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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
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
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
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
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
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
44 notably, complex 5 increases the activity of CTZ by factors of 110 and 58 against L. major and T. cru
46 Cs along with mass spectrometric analysis of CTZ-treated slices indicates that the cause is prolonged
49 ated in in vivo recordings that injection of CTZ (5 micromol in 5 microl) into the lateral ventricles
52 ivity lasts more than 48 h after washing off CTZ, suggesting a permanent change of the neural network
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)
59 ingle-channel analyses revealed further that CTZ greatly reduced the open probability of GABAA recept
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.
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
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