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1  glutamate receptor agonists (AMPA, kainate, quisqualate).
2 of Ca2+ oscillations induced by glutamate or quisqualate.
3 tered the relative efficacy of glutamate and quisqualate.
4 ion by its namesake agonist AMPA and also by quisqualate.
5 m HEK cells or cortical cell types bound [3H]quisqualate.
6 esponses evoked by the orthosteric agonist l-quisqualate.
7 ists was ibotenate > L-glutamate > kainate = quisqualate.
8 s, such as N-methyl-d-aspartate, kainate and quisqualate.
9 erebroventricular (i.c.v.) administration of quisqualate.
10 acid but were not significantly displaced by quisqualate.
11  this current is preferentially activated by quisqualate.
12 ibution, and are differentially sensitive to quisqualate.
13  in Gm, a response similar to that evoked by quisqualate.
14 was more sensitive to NEM than inhibition by quisqualate.
15 ed the peak amplitude of the Ca2+ signals to quisqualate (1 microM; Quis) in both the somatic and den
16 lication of the type I and II mGluR agonists quisqualate (10 micro;M), trans-(+/-)-1-amino-1,3-cyclop
17 -decarboxylic acid (1S,3R-ACPD; 200 microM), quisqualate (10 microM) and (2S,1'S,2'S)-2-(carboxycyclo
18           When recording with K+ electrodes, quisqualate (10-50 microM) produced an inward current wh
19            At a holding potential of -70 mV, quisqualate (2 microM) induced an inward current of abou
20  microM), N-methyl-D-aspartate (100 microM), quisqualate (300 microM), or kainate (100 microM) increa
21 rch states that non-NMDA glutamate agonists (quisqualate (5 microliters of 2 mg/ml i.c.v.), AMPA (4 m
22 lectrodes in external Ba2+ and Cs+ solution, quisqualate activated an inward current more potently th
23 ent negative cooperativity for modulation of quisqualate affinity, and the NAMs CPCCOEt and PF-064628
24 with a positive allosteric modulator or with quisqualate alone.
25              Inhibition of System X(C)- with quisqualate also decreased cystine uptake in both astroc
26 e on synaptic activity, it was observed that quisqualate also induced a slow inward current.
27                     Inhibition by DCG-IV and quisqualate also was reduced by omega-CgTx.
28 d activated both signaling pathways, whereas quisqualate and (S)-3,5-dihydroxyphenylglycine stimulate
29 abotropic glutamate receptor (mGlu) agonists quisqualate and 1S,3R-1-aminocyclopentane-1,3-dicarboxyl
30 data are consistent with the hypothesis that quisqualate and 1S,3R-ACPD in Ba2+ and Cs+ solution acti
31 -millisecond conformational dynamics because quisqualate and AMPA bind with similar affinities that a
32 and ketamine (60 mg/kg i.p.) both diminished quisqualate and AMPA hsp70 induction in the CA1, CA2, CA
33                                Inhibition by quisqualate and DCG-IV was nonocclusive in neurons respo
34                                Inhibition by quisqualate and DCG-IV was voltage-dependent.
35  rises, whereas in a smaller number of cells quisqualate and L-CCG-I showed both inhibitory and addit
36 als elicited by glutamate receptor agonists (quisqualate and NMDA) was examined in developing cerebel
37 on of responses to the orthosteric agonist l-quisqualate and the allosteric modulator Ro 67-4853 by e
38 allographic data on the interactions between quisqualate and the GluR2 receptor ion channel and its c
39 sistent with those of group 1 (high-affinity quisqualate) and group 2 (low-affinity quisqualate) mGlu
40  glutamic acid (glutamate), quisqualic acid (quisqualate), and alpha-amino-3-hydroxy-5-methyl-4-isoxa
41    Incubation of the cells with L-glutamate, quisqualate, and 1-aminocyclopentane-1S, 3R-dicarboxylic
42  by four different ligands, glutamate, AMPA, quisqualate, and 2-Me-Tet-AMPA, full agonists that vary
43 otentiates threshold responses to glutamate, quisqualate, and 3,5-dihydroxyphenylglycine in fluoromet
44 rences exist between the agonists glutamate, quisqualate, and AMPA in modulating glutamate receptor f
45 enylglycine attenuated inhibition by t-ACPD, quisqualate, and DCG-IV.
46                  These data suggest that the quisqualate- and 1S,3R-ACPD-induced currents are mediate
47                                          The quisqualate- and 1S,3R-ACPD-induced inward currents were
48 or 50 mM) or with 100 mM choline reduced the quisqualate- and 1S,3R-ACPD-induced inward currents, res
49 e LY393053 and LY367366 not only blocked [3H]quisqualate binding but also prevented nontransported ag
50               Nevertheless, the mechanism of quisqualate binding is different from that of AMPA but s
51 -CCG-I displaces both high- and low-affinity quisqualate binding sites, but unlike the other two comp
52  DCG-IV binding correlates with low-affinity quisqualate binding, whereas low-affinity DCG-IV binding
53 DCG-IV binding correlates with high-affinity quisqualate binding.
54 mate binding, corresponding to high-affinity quisqualate binding.
55 onformationally distinct from glutamate- and quisqualate-bound forms of GluR2 S1S2.
56 cs, in AMPA-bound compared to glutamate- and quisqualate-bound states.
57                   A sublethal i.c.v. dose of quisqualate caused episodes of prolonged akinesia and co
58                                          The quisqualate current with no Gm change was inhibited by i
59 IV binding by anatomic region correlate with quisqualate-defined binding subtypes: high-affinity DCG-
60                                          The quisqualate exchange current mediated through a group I
61                                              Quisqualate (group I mGluR agonist), decreases the f-IPS
62 amate, 2S,4R-4-methylglutamate, kainate, and quisqualate have now been solved.
63 had a marked reduction in cooperativity with quisqualate in IP(1) accumulation and upon extended incu
64 inate), and two full agonists (glutamate and quisqualate) in the wildtype and two mutant receptors.
65           The mGluR agonists L-glutamate and quisqualate increased the open state probability (NP(o))
66 h as glutamate induced both effects, whereas quisqualate induced only PI hydrolysis.
67 or infusion of psychosine greatly attenuated quisqualate-induced behaviors, and fully prevented destr
68          The current-voltage relation of the quisqualate-induced current was linear with a reversal p
69 on to block voltage-gated Ca2+ currents, the quisqualate-induced current was not altered, but the 1S,
70                                          The quisqualate-induced inward current was markedly reduced
71 utamate binding site (A168V) shows increased quisqualate-induced IP formation and, similar to R375G,
72 ilar to that of glutamate, illustrating that quisqualate is a faithful glutamate analogue.
73                                              Quisqualate is a high-affinity, full agonist which like
74                                              Quisqualate is a potent specific agonist for Group 1 met
75 NOS- cultures to high-dose NMDA and low-dose quisqualate is identical to the response of NOS-immunopo
76                  Modulation of glutamate and quisqualate-mediated iCa(2+) mobilization revealed probe
77 inity quisqualate) and group 2 (low-affinity quisqualate) mGluRs.
78 otoxicity and differential susceptibility to quisqualate neurotoxicity remain intact in the nNOS- cul
79 ype cultures and only a modest resistance to quisqualate neurotoxicity, confirming observations that
80 ehaviors, and fully prevented destruction by quisqualate of vulnerable hippocampal neurons.
81             During studies of the effects of quisqualate on synaptic activity, it was observed that q
82   In contrast, neither LY compound prevented quisqualate or glutamate from activating intracellular r
83 ons were unresponsive to the group I agonist quisqualate or the group II agonist 2-(2,3-dicarboxycycl
84 abotropic glutamate receptor (mGluR) agonist quisqualate (QA).
85  Extracellular ligands such as glutamate and quisqualate reach nuclear receptors via both sodium-depe
86 s to L-alpha-aminoadipate blocks or reverses quisqualate sensitization, making the neurons unresponsi
87 or reverses the persistent depolarization of quisqualate-sensitized neurons which is induced by expos
88                                  Exposure of quisqualate-sensitized slices of rat hippocampus to 400
89 s increased ERK1/2 activation in response to quisqualate stimulation.
90 trongly desensitizing agonists glutamate and quisqualate than the weakly desensitizing agonist kainat
91 None of these analogs affects binding of [3H]quisqualate to the orthosteric (glutamate) site, but the
92  partial agonist kainate or the full agonist quisqualate together with a positive allosteric modulato
93 /pyruvate, the maximal [3H]InsP1 response to quisqualate was increased by >/=75%, and the EC50 shifte
94             Both C[93]S and C[129]S bind [3H]quisqualate, whereas binding to C[57]S or C[99]S mutants
95                                              Quisqualate, which is biased toward PI hydrolysis, faile