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1                                              CTZ and TCM further slowed desensitization of L/Y mutant
2                                              CTZ inhibited the open channel of the GABA(C) receptor w
3                                              CTZ inhibition of GABA(C) receptors was subunit specific
4                                              CTZ successfully inhibited the activity evoked by group
5                                              CTZ, TCM, or L/Y mutation all essentially blocked GluR1
6 (CTZ)(2)] (4), [Ru(II)(eta(6)-p-cymene)Cl(2)(CTZ)] (5), [Ru(II)(eta(6)-p-cymene)(bipy)(CTZ)][BF(4)](2
7 Z)] (1), cis,cis,trans-[Ru(II)Cl(2)(DMSO)(2)(CTZ)(2)] (2), Na[Ru(III)Cl(4)(DMSO)(CTZ)] (3), Na[trans-
8 n synthesized, cis,fac-[Ru(II)Cl(2)(DMSO)(3)(CTZ)] (1), cis,cis,trans-[Ru(II)Cl(2)(DMSO)(2)(CTZ)(2)]
9 Cl(4)(DMSO)(CTZ)] (3), Na[trans-Ru(III)Cl(4)(CTZ)(2)] (4), [Ru(II)(eta(6)-p-cymene)Cl(2)(CTZ)] (5), [
10 ](2) (7), and [Ru(II)(eta(6)-p-cymene)(acac)(CTZ)][BF(4)] (8) (bipy = bipyridine; en = ethlylenediami
11 The long-lasting epileptiform activity after CTZ washout may also make it a very useful model in scre
12 hange of the neural network properties after CTZ treatment.
13 combined L497Y-S750Q mutations abolished all CTZ and TCM actions without disrupting CX614 activity.
14 rent rebound when co-application of GABA and CTZ was terminated suggests that the binding site for CT
15              Intermediate structures between CTZ and IDRA-21 show reduced potency, suggesting that th
16 2)(CTZ)] (5), [Ru(II)(eta(6)-p-cymene)(bipy)(CTZ)][BF(4)](2) (6), [Ru(II)(eta(6)-p-cymene)(en)(CTZ)][
17 d facilitation (CIF) was dependent upon both CTZ dose and exposure time and was accompanied by a long
18 inding to rifampicin (Rif) and clotrimazole (CTZ) by recruiting transcriptional coactivators.
19 armaceuticals ibuprofen (IBU), clotrimazole (CTZ), clofibric acid (CFA) and propranolol (PRP), found
20 ght new ruthenium complexes of clotrimazole (CTZ) with high antiparasitic activity have been synthesi
21 nificant cell death in hippocampal cultures, CTZ treatment does not result in any apparent neuronal d
22                               Cyclothiazide (CTZ) is a potent blocker of AMPA receptor desensitizatio
23                               Cyclothiazide (CTZ) is well known for its effect of enhancing glutamate
24                               Cyclothiazide (CTZ), a potentiator of AMPAR, revealed slowly rising AMP
25                               Cyclothiazide (CTZ), a selective antagonist at mGluR1, markedly reduced
26                               Cyclothiazide (CTZ), the allosteric modulator of AMPARs, potentiates re
27 ia AMPA receptors produced by cyclothiazide (CTZ) to estimate the concentration of glutamate reached
28 in the presence of 100 microM cyclothiazide (CTZ) causes an increase in [Ca(2+)](i) in cultured cereb
29 sive, AMPA receptor modulator cyclothiazide (CTZ) induces a profound and long-lasting increase in the
30            The application of cyclothiazide (CTZ) revealed that desensitization of postsynaptic recep
31      We tested the effects of cyclothiazide (CTZ), an agent used to block desensitization of AMPA-typ
32                    Effects of cyclothiazide (CTZ), trichlormethiazide (TCM), and CX614 were compared
33 on is commonly achieved using cyclothiazide (CTZ), the most potent modulator of the benzothiadiazide
34 that chronic stimulation with cyclothiazide (CTZ) or kainic acid (KA) induces robust epileptiform act
35 DMSO)(2)(CTZ)(2)] (2), Na[Ru(III)Cl(4)(DMSO)(CTZ)] (3), Na[trans-Ru(III)Cl(4)(CTZ)(2)] (4), [Ru(II)(e
36 ne to proline on the rho2 subunit eliminated CTZ sensitivity, whereas switching proline to serine on
37 [BF(4)](2) (6), [Ru(II)(eta(6)-p-cymene)(en)(CTZ)][BF(4)](2) (7), and [Ru(II)(eta(6)-p-cymene)(acac)(
38 erminated suggests that the binding site for CTZ on the GABA(C) receptor is distinct from that for GA
39 C50, 1810 microM in control vs 304 microM in CTZ), we estimate that the extrasynaptic transmitter con
40 -known epileptogenic agent kainic acid (KA), CTZ affects neuronal activity mainly through modulating
41 ver, the effect of the allosteric modulator, CTZ on agonist activation of AMPAR can also be modified
42 RP), found responses to IBU and CFA, but not CTZ or PRP.
43                               The ability of CTZ to interact with various types of neurotransmitter r
44 notably, complex 5 increases the activity of CTZ by factors of 110 and 58 against L. major and T. cru
45                                The amount of CTZ-induced facilitation (CIF) was dependent upon both C
46 Cs along with mass spectrometric analysis of CTZ-treated slices indicates that the cause is prolonged
47 at the cause is prolonged bioavailability of CTZ.
48                  The epileptogenic effect of CTZ is probably due to its enhancing glutamatergic neuro
49 ated in in vivo recordings that injection of CTZ (5 micromol in 5 microl) into the lateral ventricles
50        Additionally, AMPA in the presence of CTZ causes a depletion of thapsigargin-sensitive intrace
51                 The inhibitory properties of CTZ were consistent with its action as a channel blocker
52 ivity lasts more than 48 h after washing off CTZ, suggesting a permanent change of the neural network
53 serine on the rho1 subunit made the receptor CTZ sensitive.
54 in addition to its action on AMPA receptors, CTZ also exerts a powerful but opposite effect on GABAA
55 tor is distinct from that for GABA, and that CTZ acts as a non-competitive antagonist on the GABA(C)
56               These results demonstrate that CTZ interacts with both glutamate and GABAA receptors an
57           We have recently demonstrated that CTZ also inhibits GABA(A) receptors.
58                                We found that CTZ reversibly inhibited both evoked and spontaneous inh
59 ingle-channel analyses revealed further that CTZ greatly reduced the open probability of GABAA recept
60                        Results indicate that CTZ and TCM target deactivation and agonist potency inde
61                          Here we report that CTZ induces robust epileptiform activity in hippocampal
62                               Therefore, the CTZ-induced epilepsy model may provide a novel research
63 hermore, GluR1L3T was totally insensitive to CTZ potentiation of KA and glutamate-activated currents
64 ant receptor currents were more sensitive to CTZ potentiation than the wild-type receptor current.
65      This is in contrast with mammals, where CTZ is a potent PXR-agonist.
66 ronic treatment of hippocampal cultures with CTZ (5 microM, 48 h) results in epileptiform activity in
67 nic pretreatment of hippocampal neurons with CTZ or KA resulted in a marked reduction in GABAergic in
68                  Treatment of the slice with CTZ (90 muM) for 1 h increased the integrated XII ( XII)

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