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1 glutamate receptors (AMPA and NMDA, but not kainate).
2 of 2e and 2f shows a similar binding mode as kainate.
3 activity were evoked by local application of kainate.
4 highest sensitivity of all inner neurons to kainate.
5 omplex with 2i comparable to that induced by kainate.
6 arable to those of the distal carboxylate in kainate.
8 some 1 (GRIK3 (glutamate receptor ionotropic kainate 3)), chromosome 4 (KLHL2 (Kelch-like protein 2))
11 ctive a dorsomedial subdivision; 3) distinct kainate, alpha2 , and muscarinic receptor densities that
13 he transient OFF bipolar cells, whereas both kainate and AMPA receptors contributed in the other cell
14 tabilities of homodimers and heterodimers of kainate and AMPA receptors using fluorescence-detected s
18 We therefore designed experiments to compare kainate and glutamate desensitization and efficacy in wi
20 p5I and CVNs were completely blocked by AMPA/kainate and NMDA glutamatergic receptor antagonists.
21 ynaptic pathways via modulation of both AMPA/kainate and NMDA receptors at different synapses in the
23 in addition to the NMDA receptor, the AMPA, kainate and the metabotropic GluRs may be targets for th
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 inct clade from the well-characterized AMPA, kainate, and NMDA iGluR subtypes found in vertebrates.
28 that is notably absent from vertebrate AMPA, kainate, and NMDA iGluRs greatly increases the rate of r
31 the proconvulsant activity of systemic AMPA, kainate, and pentylenetetrazol is not mediated by GluK1
32 aneo), and here we compare the properties of kainate- and carbachol-induced oscillatory activity gene
33 vey of iGluR gene expression revealed AMPA-, Kainate-, and NMDA-type subunits are expressed in zebraf
37 ull agonist glutamate or the partial agonist kainate, consistent with conductance state-dependent blo
38 ith stargazin was the result of both reduced kainate desensitization and increased kainate efficacy.
40 A receptor-mediated responses to the agonist kainate differ from those of glutamate in two important
43 ls of GluK2/3 in primary neurons and reduced kainate-evoked currents in CA1 pyramidal neurons in acut
45 luN1/GluN2B NMDA receptors, as well as AMPA, kainate, GABA, glycine, nicotinic, serotonin, and purine
46 e densities for glutamatergic AMPA, NMDA and kainate, GABAergic GABAA , muscarinic M1 , M2 and nicoti
49 ious studies, stimulation of ionotropic AMPA/kainate glutamate receptors on cultured oligodendrocyte
51 the relative efficacy of the partial agonist kainate (I(KA)/I(Glu) ratio 0.4) and a greater than five
54 nction persists, indicated by alterations in kainate-induced gamma oscillations and impaired nest bui
55 ated deSUMOylation of PKC is involved in the kainate-induced GlyR endocytosis and thus plays an impor
56 2-expressing astrocytes reduces the power of kainate-induced hippocampal ex vivo gamma oscillation.
57 We found that 5-HT decreases the power of kainate-induced hippocampal gamma oscillations in both s
59 f an M-channel inhibitor that did not affect kainate-induced seizure transiently eliminated the antic
61 at model of massive neuronal activation upon kainate-induced seizures we found that elevated neuronal
62 and SCaMC-3 KO mice are more susceptible to kainate-induced seizures, showing that early PARP-1-depe
66 irm that horizontal cell depolarization with kainate inhibits and horizontal cell hyperpolarization w
69 ts strongly desensitizing responses, whereas kainate is a partial agonist with responses that are oft
70 CRMP4 proteins with the GluK5 subunit of the kainate (KA) receptor (KAR) and investigated the role of
76 able in the two species in layers III-Va for kainate, NMDA, gamma-aminobutyric acid (GABA)B , BZ, and
80 mplex in the presence of the partial agonist kainate or the full agonist quisqualate together with a
82 ligand-binding domain gating ring, enhancing kainate potency and diminishing the ensemble of desensit
86 Neto) 1 and Neto2, the auxiliary subunits of kainate receptor (KARs), are phosphorylated by multiple
87 ed antidepressant-like effects required AMPA/kainate receptor activation, as evidenced by the ability
88 in GluK5 expression is sufficient to enhance kainate receptor activity by modulating receptor channel
89 at loss of synaptic AMPA receptors increased kainate receptor activity in cerebellar granule cells wi
90 acological inhibition or genetic ablation of kainate receptor activity reduces pain behaviors in a nu
91 ochemistry, and pharmacology to identify the kainate receptor and auxiliary subunits in ground squirr
92 on treatment of an acutely administered AMPA/kainate receptor antagonist and delayed transplantation
93 These findings show that a highly selective kainate receptor antagonist can affect the deficits in s
94 no-3-hydroxy-5-methyl-4-isoxazole propionate/kainate receptor antagonist CNQX (0, .01, .03, .1 mug/si
95 finding that intracore injection of the AMPA/kainate receptor antagonist CNQX attenuated the ability
98 havioral responses to kainic acid and that a kainate receptor antagonist normalized altered behaviors
100 t work examined effects of another selective kainate receptor antagonist, (S)-1-(2-Amino-2-carboxyeth
101 A) receptor antagonist, but not an NMDA/AMPA/kainate receptor antagonist, suggesting that they were m
102 further support for the idea that selective kainate receptor antagonists could be novel therapeutic
103 Compounds 18i and (-)-4 were the most potent kainate receptor antagonists, and 18i was selective for
106 al/pharmacological data showed that CeA AMPA/kainate receptor blockade attenuates cisplatin-induced p
107 d knockdown, we determine that Tm5c uses the kainate receptor Clumsy to receive excitatory glutamate
109 tly as auxiliary proteins that slowed GluK2a kainate receptor current kinetics without impacting rece
111 r, heterologous expression of the Drosophila kainate receptor DKaiR1D and the AMPA receptor DGluR1A r
115 new roles for Neto1 and Neto2 in regulating kainate receptor function and identify domains within th
118 Here, by determining the structure of the kainate receptor GluK2 subtype in its desensitized state
119 entified some known SAP102 binding partners, kainate receptor GluR6/7 and inward rectifier potassium
121 he present study highlights the role of AMPA-kainate receptor in IVH-induced white matter injury and
122 pharmacogenetic findings also implicate the kainate receptor in the mechanism of topiramate's effect
126 via AMPA receptor activation, and that AMPA-kainate receptor inhibition suppresses inflammation and
127 normal LTP, as did an artificially expressed kainate receptor not normally found at these synapses.
129 utive mGluR7 recruitment and regulated GluK2 kainate receptor recruitment, revealing a mechanism that
131 oxy-5-methyl-4-isoxazole propionic acid) and kainate receptor subtypes in their major functional stat
132 resting and desensitized states of AMPA and kainate receptor subtypes, the ion channels are closed,
133 of a single gene coding for a high-affinity kainate receptor subunit (i.e., grik4) in a limited area
134 g that fusing the N-terminal 150 residues of kainate receptor subunit 2 (KA2) to the recently discove
136 hippocampal neurons, we discovered that the kainate receptor subunit GluK2 and the auxiliary subunit
138 We conclude that GluK1 is the predominant kainate receptor subunit in cb1 and cb3 Off bipolar cell
141 -expression of Neto1 and 2 with pore-forming kainate receptor subunits also increases the duration of
142 Here we report that the GluK1 and GluK2 kainate receptor subunits interact with the spectrin-act
143 ction with mice deficient in GluK1 and GluK2 kainate receptor subunits to assess the role of GluK1 ka
144 FB9s-b selectively inhibited GluK1 and GluK2 kainate receptor subunits, and also GluK1/GluK5 and GluK
145 ans in the disease state, including AMPA and kainate receptor subunits, glutamate transporters EAAT1
151 ction of both NMDA receptor (NMDAR) and AMPA/kainate receptor-mediated evoked excitatory postsynaptic
152 e activity of MSNs via a glutamatergic, AMPA/kainate receptor-mediated mechanism, indicated by increa
161 mit high temporal frequency signals, whereas kainate receptors (KARs) are presumed to encode lower te
166 e classes of ionotropic glutamate receptors, kainate receptors (KARs) have a unique brain distributio
169 coassemble with NMDA receptors (NMDARs) and kainate receptors (KARs) to modulate their function.
171 ons of the dorsal root ganglia (DRG) express kainate receptors (KARs), a subfamily of glutamate recep
172 urons in the neonatal DRG express functional kainate receptors (KARs), one of three subfamilies of io
174 ; a presynaptic form (pre-LTP) that requires kainate receptors and a postsynaptic form (post-LTP) tha
175 pathway requires the metabotropic action of kainate receptors and activation of G protein, protein k
176 ke-2 (Neto2) as a novel accessory subunit of kainate receptors and showed that Neto2 modulates the ga
177 l-4-isoxazolepropionic acid, and heteromeric kainate receptors are all downstream targets of GPCR sig
183 uK2 knock-out mice, demonstrating that GluK1 kainate receptors are not required for epileptogenesis o
184 properties and kinetic behaviour of AMPA and kainate receptors at the level of single receptor molecu
185 -5-methylisoxazol-4-yl)propanoate (AMPA) and kainate receptors bound to full and partial agonists.
191 tropic glutamate receptor 7) and GluK2-KARs (kainate receptors containing glutamate receptor, ionotro
192 We conclude that selective activation of kainate receptors containing the GluK1 subunit can trigg
194 than other glutamate receptors, and synaptic kainate receptors display properties that differ from re
197 nglion cells confirmed the essential role of kainate receptors for signaling in both transient and su
198 n of Neto subunits with recombinant GluK2(Q) kainate receptors greatly reduced inward rectification w
199 good evidence that both heteromeric AMPA and kainate receptors have a 2:2 subunit stoichiometry and a
200 sed 4.1N interaction with GluK2/3-containing kainate receptors in acute brain slices, an effect that
201 d with combined activation of muscarinic and kainate receptors in different subregions of the medial
204 eceptor subunits to assess the role of GluK1 kainate receptors in provoking seizures and in kindling
205 previously unsuspected role for postsynaptic kainate receptors in the induction of functional and str
206 ceptors was mediated exclusively through the kainate receptors in the transient OFF bipolar cells, wh
213 identified glutamate receptors, for example, kainate receptors on which NMDA acts as a competitive an
214 NMDAR antagonists, but not blockers of AMPA/kainate receptors or voltage-gated sodium channels, prev
215 r results have revealed a mechanism by which kainate receptors regulate KCC2 expression in the hippoc
218 1a/b cells were mediated by GluK1-containing kainate receptors that behaved differently from the rece
219 id (ATPA), a potent and selective agonist of kainate receptors that include the GluK1 subunit, in con
221 mately 21 A resolution, of full-length GluK2 kainate receptors trapped in antagonist-bound resting an
222 at an aberrant readout of synaptic inputs by kainate receptors triggered a long-lasting impairment of
223 erologous systems, the temporal responses of kainate receptors vary when different channel-forming an
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
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
237 ntagonists of these receptors, especially of kainate receptors, is useful for developing potential tr
238 c glutamate receptors (iGluRs), the NMDA and kainate receptors, mediate a majority of excitatory neur
240 ndly slows the desensitization rate of GluK1 kainate receptors, promotes plasma membrane localization
241 ubunits that combined segments from NMDA and kainate receptors, subtypes with distinct pharmacologica
243 promoting the insertion and stabilization of kainate receptors, which may be important for tuning neu
267 densities for glutamatergic AMPA, NMDA, and kainate receptors; GABAA receptors; muscarinic M1 , M2 a
268 no-terminal domain tetramer in AMPA, but not kainate, receptors with a two-fold to four-fold symmetry
270 and a greater than fivefold potentiation of kainate responses by cyclothiazide-suggest AMPAR associa
272 acrine (ACs) and ganglion cells (GCs) showed kainate responses with different sensitivities between m
277 uanidobutane agmatine (AGB), we investigated kainate sensitivity of neurochemically identified cell p
279 er, hyperactive shifts in neuronal activity (kainate status epilepticus and CaMKIIa Gq DREADD activat
280 a selective impairment of depolarization- or kainate-stimulated glutamate and [(3)H]d-aspartate relea
281 -methyl-3-hydroxy-4-isoxazole propionate and kainate subtypes of the ionotropic glutamate receptors.
282 non-NMDA glutamate receptors (both AMPA and kainate subtypes) are modulated by the association of th
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
287 f episodic-like memory in rats, we show that kainate-treated TLE rats exhibit a selective impairment
294 mammals, the selective expression of AMPA or kainate-type glutamate receptors in the dendrites of dif
298 s restricted period of synaptic development, kainate-type of ionotropic glutamate receptors (KARs) ar
299 ropic glutamate subfamilies (i.e. AMPA-type, kainate-type, and NMDA-type) assemble as tetramers of fo
300 ed cholinergic ACs were highly responsive to kainate, whereas dopaminergic ACs do not appear to expre