ライフサイエンスコーパス: AMPA receptor

1 oter to express AMPApHluorin (pHluorin on an AMPA receptor).

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

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

4 units, as we show for both kainate and GluA2 AMPA receptors.

5 lies comprising a major population of native AMPA receptors.

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

7 reduced levels of membrane GluA1-containing AMPA receptors.

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

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

10 h disordered regulation of calcium-permeable AMPA receptors.

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

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

13 post-synaptic scaffold that captures surface AMPA receptors.

14 designed to individually inhibit kainate and AMPA receptors.

15 is due to the effect of this polymer on the AMPA receptors.

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

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

18 s in postsynaptic response to GABA, and also AMPA, receptor activation include regulation of voltage-

19 Furthermore, FB9s-r blocked AMPA receptor activity.

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

21 as patients' CSF did not alter responses to AMPA receptor agonists and was abrogated by preabsorptio

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

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

24 rly gene (IEG) expression and changes in BLA AMPA receptor (AMPAR) and NMDA receptor (NMDAR) subunit

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

26 nel, a Food and Drug Administration-approved AMPA receptor (AMPAR) antagonist, during a follow-on 24-

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

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

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

30 Regulation of AMPA receptor (AMPAR) expression is central to synaptic

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

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

33 Transmembrane AMPA receptor (AMPAR) regulatory proteins (TARPs) modula

34 The AMPA receptor (AMPAR) subunit GluA3 has been suggested t

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

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

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

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

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

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

41 nnings for these memory dynamics, we studied AMPA receptor (AMPAR)-silent excitatory synapses, which

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

43 -hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (AMPAR) abundance, which is modulated by

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

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

46 al gene expression levels between excitatory AMPA receptors (AMPARs) and inhibitory GABA(A) receptors

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

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

49 stsynaptic ligand-gated ion channels such as AMPA receptors (AMPARs) are organized into so-called nan

50 AMPA receptors (AMPARs) are tetrameric ion channels that

51 AMPA receptors (AMPARs) are tetrameric ligand-gated chan

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

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

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

55 domains of both NMDA receptors (NMDARs) and AMPA receptors (AMPARs) have distinct motifs, which are

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

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

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

59 of synaptic strength through trafficking of AMPA receptors (AMPARs) is a fundamental mechanism under

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

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

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

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

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

65 but also ones including the GluA2 subunit of AMPA receptors (AMPARs).

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

67 we examined the involvement of the glutamate AMPA receptor and brain-derived neurotrophic factor (BDN

68 sed levels of the GluA1 subunit of glutamate AMPA receptor and display increased anxiety-like behavio

69 ased by vagal afferents, glutamate acting at AMPA receptors and 5-HT acting at 5-HT(2A) receptors.

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

71 g in the accumulation of excess postsynaptic AMPA receptors and defective synaptic plasticity.

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

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

74 ion but, instead, requires Ca(2+) -permeable AMPA receptors and group I metabotropic glutamate recept

75 AMPA receptors and interacting proteins are importantly

76 dendritic spine pruning, internalization of AMPA receptors and long-term depression.

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

78 itro blocked LTP-induced surface delivery of AMPA receptors and spine enlargement.

79 Previously we reported that GluA1-containing AMPA receptors and their interaction with PDZ-proteins a

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

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

82 creased synaptic expression of GluA2-lacking AMPA receptors, and blocked synaptic scaling, whereas in

83 These synapses have larger AMPA receptor- and NMDA receptor-mediated events.

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

85 Consistently, AMPA receptor antagonist CNQX or calcineurin inhibitor F

86 scimol (1/0.1 mM) into unilateral PL and the AMPA receptor antagonist NBQX (1 mM) into contralateral

87 f 8-OH-DPAT are blocked by co-infusion of an AMPA receptor antagonist or an anti-BDNF neutralizing an

88 owth are also reduced by anaesthesia and the AMPA receptor antagonist perampanel, respectively.

89 hydrobromide (IEM-1460), a calcium-permeable AMPA receptor antagonist, was determined.

90 se antidepressant effects were blocked by an AMPA receptor antagonist.

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

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

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

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

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

96 Negative allosteric modulators of AMPA receptors are considered to have significant therap

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 Under basal conditions, endocytosed AMPA receptors are rapidly recycled back to the plasma m

100 AMPA receptors are tetrameric assemblies composed of fou

101 -hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors are glutamate-gated ion channels that me

102 -hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors are two major, closely related receptor

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

104 xample, the ratio to PSD-95 of Transmembrane AMPA-Receptor-associated Proteins (TARPs), which mediate

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

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

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

108 and strong upregulation of genes coding for AMPA receptor auxiliary subunits.

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

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

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

112 ntidepressant-like effects via activation of AMPA receptor/BDNF/mTOR signaling in mice, which subsequ

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

114 trate that positive allosteric modulation of AMPA receptors by PAM-AMPA treatment reverted memory, bu

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

116 ng through positive allosteric modulation of AMPA receptors, by the use of a PAM-AMPA compound.

117 tase 2B (PP2B)-mediated dephosphorylation of AMPA receptors can determine whether LTD or LTP occurs i

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

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

120 In mature neurons AMPA receptors cluster at excitatory synapses primarily

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

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

123 ucidate the structures of 10 distinct native AMPA receptor complexes by single-particle cryo-electron

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

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

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

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

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

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

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

131 ulation of high conductance Ca(2+)-permeable AMPA receptors (CP-AMPARs) that is detectable with elect

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

133 nvolvement of GluA2-lacking Ca(2+)-permeable AMPA receptors (CP-AMPARs) using IEM-1460, which has bee

134 -hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (CP-AMPAR) currents after brain injury.

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

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

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

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

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

140 ctrochemical communication through bona fide AMPA receptor-dependent neuron-glioma synapses.

141 Second, a reduction of functional AMPA receptors depends upon the phosphorylation of at le

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

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

144 We modeled AMPA receptor diffusion in synapses where the distributi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 t miRNA-mediated mechanism for regulation of AMPA receptor expression.

160 ng an EE experience not only restored normal AMPA-receptor expression levels but also reversed the in

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

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

163 Its expression is mediated by the removal of AMPA receptors from postsynaptic membranes.

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

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

166 in dentate granule neurons reduces synaptic AMPA receptor function and causes dendritic spines to ad

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

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

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

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

171 We also determined whether modified AMPA receptors generated during status epilepticus could

172 kinase A (PKA), protein kinase C (PKC), and AMPA receptor genes that play a pivotal role in memory f

173 r the crystal structures in complex with the AMPA receptor GluA2 agonist-binding domain.

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

175 te within the 3'UTR of the mRNA encoding the AMPA receptor GluA2 subunit, and demonstrate that GluA2

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

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

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

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

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

181 In AMPA receptor heteromers, TARP stoichiometry further mod

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

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

184 ls and altered organization of glutamatergic AMPA receptors in LRRK2 mutants.

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

186 ces, PolyP reduced ion flux through NMDA and AMPA receptors in native neurons.

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

188 est that the endocytosis of GluR2-containing AMPA receptors in the amygdala regulates retrieval-induc

189 -hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in vitro after exposure to patients' CSF

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

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

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

193 to find that mGluR activation causes LTD and AMPA receptor internalization, but no spine shrinkage in

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

195 nclear if the expression of GluA1-containing AMPA receptors is affected by this type of behavior.

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

197 n Vglut3(WT) were maintained as postsynaptic AMPA receptors juxtaposed with presynaptic ribbons and v

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

199 d in animals (e.g., antibodies against NMDA, AMPA receptors, LGI1 protein) or in cultured neurons (e.

200 AMPA receptors mediate fast excitatory neurotransmission

201 Glutamate-gated AMPA receptors mediate the fast component of excitatory

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

203 ce levels and the amplitude and frequency of AMPA receptor-mediated currents, and mimicked excitatory

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

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

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

207 dministration revealed that both drugs alter AMPA receptor-mediated synaptic transmission in CA3.

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

209 ptor surface expression and trafficking, and AMPA receptor-mediated synaptic transmission.

210 tively increased dendritic spine density and AMPA-receptor-mediated EPSCs in wild-type neurons, but n

211 r model, which permits the estimation of the AMPA-receptor-mediated maximal synaptic conductance base

212 neurexin-2 at SS4 had no effect on NMDA- or AMPA-receptor-mediated responses.

213 alter synaptic connectivity as measured via AMPA-receptor-mediated synaptic responses at Schaffer-co

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

215 ive splicing of neurexin-3 at SS4 suppressed AMPA-receptor-mediated, but not NMDA-receptor-mediated,

216 postsynaptic NMDA-receptor-mediated, but not AMPA-receptor-mediated, synaptic responses without alter

217 Calcium-permeable AMPA receptors modified during status epilepticus can be

218 omain, which controls motions in the distant AMPA receptor N-terminal domain (NTD).

219 nt amplitude and alter kinetic properties of AMPA receptors on slow time scale, such as desensitizati

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

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

224 We present the first model of AMPA receptor phosphorylation that simulates the inducti

225 AMPA receptor plasticity mediated by the GluA1 subunit p

226 -hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor plasticity plays a role in sustaining sei

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

228 (AMPA)-type ionotropic glutamate receptors (AMPA receptors) predetermines responsiveness to neurotra

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

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

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

232 Glioma-cell-specific genetic perturbation of AMPA receptors reduces calcium-related invasiveness of t

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

234 As auxiliary subunits, transmembrane AMPA receptor regulatory proteins (TARPs) are known to e

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

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

237 rangement, and molecular structure of native AMPA receptors remain unknown.

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

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

240 95 induction following learning impairs both AMPA receptor response maturation and infantile memory,

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

242 ggest that positive allosteric modulation of AMPA receptors restores synaptic integrity and cognitive

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

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

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

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

247 to induce spinogenesis and the generation of AMPA receptor-silent glutamatergic synapses in the adult

248 tion led to an increase in surface-expressed AMPA receptors specifically in the neurons with MAP2 spi

249 ydroxy-5-methyl-4-isoxazolyl)propionic acid (AMPA) receptor subtypes, confirmed also by an unusual bi

250 -5-methyl-4-isoxazolepropionic acid receptor AMPA receptor subunit 1 (GluA1) through phosphorylation

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

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

253 ic receptors regulate the phosphorylation of AMPA receptor subunit GluA1 via a signaling pathway link

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

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

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

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

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

259 hrough age-dependent suppression of amygdala AMPA receptor subunit trafficking, (2) maternal presence

260 isengage both the BLA and plasticity-related AMPA receptor subunit trafficking.

261 teral amygdala (BLA), and plasticity-related AMPA receptor subunit trafficking.

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

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

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

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

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

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

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

269 of Bin1 lead to changes in spine morphology, AMPA receptor surface expression and trafficking, and AM

270 in and PSD-95, and significant maturation of AMPA receptor synaptic responses.

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

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

273 We developed a statistical AMPA-receptor-tetramer model, which permits the estimati

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

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

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

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

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

279 functions transsynaptically control NMDA and AMPA receptors, thereby mediating presynaptic control of

280 PolyP reduced calcium signal acting through AMPA receptors, thus protecting neurons against glutamat

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

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

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

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

285 at the acute involvement of GluA1-containing AMPA receptors tor forced swim behavior is a result of n

286 ctin-dependent cellular processes, including AMPA receptor trafficking at synapses.

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

288 ing in hippocampal neurons, without altering AMPA receptor trafficking.

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

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

291 akin to Hebbian plasticity: Ca(2+)-permeable AMPA receptor upregulation, L-type Ca(2+) channel activa

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

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

294 f PolyP on glutamate and specifically on the AMPA receptors was dependent on the presence of P2Y1 but

295 loss of presynaptic ribbons or postsynaptic AMPA receptors was not observed in Vglut3(KO) , demonstr

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

297 ular insight into how NAMs interact with the AMPA receptor, which is of potential use for future desi

298 sites at the GluA1 subunit of the glutamate AMPA receptors, which has been characterized as a critic

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

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