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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  by the luciferase substrate coelenterazine (CTZ).
22 nificant cell death in hippocampal cultures, CTZ treatment does not result in any apparent neuronal d
23                               Cyclothiazide (CTZ) is a potent blocker of AMPA receptor desensitizatio
24                               Cyclothiazide (CTZ) is well known for its effect of enhancing glutamate
25                               Cyclothiazide (CTZ), a potentiator of AMPAR, revealed slowly rising AMP
26                               Cyclothiazide (CTZ), a selective antagonist at mGluR1, markedly reduced
27                               Cyclothiazide (CTZ), the allosteric modulator of AMPARs, potentiates re
28 ia AMPA receptors produced by cyclothiazide (CTZ) to estimate the concentration of glutamate reached
29 in the presence of 100 microM cyclothiazide (CTZ) causes an increase in [Ca(2+)](i) in cultured cereb
30 sive, AMPA receptor modulator cyclothiazide (CTZ) induces a profound and long-lasting increase in the
31            The application of cyclothiazide (CTZ) revealed that desensitization of postsynaptic recep
32      We tested the effects of cyclothiazide (CTZ), an agent used to block desensitization of AMPA-typ
33                    Effects of cyclothiazide (CTZ), trichlormethiazide (TCM), and CX614 were compared
34 on is commonly achieved using cyclothiazide (CTZ), the most potent modulator of the benzothiadiazide
35 that chronic stimulation with cyclothiazide (CTZ) or kainic acid (KA) induces robust epileptiform act
36 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
37 ne to proline on the rho2 subunit eliminated CTZ sensitivity, whereas switching proline to serine on
38 [BF(4)](2) (6), [Ru(II)(eta(6)-p-cymene)(en)(CTZ)][BF(4)](2) (7), and [Ru(II)(eta(6)-p-cymene)(acac)(
39 erminated suggests that the binding site for CTZ on the GABA(C) receptor is distinct from that for GA
40 C50, 1810 microM in control vs 304 microM in CTZ), we estimate that the extrasynaptic transmitter con
41 -known epileptogenic agent kainic acid (KA), CTZ affects neuronal activity mainly through modulating
42 ver, the effect of the allosteric modulator, CTZ on agonist activation of AMPAR can also be modified
43 RP), found responses to IBU and CFA, but not CTZ or PRP.
44 roke mice received the combined LMO3-iPS-NPC/CTZ treatment, but not cell or CTZ alone, showed enhance
45                               The ability of CTZ to interact with various types of neurotransmitter r
46 notably, complex 5 increases the activity of CTZ by factors of 110 and 58 against L. major and T. cru
47 ells with daily intranasal administration of CTZ enhanced axonal myelination, synaptic transmission,
48                                The amount of CTZ-induced facilitation (CIF) was dependent upon both C
49 Cs along with mass spectrometric analysis of CTZ-treated slices indicates that the cause is prolonged
50 at the cause is prolonged bioavailability of CTZ.
51                  The epileptogenic effect of CTZ is probably due to its enhancing glutamatergic neuro
52 ated in in vivo recordings that injection of CTZ (5 micromol in 5 microl) into the lateral ventricles
53        Additionally, AMPA in the presence of CTZ causes a depletion of thapsigargin-sensitive intrace
54                 The inhibitory properties of CTZ were consistent with its action as a channel blocker
55 ivity lasts more than 48 h after washing off CTZ, suggesting a permanent change of the neural network
56  LMO3-iPS-NPC/CTZ treatment, but not cell or CTZ alone, showed enhanced neural network connections in
57 serine on the rho1 subunit made the receptor CTZ sensitive.
58 in addition to its action on AMPA receptors, CTZ also exerts a powerful but opposite effect on GABAA
59 tor is distinct from that for GABA, and that CTZ acts as a non-competitive antagonist on the GABA(C)
60               These results demonstrate that CTZ interacts with both glutamate and GABAA receptors an
61           We have recently demonstrated that CTZ also inhibits GABA(A) receptors.
62                                We found that CTZ reversibly inhibited both evoked and spontaneous inh
63 ingle-channel analyses revealed further that CTZ greatly reduced the open probability of GABAA recept
64                        Results indicate that CTZ and TCM target deactivation and agonist potency inde
65                          Here we report that CTZ induces robust epileptiform activity in hippocampal
66 array recordings in brain slices showed that CTZ or light stimulation facilitated synaptic transmissi
67                               Therefore, the CTZ-induced epilepsy model may provide a novel research
68 hermore, GluR1L3T was totally insensitive to CTZ potentiation of KA and glutamate-activated currents
69 ant receptor currents were more sensitive to CTZ potentiation than the wild-type receptor current.
70      This is in contrast with mammals, where CTZ is a potent PXR-agonist.
71 ronic treatment of hippocampal cultures with CTZ (5 microM, 48 h) results in epileptiform activity in
72 nic pretreatment of hippocampal neurons with CTZ or KA resulted in a marked reduction in GABAergic in
73                  Treatment of the slice with CTZ (90 muM) for 1 h increased the integrated XII ( XII)