAA receptor, and the AMPA receptor using live cell-based assays.

291 f homodimers and heterodimers of kainate and AMPA receptors using fluorescence-detected sedimentation

292 om Ca(2+) influxes through calcium-permeable AMPA receptors, voltage-gated Ca(2+) channels, and trans

293 Using live-cell imaging of a pH-sensitive AMPA receptor, we found that during LTP-inducing stimula

294 modulates the pharmacological properties of AMPA receptors, we discovered that LY3130481 selectively

295 ain, proteins of GluA1 subunits of glutamate AMPA receptors were upregulated during morphine withdraw

296 by NMDA receptors and to a lesser extent by AMPA receptors, whereas an AMPA receptor-mediated excita

297 -hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, which trigger mammalian target of rapam

298 that the two synaptic components arise from AMPA receptors with different functional signatures and

299 ptic sodium entry is almost entirely through AMPA receptors with little contribution from entry throu

300 We hypothesized that blockade of forebrain AMPA receptors without blocking cerebellar AMPA receptor

301 n AMPA receptors without blocking cerebellar AMPA receptors would be antiepileptic and devoid of moto