ライフサイエンスコーパス: AMPA

1 AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propion

2 AMPA and kainate receptors share a high degree of sequen

3 AMPA and kainate receptors, along with NMDA receptors, r

4 AMPA and NMDA receptors are glutamate-gated ion channels

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

6 AMPA receptors (AMPARs) are tetrameric ion channels that

7 AMPA receptors are glutamate-gated cation channels assem

8 AMPA receptors mediate fast excitatory neurotransmission

9 AMPA subtype ionotropic glutamate receptors mediate fast

10 AMPA-kainate receptor induced excitotoxicity contributes

11 AMPA-type glutamate receptors (AMPARs) lacking an edited

12 AMPA-type glutamate receptors (AMPARs) mediate fast exci

13 AMPA-type glutamate receptors (AMPARs), which are centra

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

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

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

17 d its metabolite aminomethylphosphonic acid (AMPA) could be detected in milk and urine produced by la

18 -hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate system.

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

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

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

22 hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) and N-methyl-D-aspartate currents and the ability

23 hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) to N-methyl-D-aspartate (NMDA) ratios, and matrix

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

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

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

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

28 l cortex pyramidal neurons without affecting AMPA EPSC currents.

29 hows weak activation by its namesake agonist AMPA and also by quisqualate.

30 ght to the mechanism by which cocaine alters AMPA surface expression.

31 educed by M1 infusion of a D1 antagonist, an AMPA antagonist, or a GABAA agonist.

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

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

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

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

36 postsynaptic scaffolding protein PSD-95 and AMPA glutamate receptors (AMPARs).

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

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

39 whereas ventromedial prefrontal cortex, and AMPA signaling therein, modulates the duration of indivi

40 ur data provide evidence that glyphosate and AMPA are not detectable in milk produced by women living

41 difference was found in urine glyphosate and AMPA concentrations between subjects consuming organic c

42 Mean +/- SD glyphosate and AMPA concentrations in urine were 0.28 +/- 0.38 and 0.30

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

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

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

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

47 inutes later, dendritic spine morphology and AMPA to NMDA ratios were restored as animals became moti

48 LTP of NMDA and AMPA EPSCs after high-frequency stimulation was reduced

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

50 We recorded neuronal glutamatergic (NMDA and AMPA) responses in prefrontal cortex (PFC) neurons and u

51 city that converge on regulation of NMDA and AMPA-type glutamate receptors (NMDAR, AMPAR), including

52 stitutive, internalization of both NMDA- and AMPA-type glutamate receptors.

53 the cell surface expression of NMDA-type and AMPA-type glutamate receptors, along with prominent func

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

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

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

57 cNIC decreased baseline AMPA/NMDA ratio, arising from increased NMDA currents en

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

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

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

61 dual activity for effectively blocking both AMPA and kainate receptors.

62 A aptamers that can potentially inhibit both AMPA and kainate receptors.

63 , its shorter version (55 nt) inhibited both AMPA and kainate receptors.

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

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

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

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

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

69 otentiation at these synapses as measured by AMPA/N-methyl-D-aspartate currents.

70 excitatory neurotransmission is mediated by AMPA-subtype ionotropic glutamate receptors (AMPARs).

71 itatory synaptic transmission is mediated by AMPA-type glutamate receptors (AMPARs).

72 Synaptic transmission mediated by AMPA-type glutamate receptors was potentiated in the NAc

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

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

75 reduced levels of membrane GluA1-containing AMPA receptors.

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

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

78 Correspondingly, AMPA-subtype ionotropic glutamate receptors, which media

79 uld be reduced by local M1 modulation of D1, AMPA, and GABAA receptors, providing preclinical support

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

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

82 ng behavior by amplifying D1DR/PKA-dependent AMPA transmission in the nucleus accumbens.

83 c index relative to known non-TARP-dependent AMPA antagonists.

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

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

86 cluded eight pesticides (desulfinylfipronil, AMPA, chlorpyrifos, dieldrin, metolachlor, atrazine, CIA

87 distinct subdivisions of ACC with different AMPA/N-methyl-D-aspartate receptor profiles.

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

89 t nAcc photoactivation of these fibers drove AMPA-mediated cellular firing of parvalbumin GABAergic i

90 by the presence of glutamate receptors (i.e. AMPA, NMDA, and kainate receptors) at the synapse.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 molecular dynamics simulations of the GluA2 AMPA subtype glutamate receptor ligand-binding domain (L

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

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

108 In the continual presence of glutamate, AMPA and NMDA receptors containing the GluN2A or GluN2B

109 zed binding site densities for glutamatergic AMPA, NMDA and kainate, GABAergic GABAA , muscarinic M1

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

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

112 se effects are not accompanied by changes in AMPA and NMDA receptor properties at cortical, amygdaloi

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

114 P activation and t-SP induction (increase in AMPA currents in MSNs).

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

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

117 pamine neurons and a concomitant increase in AMPA synaptic transmission to ex vivo dopamine neurons w

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

119 some antigen 1 (EEA1), a protein involved in AMPA-type glutamate receptor endocytosis.

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

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

122 ffects their neuronal activity and increases AMPA-mediated over NMDA-mediated excitatory synaptic cur

123 hat self-administration of cocaine increases AMPA glutamate receptors in the VTA, and this effect enh

124 ked LTD induction and prevented NMDA-induced AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropioni

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

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

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

128 tor subunit B, glutamate receptor ionotropic AMPA 2 (GRIA2), modifies a codon, replacing the genomica

129 changes is the remodeling of the ionotropic AMPA-type glutamate receptors that underlie fast excitat

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

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

132 naptic density protein-95 (PSD-95) localizes AMPA-type glutamate receptors (AMPARs) to postsynaptic s

133 e hydrophobic box differed between mammalian AMPA and NMDA receptors.

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

135 We modeled AMPA receptor diffusion in synapses where the distributi

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

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

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

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

140 Phrenic motoneuron AMPA glutamate receptor 2 (GluR2) subunit mRNA expressio

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

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

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

144 In mature neurons AMPA receptors cluster at excitatory synapses primarily

145 th analytes, detected neither glyphosate nor AMPA in any milk sample.

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

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

148 EAAT2 buffers basal glutamate activation of AMPA-type glutamate receptors and therefore decreases ba

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

150 Although we observed no alterations of AMPA and NMDA receptor properties, we found that the AMP

151 Prolonged application of AMPA caused loss of afferent terminal responsiveness, wh

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

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

154 Pharmacological blockade of AMPA-kainate receptors with systemic NBQX, or selective

155 ing were mimicked by intra-vmPFC blockade of AMPA-type but not NMDA-type glutamate receptors.

156 Distinct complements of AMPA and NMDA receptors within different interneuron sub

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

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

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

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

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

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

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

164 ocomotor responses to intra-VTA infusions of AMPA, suggesting a paradoxical increase in VTA AMPA rece

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

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

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

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

169 The free energy maps of AMPA and kainate receptor ATD dimers provide a framework

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

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

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

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

174 ration of a positive allosteric modulator of AMPA-type glutamate receptors.

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

176 igate the relationship between the number of AMPA-type glutamate receptors in the PSD and synaptic st

177 A receptors also blocked the potentiation of AMPA-mediated currents.

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

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

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

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

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

183 Regulation of AMPA-type glutamate receptor (AMPAR) number at synapses

184 ity is the regulated addition and removal of AMPA-type glutamate receptors (AMPARs) at excitatory syn

185 have evolved to optimize rapid responses of AMPA-type iGluRs at synapses.

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

187 ce, the present study highlights the role of AMPA-kainate receptor in IVH-induced white matter injury

188 orm of homeostatic plasticity, up-scaling of AMPA-glutamate receptors.

189 ng other kinetic properties, for a series of AMPA channels with different arginine/glycine (R/G) edit

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

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

192 d of synaptic levels of the GluA1 subunit of AMPA-type glutamate receptors after 48 h silencing with

193 GRIA3 encodes GluA3, a subunit of AMPA-type ionotropic glutamate receptors (AMPARs).

194 ne dependence to show that GluA1 subunits of AMPA glutamate receptors in the nucleus accumbens (NAc),

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

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

197 ent with the role of synaptic trafficking of AMPA-type of glutamate receptors in HSP, Mecp2 KO neuron

198 The regulated transport of AMPA-type glutamate receptors (AMPARs) to the synaptic m

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

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

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

202 ve iontophoresis (or puffs) of glutamate (or AMPA) onto the dendrites of amacrine cells also signific

203 no immediate effect on glutamate release or AMPA-mediated neurotransmission.

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

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

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

207 ation through Ca(2+)- (and Zn(2+))-permeable AMPA channels in CA3 and Zn(2+) mobilization from MT-III

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

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

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

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

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

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

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

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

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

217 h disordered regulation of calcium-permeable AMPA receptors.

218 turation by recruitment of calcium-permeable AMPA-type glutamate receptors (CP-AMPARs) after drug wit

219 piny neurons as a primary site of persistent AMPA-type glutamate receptor plasticity by two widely us

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

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

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

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

224 se or by direct modification of postsynaptic AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropioni

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

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

227 -3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) throughput.

228 ere, we report crystal structures of the rat AMPA-subtype GluA2 receptor in complex with three noncom

229 of excitatory ionotropic glutamate receptor AMPA subunits in Xenopus oocytes, we show that this effe

230 targeting pre- and post-synaptic receptors (AMPA, NMDA, GABA-A, mGluR2/3 receptors and Nav, Cav volt

231 of active excitatory synapses by recruiting AMPA glutamate receptors to the postsynaptic cell surfac

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

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

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

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

236 A survey of iGluR gene expression revealed AMPA-, Kainate-, and NMDA-type subunits are expressed in

237 Phylogenetic analysis reveals AMPA, kainate, and NMDA receptor families in insect geno

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

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

240 generate action potentials evoked by single AMPA-dependent EPSPs.

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

242 ancement in membrane AMPA receptor subunits, AMPA responsiveness, and the motivation for cocaine.

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

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

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

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

247 Single-synapse AMPA conductance was much larger than previously appreci

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

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

250 +) influx stimulates recruitment of synaptic AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propion

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

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

253 gh removal and dephosphorylation of synaptic AMPA-type glutamate receptors.

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

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

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

257 atter via AMPA receptor activation, and that AMPA-kainate receptor inhibition suppresses inflammation

258 Our data suggest that AMPA-kainate receptor inhibition alleviates OPC loss and

259 Evidence suggests that AMPA glutamate-receptor-dependent synaptic plasticity wi

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

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

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

263 AMPK targets both the AMPA-type glutamate receptor GLR-1 and the metabotropic

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

265 MPA receptor antagonists and mimicked by the AMPA-positive allosteric modulator CX614.

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

267 Following ER exit, the AMPA-type glutamate receptor GluA1 and neuroligin 1 unde

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

269 eceptors after cocaine, but no change in the AMPA-to-NMDA ratio.

270 CIE mice also showed an increase in the AMPA/NMDA ratio, and this was associated with an increas

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

272 l with an increase in phosphorylation of the AMPA GluA1 receptor subunit at serine 831 (S831), a CaMK

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

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

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

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

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

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

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

280 KEY POINTS: The AMPA-type ionotropic glutamate receptors (AMPARs) mediat

281 led to PPN-innervated synapses reducing the AMPA-to-NMDA receptor-mediated current ratio.

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

283 NMDA receptor properties, we found that the AMPA/NMDA ratio increased at cortical and amygdaloid inp

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

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

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

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

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

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

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

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

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

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

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

295 ional synaptic potentials are dependent upon AMPA (GluA) receptors, are GABAA independent, and origin

296 ridge that is notably absent from vertebrate AMPA, kainate, and NMDA iGluRs greatly increases the rat

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

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

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

300 how conformation regulated interactions with AMPA-type and NMDA-type glutamate receptors (AMPARs/NMDA