コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
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
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
27 d activated both signaling pathways, whereas quisqualate and (S)-3,5-dihydroxyphenylglycine stimulate
28 abotropic glutamate receptor (mGlu) agonists quisqualate and 1S,3R-1-aminocyclopentane-1,3-dicarboxyl
29 data are consistent with the hypothesis that quisqualate and 1S,3R-ACPD in Ba2+ and Cs+ solution acti
30 -millisecond conformational dynamics because quisqualate and AMPA bind with similar affinities that a
31 and ketamine (60 mg/kg i.p.) both diminished quisqualate and AMPA hsp70 induction in the CA1, CA2, CA
34 rises, whereas in a smaller number of cells quisqualate and L-CCG-I showed both inhibitory and addit
35 als elicited by glutamate receptor agonists (quisqualate and NMDA) was examined in developing cerebel
36 on of responses to the orthosteric agonist l-quisqualate and the allosteric modulator Ro 67-4853 by e
37 allographic data on the interactions between quisqualate and the GluR2 receptor ion channel and its c
38 sistent with those of group 1 (high-affinity quisqualate) and group 2 (low-affinity quisqualate) mGlu
39 glutamic acid (glutamate), quisqualic acid (quisqualate), and alpha-amino-3-hydroxy-5-methyl-4-isoxa
40 Incubation of the cells with L-glutamate, quisqualate, and 1-aminocyclopentane-1S, 3R-dicarboxylic
41 by four different ligands, glutamate, AMPA, quisqualate, and 2-Me-Tet-AMPA, full agonists that vary
42 otentiates threshold responses to glutamate, quisqualate, and 3,5-dihydroxyphenylglycine in fluoromet
43 rences exist between the agonists glutamate, quisqualate, and AMPA in modulating glutamate receptor f
47 or 50 mM) or with 100 mM choline reduced the quisqualate- and 1S,3R-ACPD-induced inward currents, res
48 e LY393053 and LY367366 not only blocked [3H]quisqualate binding but also prevented nontransported ag
50 -CCG-I displaces both high- and low-affinity quisqualate binding sites, but unlike the other two comp
51 DCG-IV binding correlates with low-affinity quisqualate binding, whereas low-affinity DCG-IV binding
58 IV binding by anatomic region correlate with quisqualate-defined binding subtypes: high-affinity DCG-
62 inate), and two full agonists (glutamate and quisqualate) in the wildtype and two mutant receptors.
65 or infusion of psychosine greatly attenuated quisqualate-induced behaviors, and fully prevented destr
67 on to block voltage-gated Ca2+ currents, the quisqualate-induced current was not altered, but the 1S,
69 utamate binding site (A168V) shows increased quisqualate-induced IP formation and, similar to R375G,
73 NOS- cultures to high-dose NMDA and low-dose quisqualate is identical to the response of NOS-immunopo
75 otoxicity and differential susceptibility to quisqualate neurotoxicity remain intact in the nNOS- cul
76 ype cultures and only a modest resistance to quisqualate neurotoxicity, confirming observations that
79 In contrast, neither LY compound prevented quisqualate or glutamate from activating intracellular r
80 ons were unresponsive to the group I agonist quisqualate or the group II agonist 2-(2,3-dicarboxycycl
82 Extracellular ligands such as glutamate and quisqualate reach nuclear receptors via both sodium-depe
83 s to L-alpha-aminoadipate blocks or reverses quisqualate sensitization, making the neurons unresponsi
84 or reverses the persistent depolarization of quisqualate-sensitized neurons which is induced by expos
87 trongly desensitizing agonists glutamate and quisqualate than the weakly desensitizing agonist kainat
88 None of these analogs affects binding of [3H]quisqualate to the orthosteric (glutamate) site, but the
89 partial agonist kainate or the full agonist quisqualate together with a positive allosteric modulato
90 /pyruvate, the maximal [3H]InsP1 response to quisqualate was increased by >/=75%, and the EC50 shifte
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。