ライフサイエンスコーパス: kainate receptor

1 nd-binding domain of a light-gated mammalian kainate receptor.

2 1 prevents kainate-evoked endocytosis of the kainate receptor.

3 ivity for effectively blocking both AMPA and kainate receptors.

4 s that can potentially inhibit both AMPA and kainate receptors.

5 combinant homomeric and heteromeric AMPA and kainate receptors.

6 discharges in BLA slices in vitro via GluK1 kainate receptors.

7 rgic ACs do not appear to express functional kainate receptors.

8 tly the activity of both the GluK1 and GluK2 kainate receptors.

9 on structure currently exists of heteromeric kainate receptors.

10 e involvement of Ca(2+)/calcineurin and AMPA/kainate receptors.

11 ties by having subnanomolar IC(50) values at kainate receptors.

12 st that Neto2 modulates the function of most kainate receptors.

13 ferent from those of the homologous AMPA and kainate receptors.

14 es that contained GluK1, GluK1/5, or GluK2/5 kainate receptors.

15 hyl-4-isoxazolepropionic acid receptors, and kainate receptors.

16 c currents in neurons expressing recombinant kainate receptors.

17 for recombinant NMDA receptors over AMPA and kainate receptors.

18 tion of inhibitory presynaptic terminals via kainate receptors.

19 rter version (55 nt) inhibited both AMPA and kainate receptors.

20 oxicity, mediated through activation of AMPA/kainate receptors.

21 n the activation properties of the remaining kainate receptors.

22 m that resembles desensitization at AMPA and kainate receptors.

23 or sodium in order for glutamate to activate kainate receptors.

24 r dissection of ligand binding and gating in kainate receptors.

25 positive for mGluR5 and GLU(K5-7)-containing kainate receptors.

26 luR3 for AMPA, and KA2>GluR5>GluR7>GluR6 for kainate receptors.

27 y selective antagonist of GLU(K5)-containing kainate receptors.

28 ions are essential structural components of kainate receptors.

29 chemic axonal injury is not mediated by AMPA/kainate receptors.

30 , ischemic axonal damage is mediated by AMPA/kainate receptors.

31 nsures a high level of GluR6/KA2 heteromeric kainate receptors.

32 YM 2081, was used to confirm the presence of kainate receptors.

33 to the unique kinetic properties of AMPA and kainate receptors.

34 F bipolar cells were exclusively mediated by kainate receptors.

35 -hydroxy-5-methyl-4-isoxazolepropionic acid)/kainate receptors.

36 e granule cells and operate via postsynaptic kainate receptors.

37 found in all vertebrate NMDA but not AMPA or kainate receptors.

38 xcitability through their actions on AMPA or kainate receptors.

39 roxy-5-methyl-4-isoxazolepropionic acid] and kainate receptors.

40 ontaining NMDA receptors as well as AMPA and kainate receptors.

41 about the role of protein kinase C (PKC) in kainate receptor actions by demonstrating that direct po

42 AMPA/kainate receptor activation alone elicited calcium signa

43 Combined NMDA and AMPA/kainate receptor activation elicited calcium signals in

44 We therefore investigated the effects of kainate receptor activation on GABA release in rat prefr

45 ggest that the balance between NMDA and AMPA/kainate receptor activation regulates the axonal arboriz

46 ed antidepressant-like effects required AMPA/kainate receptor activation, as evidenced by the ability

47 in GluK5 expression is sufficient to enhance kainate receptor activity by modulating receptor channel

48 at loss of synaptic AMPA receptors increased kainate receptor activity in cerebellar granule cells wi

49 acological inhibition or genetic ablation of kainate receptor activity reduces pain behaviors in a nu

50 e demonstrate that the desensitized state of kainate receptors acts as a deep energy well offsetting

51 as occurs in all previously solved AMPA and kainate receptor agonist and antagonist complexes.

52 nals at synapses that contain either AMPA or kainate receptors, all with different temporal propertie

53 ed EPSCs, whether they were mediated by AMPA/kainate receptors alone or in combination with NMDA rece

54 AMPA and kainate receptors, along with NMDA receptors, represent

55 ochemistry, and pharmacology to identify the kainate receptor and auxiliary subunits in ground squirr

56 lation of GluR6 regulates endocytosis of the kainate receptor and modifies synaptic transmission.

57 ; a presynaptic form (pre-LTP) that requires kainate receptors and a postsynaptic form (post-LTP) tha

58 he agonist-bound state that are conserved in kainate receptors and absent in AMPA receptors.

59 pathway requires the metabotropic action of kainate receptors and activation of G protein, protein k

60 3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate receptors and of N-methyl-D-aspartate (NMDA) rec

61 ke-2 (Neto2) as a novel accessory subunit of kainate receptors and showed that Neto2 modulates the ga

62 d pentylenetetrazol is not mediated by GluK1 kainate receptors, and deletion of these receptors does

63 The AMPA/kainate receptor antagonist 2,3-dihydroxy-6-nitro-7-sulf

64 The AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2

65 on treatment of an acutely administered AMPA/kainate receptor antagonist and delayed transplantation

66 These findings show that a highly selective kainate receptor antagonist can affect the deficits in s

67 These data suggest that an AMPA/kainate receptor antagonist can represent a novel therap

68 no-3-hydroxy-5-methyl-4-isoxazole propionate/kainate receptor antagonist CNQX (0, .01, .03, .1 mug/si

69 sent experiments, administration of the AMPA/kainate receptor antagonist CNQX (0, 0.03, or 0.3 mug) i

70 finding that intracore injection of the AMPA/kainate receptor antagonist CNQX attenuated the ability

71 NMDAR antagonist MK801, and also by the AMPA/kainate receptor antagonist CNQX.

72 The AMPA/kainate receptor antagonist NBQX was directly administer

73 havioral responses to kainic acid and that a kainate receptor antagonist normalized altered behaviors

74 t work examined effects of another selective kainate receptor antagonist, (S)-1-(2-Amino-2-carboxyeth

75 further support for the idea that selective kainate receptor antagonists could be novel therapeutic

76 These findings suggest that selective kainate receptor antagonists could be novel therapeutic

77 Compounds 18i and (-)-4 were the most potent kainate receptor antagonists, and 18i was selective for

78 carboxybenzyl substituents produces AMPA and kainate receptor antagonists.

79 l-4-isoxazolepropionic acid, and heteromeric kainate receptors are all downstream targets of GPCR sig

80 Kainate receptors are also expressed throughout central

81 Kainate receptors are further classified into low-affini

82 AMPA and kainate receptors are glutamate-gated ion channels whose

83 Recombinant kainate receptors are inhibited in a subunit-dependent m

84 Kainate receptors are less well understood than other gl

85 n performed on homomeric GluK2 but, in vivo, kainate receptors are likely heterotetramers.

86 uK2 knock-out mice, demonstrating that GluK1 kainate receptors are not required for epileptogenesis o

87 Neuronal kainate receptors are typically heteromeric complexes co

88 Kainate receptors are widely expressed in the brain, and

89 AMPA/kainate receptors as well as metabotropic glutamate rece

90 g the different temporal signalling roles of kainate receptors, as cones release glutamate over a ran

91 ptically released zinc inhibits postsynaptic kainate receptors at mossy fiber synapses and limits fre

92 properties and kinetic behaviour of AMPA and kainate receptors at the level of single receptor molecu

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

94 ntly solved crystal structures for the GluK2 kainate receptor ATD as a guide, we performed cysteine m

95 The association of kainate receptor ATD dimers is generally weaker than the

96 The free energy maps of AMPA and kainate receptor ATD dimers provide a framework for the

97 AMPA/kainate receptor blockade (NBQX, 100 microM) or Group II

98 al/pharmacological data showed that CeA AMPA/kainate receptor blockade attenuates cisplatin-induced p

99 n trained rabbits was injected with the AMPA/kainate receptor blocker, 1,2,3,4-tetrahydro-6-nitro-2,3

100 -5-methylisoxazol-4-yl)propanoate (AMPA) and kainate receptors bound to full and partial agonists.

101 bipolar cells was blocked by antagonists to kainate receptors but not AMPA receptors.

102 -methyl-4-isoxazolepropionic acid (AMPA) and kainate receptors, but only oscillations in the DP were

103 Strikingly, the activation of kainate receptors by glutamate requires the presence of

104 e presence of zinc, a fall in pH potentiates kainate receptors by relieving zinc inhibition.

105 In neurons, kainate receptors can associate with the auxiliary subun

106 In contrast, desensitization of kainate receptors can be slowed, but not blocked, by sim

107 Kainate receptors can be subject to voltage-dependent bl

108 While some AMPA and kainate receptors can form functional homomeric ion chan

109 systemic ATPA, acting specifically via GluK1 kainate receptors, causes locomotor arrest and forelimb

110 operties of single AMPA receptor (AMPAR) and kainate receptor channels present in CA1 cells in hippoc

111 d knockdown, we determine that Tm5c uses the kainate receptor Clumsy to receive excitatory glutamate

112 just through the NMDA but also mGlu and AMPA/Kainate receptors, completely reversed the cell death ph

113 We conclude that selective activation of kainate receptors containing the GluK1 subunit can trigg

114 Kainate receptors containing the GluK1 subunit have an i

115 The dendrites of kainate receptor-containing cells make basal contacts an

116 Kainate receptors contribute to synaptic plasticity and

117 Although annotated as glutamate and kainate receptors, crystal structures of the ML032222a a

118 tly as auxiliary proteins that slowed GluK2a kainate receptor current kinetics without impacting rece

119 ulted in a significant reduction in synaptic kainate receptor currents.

120 itin ligase to provide a novel mechanism for kainate receptor degradation.

121 ) a dorsomedial region characterized by high kainate receptor density.

122 Like classical LTP, kainate-receptor-dependent LTP recruits recycling endoso

123 isulfides has been previously shown to block kainate receptor desensitization completely.

124 show that sodium and chloride ions modulate kainate receptor dimer affinity as much as 50-fold, and

125 tor mutants and directly measured changes in kainate receptor dimer stability by analytical ultracent

126 the energetic effects of allosteric ions on kainate receptor dimer stability in solution, using a Gl

127 than other glutamate receptors, and synaptic kainate receptors display properties that differ from re

128 r, heterologous expression of the Drosophila kainate receptor DKaiR1D and the AMPA receptor DGluR1A r

129 ptic Ca(2+) influx through calcium-permeable kainate receptors during its induction.

130 Kainate receptors exhibit a highly compartmentalized dis

131 tective effect is mediated through increased kainate receptor expression.

132 ropic receptor with metabotropic properties (kainate receptors) failed to prevent depolarization-indu

133 However, the kainate receptor family consists of five different subun

134 The kainate receptor family of glutamate-gated ion channels

135 selectivity among the more distantly related kainate receptor family.

136 us the plasma membrane localization of GluR6 kainate receptors following mutagenesis of the LBD.

137 aturated in CSF, and that the requirement of kainate receptors for Na(+) occurs simply because other

138 nglion cells confirmed the essential role of kainate receptors for signaling in both transient and su

139 or the high-affinity subunits for ionotropic kainate receptor function and further demonstrate that k

140 new roles for Neto1 and Neto2 in regulating kainate receptor function and identify domains within th

141 This review will cover kainate receptor function and participation in pain sign

142 ould underlie some of the unusual aspects of kainate receptor function in the mammalian CNS.

143 for the PKC-dependent regulation of synaptic kainate receptor function observed during various forms

144 caused complete loss of synaptic ionotropic kainate receptor function.

145 a potentially useful new tool for dissecting kainate receptor function.

146 densities for glutamatergic AMPA, NMDA, and kainate receptors; GABAA receptors; muscarinic M1 , M2 a

147 sitizing D776K mutant provides insights into kainate receptor gating and represents a potentially use

148 Here, by determining the structure of the kainate receptor GluK2 subtype in its desensitized state

149 expression are decreased in mice lacking the kainate receptor GluR6.

150 entified some known SAP102 binding partners, kainate receptor GluR6/7 and inward rectifier potassium

151 n of Neto subunits with recombinant GluK2(Q) kainate receptors greatly reduced inward rectification w

152 Delineating the roles of kainate receptors has been hampered by sub-optimal pharm

153 good evidence that both heteromeric AMPA and kainate receptors have a 2:2 subunit stoichiometry and a

154 Kainate receptors have been implicated in excitotoxic ne

155 Kainate receptor heteromerization and auxiliary subunits

156 he present study highlights the role of AMPA-kainate receptor in IVH-induced white matter injury and

157 the desensitization properties of the GluR6 kainate receptor in response to glutamate application, a

158 pharmacogenetic findings also implicate the kainate receptor in the mechanism of topiramate's effect

159 sed 4.1N interaction with GluK2/3-containing kainate receptors in acute brain slices, an effect that

160 d with combined activation of muscarinic and kainate receptors in different subregions of the medial

161 Neuronal kainate receptors in dorsal root ganglia were sensitive

162 roblasts express mGluR5 and Ca(2+)-permeable kainate receptors in mouse slices.

163 uously released in darkness, activating AMPA/kainate receptors in postsynaptic neurons.

164 eceptor subunits to assess the role of GluK1 kainate receptors in provoking seizures and in kindling

165 We investigated the role of kainate receptors in the generation of theta oscillation

166 previously unsuspected role for postsynaptic kainate receptors in the induction of functional and str

167 y, it was reported that inactivation of AMPA/kainate receptors in the IO produces extinction of condi

168 ceptors was mediated exclusively through the kainate receptors in the transient OFF bipolar cells, wh

169 ical studies demonstrated that activation of kainate receptors increased the frequency, but not the a

170 AMPA-kainate receptor induced excitotoxicity contributes to o

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

172 Here, we show that AMPA-kainate receptor inhibition by NBQX suppresses inflammat

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

174 selectivity toward native GLU(K5)-containing kainate receptors (K(D) 0.105 +/- 0.007 microM vs kainat

175 Here, we show that kainate receptor (KAR) heteromerization and association

176 Phosphorylation or SUMOylation of the kainate receptor (KAR) subunit GluK2 have both individua

177 ole(s) of Rab17 in AMPA receptor (AMPAR) and kainate receptor (KAR) trafficking.

178 Kainate receptor (KAR)-mediated currents are particularl

179 Neto) 1 and Neto2, the auxiliary subunits of kainate receptor (KARs), are phosphorylated by multiple

180 Kainate receptors (KARs) are a subfamily of ionotropic g

181 Kainate receptors (KARs) are found ubiquitously in the C

182 Kainate receptors (KARs) are important modulators of syn

183 Kainate receptors (KARs) are involved in the modulation

184 Kainate receptors (KARs) are ionotropic glutamate recept

185 Kainate receptors (KARs) are ionotropic glutamate recept

186 Kainate receptors (KARs) are neuronal proteins that exhi

187 mit high temporal frequency signals, whereas kainate receptors (KARs) are presumed to encode lower te

188 Heteromeric kainate receptors (KARs) can be assembled from varying c

189 Here we show that activation of kainate receptors (KARs) causes GlyR endocytosis in a ca

190 Kainate receptors (KARs) consist of a class of ionotropi

191 Kainate receptors (KARs) contribute to postsynaptic exci

192 Presynaptic kainate receptors (KARs) exert a modulatory action on tr

193 Activation of presynaptic kainate receptors (KARs) has been shown to reduce inhibi

194 e classes of ionotropic glutamate receptors, kainate receptors (KARs) have a unique brain distributio

195 Kainate receptors (KARs) have been implicated in a numbe

196 Kainate receptors (KARs) have been shown to be involved

197 Interneuronal kainate receptors (KARs) regulate GABAergic transmission

198 coassemble with NMDA receptors (NMDARs) and kainate receptors (KARs) to modulate their function.

199 Kainate receptors (KARs), a family of ionotropic glutama

200 ons of the dorsal root ganglia (DRG) express kainate receptors (KARs), a subfamily of glutamate recep

201 urons in the neonatal DRG express functional kainate receptors (KARs), one of three subfamilies of io

202 , little is known about the effect of ACh on kainate receptors (KARs).

203 lutamate receptors (mGluRs) and augmented by kainate receptors (KARs).

204 nabling efficient 2P activation of the GluK2 kainate receptor, LiGluR.

205 Postsynaptic kainate receptors mediate excitatory synaptic transmissi

206 AMPA and kainate receptors mediate fast synaptic transmission.

207 Kainate receptors mediate fast, excitatory synaptic tran

208 c glutamate receptors (iGluRs), the NMDA and kainate receptors, mediate a majority of excitatory neur

209 Kainate receptors mediated approximately 80% of the syna

210 Kainate receptors mediated responses to contrast modulat

211 Although the kainate receptors mediated the light responses in the su

212 ne or PKA with either H89 or RpcAMPs blocked kainate receptor-mediated actions but did not prevent th

213 ted bursts and reduced the magnitude of AMPA/kainate receptor-mediated bursts.

214 cologically isolated NMDA receptor- and AMPA/kainate receptor-mediated components of the fully develo

215 The augmentation of kainate receptor-mediated currents in the absence of AMP

216 CT depolarisation evoked short-latency, AMPA/kainate receptor-mediated EPSCs in connected GCL neurons

217 Both cell types receive predominantly AMPA/kainate receptor-mediated excitatory synaptic input that

218 for the cAMP/PKA system as a requirement for kainate receptor-mediated inhibition of I(sAHP).

219 Despite this, kainate receptor-mediated inhibition of the slow afterhy

220 e activity of MSNs via a glutamatergic, AMPA/kainate receptor-mediated mechanism, indicated by increa

221 primarily controlled by two classes of AMPA/kainate receptor-mediated synaptic inputs derived from o

222 dings in hippocampal slices demonstrate that kainate-receptor-mediated excitatory postsynaptic curren

223 fficking of the receptors and also modulates kainate-receptor-mediated mEPSCs.

224 gate this, we constructed a library of GluR6 kainate receptor mutants and directly measured changes i

225 tive activity, may therefore serve to unmask kainate receptor neurotransmission.

226 Relative to the homologous AMPA and kainate receptors, NMDA receptors have additional inters

227 normal LTP, as did an artificially expressed kainate receptor not normally found at these synapses.

228 The kainate receptor occupies a position distinct from that

229 Kainate receptors of astrocytes act as sensors of extrac

230 Within individual neurons, kainate receptors of different subunit compositions are

231 utamate as a neurotransmitter acting on AMPA/kainate receptors of second-order neurons.

232 the long duration of metabotropic actions of kainate receptors on I(sAHP).

233 NMDAR antagonists, but not blockers of AMPA/kainate receptors or voltage-gated sodium channels, prev

234 ceptor function and further demonstrate that kainate receptor participation in metabotropic signaling

235 NMDA receptors and kainate receptors play roles in synaptic transmission, b

236 ndly slows the desensitization rate of GluK1 kainate receptors, promotes plasma membrane localization

237 receptor; GluR5-7 and KA1-2 subunits of the kainate receptor; PSD95), all but two (GluR4 and KA1) we

238 r results have revealed a mechanism by which kainate receptors regulate KCC2 expression in the hippoc

239 Furthermore, we found that kainate receptors regulate the surface expression of NET

240 Kainate receptors require the presence of external ions

241 relate of this action - activation of PKC by kainate receptors - requires G alpha(i/o) proteins.

242 erface mutants, and that the deactivation of kainate receptor responses is dominated by entry into de

243 Kainate receptor responses to domoate are characterized

244 receptor, along with the wild-type rat GluK2 kainate receptor (rGluK2) as the control.

245 We conclude that zinc modulation of kainate receptors serves an important role in shaping ka

246 AMPA and kainate receptors share a high degree of sequence and st

247 The 7.6 A structure of a desensitized kainate receptor shows how these changes accommodate cha

248 hly with expression of Ca(2+)-permeable AMPA/kainate receptors, shows a laminar pattern of distributi

249 Kainate receptors signal through both ionotropic and met

250 Incorporation of NETO proteins into kainate receptor-signaling complexes therefore extends t

251 oxy-5-methyl-4-isoxazole propionic acid) and kainate receptor subtypes in their major functional stat

252 resting and desensitized states of AMPA and kainate receptor subtypes, the ion channels are closed,

253 ubunits that combined segments from NMDA and kainate receptors, subtypes with distinct pharmacologica

254 of a single gene coding for a high-affinity kainate receptor subunit (i.e., grik4) in a limited area

255 g that fusing the N-terminal 150 residues of kainate receptor subunit 2 (KA2) to the recently discove

256 The grik2 gene, coding for the kainate receptor subunit GluK2 (formerly GluR6), is asso

257 hippocampal neurons, we discovered that the kainate receptor subunit GluK2 and the auxiliary subunit

258 loop apex and the transmembrane M3 helix of kainate receptor subunit GluK2.

259 -I mRNA editing at the Q/R site of the human kainate receptor subunit GluR5 and was compared with two

260 d the splicing pattern and expression of the kainate receptor subunit GluR6 in human fibroblast cell

261 are present at synapses and we show that the kainate receptor subunit GluR6 is a SUMO substrate.

262 We conclude that GluK1 is the predominant kainate receptor subunit in cb1 and cb3 Off bipolar cell

263 as a critical mechanism for retention of the kainate receptor subunit KA2 in the endoplasmic reticulu

264 GluK2 is a kainate receptor subunit that is alternatively spliced a

265 wn about the molecular mechanisms regulating kainate receptor subunit trafficking.

266 The results show that NETO2 is a kainate receptor subunit with significant effects on glu

267 reased expression of the GluK5 high-affinity kainate receptor subunit.

268 sphorylation in the trafficking of the GluR6 kainate receptor subunit.

269 with homologous segments from the rat GluK2 kainate receptor subunit.

270 -expression of Neto1 and 2 with pore-forming kainate receptor subunits also increases the duration of

271 Kainate receptor subunits can form functional channels a

272 Here we report that the GluK1 and GluK2 kainate receptor subunits interact with the spectrin-act

273 ction with mice deficient in GluK1 and GluK2 kainate receptor subunits to assess the role of GluK1 ka

274 Xenopus oocytes injected with cRNA encoding kainate receptor subunits, we have observed that heterom

275 In particular, the slow decay of kainate receptor synaptic currents contrasts with the ra

276 ained 25 genes involved in the regulation of kainate receptors, TGF-beta and Wnt signaling, as well a

277 1a/b cells were mediated by GluK1-containing kainate receptors that behaved differently from the rece

278 much less well understood, particularly for kainate receptors that exist as multiple subtypes with a

279 id (ATPA), a potent and selective agonist of kainate receptors that include the GluK1 subunit, in con

280 ty and by synaptic activation of presynaptic kainate receptors that increase release probability on s

281 xcitatory neurotransmitter that binds to the kainate receptor, the N-methyl-D-aspartate (NMDA) recept

282 could be related to increased sensitivity of kainate receptors to endogenous glutamate, effects of th

283 However, allocation of functional kainate receptors to known cell types and their sensitiv

284 mately 21 A resolution, of full-length GluK2 kainate receptors trapped in antagonist-bound resting an

285 at an aberrant readout of synaptic inputs by kainate receptors triggered a long-lasting impairment of

286 Similarly, the most common phenotype for kainate receptor variants is intellectual disability.

287 erologous systems, the temporal responses of kainate receptors vary when different channel-forming an

288 Galectin modulation of GluK2 kainate receptors was dependent upon complex oligosaccha

289 ts the channel properties of the human GluK2 kainate receptor, we have systematically characterized t

290 fferent fibers express Ca(2+)-permeable AMPA/kainate receptors, we utilized kainate-stimulated uptake

291 and growth cone splitting when NMDA and AMPA/kainate receptors were activated.

292 In contrast, when AMPA/kainate receptors were selectively activated, axon growt

293 ese findings place GluRdelta2 among AMPA and kainate receptors, where the dimer interface is not only

294 Hyperpolarizing bipolar cells express AMPA/kainate receptors, whereas depolarizing bipolar cells (D

295 In contrast, the lesser-studied kainate receptors, which are often present at both pre-

296 promoting the insertion and stabilization of kainate receptors, which may be important for tuning neu

297 on of the CRH system following activation of kainate receptors, which may result in long-term changes

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

299 no-terminal domain tetramer in AMPA, but not kainate, receptors with a two-fold to four-fold symmetry

300 channel properties of recombinant and native kainate receptors without affecting trafficking of the r