ライフサイエンスコーパス: kainate

1 glutamate receptors (AMPA and NMDA, but not kainate).

2 highest sensitivity of all inner neurons to kainate.

3 omplex with 2i comparable to that induced by kainate.

4 after microinjection of a neurotoxic dose of kainate.

5 wild type mouse after prolonged exposure to kainate.

6 restored by Epo in the continued presence of kainate.

7 arable to those of the distal carboxylate in kainate.

8 of 2e and 2f shows a similar binding mode as kainate.

9 activity were evoked by local application of kainate.

10 some 1 (GRIK3 (glutamate receptor ionotropic kainate 3)), chromosome 4 (KLHL2 (Kelch-like protein 2))

11 ogenetic modulation of gamma oscillations in kainate-activated hippocampal slices.

12 eversing behavioral effects of the selective kainate agonist ATPA.

13 ctive a dorsomedial subdivision; 3) distinct kainate, alpha2 , and muscarinic receptor densities that

14 he transient OFF bipolar cells, whereas both kainate and AMPA receptors contributed in the other cell

15 These results establish that kainate and AMPA receptors have a conserved extracellula

16 tabilities of homodimers and heterodimers of kainate and AMPA receptors using fluorescence-detected s

17 osing effects on 4.1N association with GluK2 kainate and GluA1 AMPA receptors.

18 We therefore designed experiments to compare kainate and glutamate desensitization and efficacy in wi

19 p5I and CVNs were completely blocked by AMPA/kainate and NMDA glutamatergic receptor antagonists.

20 ynaptic pathways via modulation of both AMPA/kainate and NMDA receptors at different synapses in the

21 els of SE-induced epilepsy: intrahippocampal kainate and systemic administration of paraoxon.

22 in addition to the NMDA receptor, the AMPA, kainate and the metabotropic GluRs may be targets for th

23 eive glutamatergic inputs via non-NMDA (AMPA/kainate) and NMDA receptors, while VS-GCs receive additi

24 ith an antagonist (CNQX), a partial agonist (kainate), and two full agonists (glutamate and quisquala

25 ntaining the GluN2A or GluN2B subunits AMPA, kainate, and GABA or glycine receptors or a variety of o

26 ic pathway, and mature N-methyl-d-aspartate, kainate, and GABA(A) receptors did not reach the synapse

27 roxy-S-methyl-4-isoxazole propionate (AMPA), kainate, and N-methyl-d-aspartate (NMDA) receptors, are

28 inct clade from the well-characterized AMPA, kainate, and NMDA iGluR subtypes found in vertebrates.

29 that is notably absent from vertebrate AMPA, kainate, and NMDA iGluRs greatly increases the rate of r

30 Phylogenetic analysis reveals AMPA, kainate, and NMDA receptor families in insect genomes, s

31 iGluRs (AMPA, kainate, and NMDA receptor subtypes) are tetrameric asse

32 the proconvulsant activity of systemic AMPA, kainate, and pentylenetetrazol is not mediated by GluK1

33 aneo), and here we compare the properties of kainate- and carbachol-induced oscillatory activity gene

34 vey of iGluR gene expression revealed AMPA-, Kainate-, and NMDA-type subunits are expressed in zebraf

35 Area p32 contains higher kainate, benzodiazepine (BZ), and serotonin (5-HT)1A but

36 en historically defined by (3)H-radiolabeled kainate binding.

37 Notably, the dose of kainate capable of inducing an approximately 50% rate of

38 formational change relative to the wild-type:kainate complex involves a twisting motion with the effi

39 ull agonist glutamate or the partial agonist kainate, consistent with conductance state-dependent blo

40 ith stargazin was the result of both reduced kainate desensitization and increased kainate efficacy.

41 much less is known about factors that affect kainate desensitization.

42 A receptor-mediated responses to the agonist kainate differ from those of glutamate in two important

43 Kainate efficacy was affected by factors distinct from l

44 educed kainate desensitization and increased kainate efficacy.

45 s and largely rescue behavioural deficits in kainate-exposed animals.

46 e the mechanisms of binding of glutamate and kainate (full and partial agonists, respectively) to a s

47 luN1/GluN2B NMDA receptors, as well as AMPA, kainate, GABA, glycine, nicotinic, serotonin, and purine

48 e densities for glutamatergic AMPA, NMDA and kainate, GABAergic GABAA , muscarinic M1 , M2 and nicoti

49 ymorphism (rs2832407) in GRIK1, encoding the kainate GluK1 receptor subunit.

50 We examined the AMPA and kainate glutamate receptor composition in each bipolar c

51 ious studies, stimulation of ionotropic AMPA/kainate glutamate receptors on cultured oligodendrocyte

52 pplication of a GABAA receptor antagonist or kainate, glutamate receptor agonist.

53 the relative efficacy of the partial agonist kainate (I(KA)/I(Glu) ratio 0.4) and a greater than five

54 nner retinal neuron populations responded to kainate in a concentration-dependent manner.

55 However, exposure of S940A mice to kainate induced lethality within 30 min of kainate injec

56 rimary L-type Ca(2+) channel contributing to kainate-induced excitotoxic death of amacrine and gangli

57 nction persists, indicated by alterations in kainate-induced gamma oscillations and impaired nest bui

58 ated deSUMOylation of PKC is involved in the kainate-induced GlyR endocytosis and thus plays an impor

59 2-expressing astrocytes reduces the power of kainate-induced hippocampal ex vivo gamma oscillation.

60 We found that 5-HT decreases the power of kainate-induced hippocampal gamma oscillations in both s

61 In a kainate-induced murine seizure model, administration of

62 he stratum oriens lamina of CA3, but for the kainate-induced oscillations, area power became signific

63 glutamate and glutamine were studied in the kainate-induced rat model of epilepsy in the chronic pha

64 f an M-channel inhibitor that did not affect kainate-induced seizure transiently eliminated the antic

65 ctly monitor the acute structural effects of kainate-induced seizures on cortical astrocytes.

66 at model of massive neuronal activation upon kainate-induced seizures we found that elevated neuronal

67 and SCaMC-3 KO mice are more susceptible to kainate-induced seizures, showing that early PARP-1-depe

68 major brain Nav channel, Nav1.2, after acute kainate-induced seizures.

69 ease, PRS rats were also highly resistant to kainate-induced seizures.

70 Lastly, kainate-induced status epilepticus causes GIRK1 and GIRK

71 irm that horizontal cell depolarization with kainate inhibits and horizontal cell hyperpolarization w

72 o kainate induced lethality within 30 min of kainate injection and subsequent entrance into SE.

73 When isoflurane was administered during kainate injection, duration and severity of SE were not

74 ion sampled by microdialysis and the site of kainate injection, intracellular glutamine concentration

75 ts strongly desensitizing responses, whereas kainate is a partial agonist with responses that are oft

76 xy-5-methyl-4-isoxale propionate (AMPA), and kainate (KA) elicit feeding when microinjected into the

77 CRMP4 proteins with the GluK5 subunit of the kainate (KA) receptor (KAR) and investigated the role of

78 tivity in the rat hippocampus in response to kainate (KA)-induced epileptogenesis.

79 Using a combination of kainate (KA, 200 nm) and the cholinergic agonist carbach

80 campal astrocytes generated from control and kainate-lesioned rats.

81 rotransmission from AWC and through AMPA and kainate-like glutamate receptor subunits.

82 isoflurane reduced neuroinflammation in the kainate model.

83 able in the two species in layers III-Va for kainate, NMDA, gamma-aminobutyric acid (GABA)B , BZ, and

84 in all mouse OFF bipolar pathways depend on kainate, not AMPA, receptors.

85 d release acetylcholine when stimulated with kainate or a lowering in glucose concentration.

86 ny effect on other AMPA receptor subunits or kainate or NMDA receptors.

87 mplex in the presence of the partial agonist kainate or the full agonist quisqualate together with a

88 Isoflurane was either administered during (kainate) or after (paraoxon) induction of SE.

89 ligand-binding domain gating ring, enhancing kainate potency and diminishing the ensemble of desensit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 The AMPA/kainate receptor antagonist NBQX was directly administer

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

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

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

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

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

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

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

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

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

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

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

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

118 The kainate receptor family of glutamate-gated ion channels

119 selectivity among the more distantly related kainate receptor family.

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

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

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

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

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

125 Kainate receptor heteromerization and auxiliary subunits

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

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

128 AMPA-kainate receptor induced excitotoxicity contributes to o

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

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

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

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

133 The kainate receptor occupies a position distinct from that

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 Kainate receptors (KARs) are important modulators of syn

163 Kainate receptors (KARs) are ionotropic glutamate recept

164 Kainate receptors (KARs) are ionotropic glutamate recept

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

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

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

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

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

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

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

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

173 Interneuronal kainate receptors (KARs) regulate GABAergic transmission

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

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

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

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

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

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

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

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

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

183 Kainate receptors are also expressed throughout central

184 Kainate receptors are further classified into low-affini

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

186 Kainate receptors are less well understood than other gl

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

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

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

190 -5-methylisoxazol-4-yl)propanoate (AMPA) and kainate receptors bound to full and partial agonists.

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

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

193 Kainate receptors can be subject to voltage-dependent bl

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

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

196 Kainate receptors containing the GluK1 subunit have an i

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

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

199 Kainate receptors exhibit a highly compartmentalized dis

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

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

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

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

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

205 Neuronal kainate receptors in dorsal root ganglia were sensitive

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

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

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

209 Postsynaptic kainate receptors mediate excitatory synaptic transmissi

210 Kainate receptors mediate fast, excitatory synaptic tran

211 Kainate receptors mediated approximately 80% of the syna

212 Kainate receptors mediated responses to contrast modulat

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

214 Kainate receptors of astrocytes act as sensors of extrac

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

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

217 Kainate receptors require the presence of external ions

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

219 1a/b cells were mediated by GluK1-containing kainate receptors that behaved differently from the rece

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

243 ivity for effectively blocking both AMPA and kainate receptors.

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

245 xcitability through their actions on AMPA or kainate receptors.

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

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

248 combinant homomeric and heteromeric AMPA and kainate receptors.

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

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

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

252 on structure currently exists of heteromeric kainate receptors.

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

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

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

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

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

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

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

260 c currents in neurons expressing recombinant kainate receptors.

261 for recombinant NMDA receptors over AMPA and kainate receptors.

262 F bipolar cells were exclusively mediated by kainate receptors.

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

264 e granule cells and operate via postsynaptic kainate receptors.

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

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

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

268 The efficacy of kainate relative to glutamate has previously been shown

269 and a greater than fivefold potentiation of kainate responses by cyclothiazide-suggest AMPAR associa

270 The increase in kainate responses for AMPA receptors coexpressed with st

271 acrine (ACs) and ganglion cells (GCs) showed kainate responses with different sensitivities between m

272 In wild-type mice, SE induced by kainate resulted in dephosphorylation of S940 and KCC2 i

273 Brief treatment with NMDA and kainate results in loss of IHC-SGN synapses and degenera

274 Kainate seizures cause an immediate, but transient, vacu

275 that type 2 bipolar cells were part of this kainate-sensitive population.

276 uanidobutane agmatine (AGB), we investigated kainate sensitivity of neurochemically identified cell p

277 losing equilibria detected for glutamate and kainate should be useful structural measures for interpr

278 On GluA2(A621G), the partial agonist kainate showed efficacy similar to a full agonist, and c

279 a selective impairment of depolarization- or kainate-stimulated glutamate and [(3)H]d-aspartate relea

280 -methyl-3-hydroxy-4-isoxazole propionate and kainate subtypes of the ionotropic glutamate receptors.

281 non-NMDA glutamate receptors (both AMPA and kainate subtypes) are modulated by the association of th

282 Exposure of cells to 100 microM kainate suppressed cellular GSH and caused excitotoxicit

283 as studied and compared between controls and kainate-treated rats, a model of temporal lobe epilepsy,

284 the blood-brain barrier between control and kainate-treated rats, and the effect of tariquidar treat

285 B(max) was decreased in kainate-treated rats, compared with controls, but no alt

286 B(max) was decreased by 12% in kainate-treated rats, compared with controls.

287 f episodic-like memory in rats, we show that kainate-treated TLE rats exhibit a selective impairment

288 We further evaluated the effects of kainate treatment on the total number, density, and soma

289 otropic glutamate receptors (AMPA, NMDA, and kainate type), AMPA receptor activity is most regulatabl

290 ding for a glutamate receptor subunit of the kainate type.

291 d since the first report of the cloning of a kainate-type glutamate receptor (KAR) subunit.

292 Presynaptic kainate-type glutamate receptors (KARs) regulate glutama

293 Postsynaptic kainate-type glutamate receptors (KARs) regulate synapti

294 mammals, the selective expression of AMPA or kainate-type glutamate receptors in the dendrites of dif

295 by the differential expression of AMPA- and kainate-type glutamate receptors, respectively.

296 ecently identified as auxiliary subunits for kainate-type glutamate receptors.

297 ssembly occurs for homomeric and heteromeric kainate-type glutamate receptors.

298 ropic glutamate subfamilies (i.e. AMPA-type, kainate-type, and NMDA-type) assemble as tetramers of fo

299 ed cholinergic ACs were highly responsive to kainate, whereas dopaminergic ACs do not appear to expre

300 bstitution enhances the relative efficacy of kainate without increasing either LBD cleft closure or t