ライフサイエンスコーパス: cyclothiazide

1 or comparison with an existing structure for cyclothiazide.

2 dentical to those controlling sensitivity to cyclothiazide.

3 resence of the positive allosteric modulator cyclothiazide.

4 ant shown previously to impede modulation by cyclothiazide.

5 ion of the desensitization-reducing compound cyclothiazide.

6 -7-nitroquinoxaline, and were potentiated by cyclothiazide.

7 ic activity significantly lower than that of cyclothiazide.

8 MDA caused no injury even in the presence of cyclothiazide.

9 asked by reducing their desensitization with cyclothiazide.

10 Cyclothiazide (100 microM) and diazoxide (500 microM), t

11 Application of 100 microM cyclothiazide (a specific AMPA receptor desensitization

12 This decline was eliminated by cyclothiazide, a drug previously shown to block AMPA rec

13 Cyclothiazide, a drug that selectively blocks AMPA recep

14 Cyclothiazide, a drug with ten fold greater effects on '

15 an AMPA receptor anti-desensitization agent cyclothiazide abolished the LTD, but not the accommodati

16 analysis are consistent with aniracetam and cyclothiazide acting via distinct mechanisms.

17 These results point to the conclusion that cyclothiazide acts at a site on the AMPA receptor differ

18 Cyclothiazide also increased steady state currents durin

19 When NMDA receptors were blocked by MK-801, cyclothiazide, an inhibitor of desensitization at non-NM

20 by polyamines increased, and sensitivity to cyclothiazide, an inhibitor of desensitization, increase

21 Cyclothiazide and (S)-4-CPG, the mGlu receptor subtype 1

22 s studies showed that the AMPAR potentiators cyclothiazide and 4-[2-(phenylsulfonylamino)ethylthio]-2

23 strated that the differential sensitivity to cyclothiazide and aniracetam depends on a single amino a

24 Many allosteric modulators (e.g., cyclothiazide and aniracetam) preferentially affect the

25 ollectively, these results show that, unlike cyclothiazide and aniracetam, the residues that confer s

26 amate, and showed differential modulation by cyclothiazide and aniracetam.

27 receptor-specific desensitization blockers, cyclothiazide and concanavalin A.

28 h compound overlap with distinct moieties of cyclothiazide and CX614.

29 nding domain and each compound with those of cyclothiazide and CX614.

30 t of recovery from depression was reduced by cyclothiazide and enhanced when release probability was

31 Controversy exists as to whether cyclothiazide and GYKI 53655 act at a common site.

32 e effects ranging from large reductions with cyclothiazide and JM-13 to increases produced by more re

33 sitive allosteric modulators, represented by cyclothiazide and the ampakine 2H,3H,6aH-pyrrolidino(2,1

34 6, the AMPA receptor desensitization blocker cyclothiazide and the sodium channel blockers riluzole,

35 isplayed desensitization, was insensitive to cyclothiazide and was potentiated by concanavalin A, sug

36 Cyclothiazide and wheatgerm agglutinin, agents which inh

37 oxy-5-methyl-4-isoxazole propionic acid with cyclothiazide, and thapsigargin mimicked the effects of

38 al; S750D was active only in the presence of cyclothiazide, and the remaining mutants exhibited alter

39 ation of deactivation and desensitization by cyclothiazide, aniracetam, and thiocyanate.

40 Cyclothiazide at 100 microM depolarized the HC dark memb

41 Cyclothiazide attenuated or reversed this decline; after

42 The benzothiadiazide compound cyclothiazide blocked receptor desensitization in patche

43 m GluRA into GluR6, conferred sensitivity to cyclothiazide but did not increase sensitivity to 2,3-be

44 Thus, these fluxes were enhanced by cyclothiazide but not by concanavalin A and were blocked

45 o glutamine, which abolishes potentiation by cyclothiazide, can in addition block antagonism by 2,3-b

46 Cyclothiazide caused a reduction in [3H]AMPA binding in

47 00 microM AMPA in the presence of 100 microM cyclothiazide (CTZ) causes an increase in [Ca(2+)](i) in

48 , anti-hypertensive, AMPA receptor modulator cyclothiazide (CTZ) induces a profound and long-lasting

49 Cyclothiazide (CTZ) is a potent blocker of AMPA receptor

50 Cyclothiazide (CTZ) is well known for its effect of enha

51 y demonstrated that chronic stimulation with cyclothiazide (CTZ) or kainic acid (KA) induces robust e

52 The application of cyclothiazide (CTZ) revealed that desensitization of pos

53 the Bergmann glia AMPA receptors produced by cyclothiazide (CTZ) to estimate the concentration of glu

54 Cyclothiazide (CTZ), a potentiator of AMPAR, revealed sl

55 Cyclothiazide (CTZ), a selective antagonist at mGluR1, m

56 We tested the effects of cyclothiazide (CTZ), an agent used to block desensitizat

57 Cyclothiazide (CTZ), the allosteric modulator of AMPARs,

58 ceptor activation is commonly achieved using cyclothiazide (CTZ), the most potent modulator of the be

59 Effects of cyclothiazide (CTZ), trichlormethiazide (TCM), and CX614

60 AMPA and cyclothiazide damaged WM axons at P7, P10, and P21 but n

61 After reduction of desensitization with cyclothiazide, deactivation decays were strongly agonist

62 tic model of the AMPA receptor suggests that cyclothiazide does not block receptor desensitization by

63 easing release probability or application of cyclothiazide does not produce responses from these sile

64 Cyclothiazide-enhanced injury varied with the age of ast

65 hat is shorter lasting than that elicited by cyclothiazide even when the drug is left in contact with

66 no effect was observed with concanavalin A, cyclothiazide greatly enhanced the Glu-, AMPA- and kaina

67 Cyclothiazide had no effect on either the dark potential

68 In the absence of thiocyanate, however, cyclothiazide had no reliable effect on the binding of [

69 itroquinoxaline-2,3-dione and potentiated by cyclothiazide in a manner indistinguishable from that of

70 ionally, while dose dependently, 5-25 microM cyclothiazide in the presence of AMPA is highly neurotox

71 the changes in binding affinity produced by cyclothiazide in the presence of thiocyanate.

72 d chlorowillardiine (ClW) in the presence of cyclothiazide, in conjunction with crystal structures of

73 tion of a moderate-level sound together with cyclothiazide increased and subsequently abolished the s

74 and the insensitivity of desensitization to cyclothiazide indicated that they contained mostly flop

75 PA receptor desensitization was blocked with cyclothiazide, indicating that it reflects a time-depend

76 Glutamate and cyclothiazide markedly altered the conformational equili

77 Cyclothiazide markedly increased current amplitude of re

78 The effects of cyclothiazide on the properties of (R,S)-alpha-amino-3-h

79 zation of glutamate receptors was blocked by cyclothiazide or aniracetam, the BDNF potentiation of th

80 s inhibited by the coapplication of AMPA and cyclothiazide or by the use of kainate as an agonist, su

81 a similar impairment of modulation by either cyclothiazide or CX546, indicating that some residues at

82 blocking AMPA-receptor desensitization with cyclothiazide, or evoking GABA release with NMDA recepto

83 The neurotoxicity elicited by cyclothiazide persists in the presence of dizocilpine (a

84 om desensitization, as well as glutamate and cyclothiazide potency to AMPARs.

85 Benzothiadiazides such as cyclothiazide potentiate alpha-amino-3-hydroxy-5-methyl-

86 estruction of the dendrites, suggesting that cyclothiazide potentiates sound-induced Glu excitotoxici

87 emoval of AMPA receptor desensitization with cyclothiazide reduced the paired-pulse depression at lon

88 Cyclothiazide reversibly increased spontaneous activity

89 yclothiazide share a common binding site but cyclothiazide seems to bind to an additional site not re

90 willardiine binding suggested that CX614 and cyclothiazide share a common binding site but cyclothiaz

91 uilibrium desensitization and sensitivity to cyclothiazide, show only small differences in sensitivit

92 ivefold potentiation of kainate responses by cyclothiazide-suggest AMPAR association with CNIHs.

93 id not significantly influence the EC(50) of cyclothiazide, suggesting distinct sites of action.

94 54 but by less than 15% at concentrations of cyclothiazide that fully blocked desensitization in patc

95 CA3 patches and that was blocked by a drug (cyclothiazide) that slows desensitization.

96 they differ in two fundamental aspects from cyclothiazide, the most widely studied BTD: 1) D1 marked

97 4-benzothiadiazine S,S-dioxide (IDRA-21) and cyclothiazide, two negative modulators of the spontaneou

98 The effect of cyclothiazide was greatly diminished when the stimulatio

99 licited by glutamate, or AMPA coapplied with cyclothiazide, were also larger in GluR3-GFP oocytes.

100 eviously to control allosteric regulation by cyclothiazide, were analyzed for modulation of deactivat

101 TD and accommodation, one being sensitive to cyclothiazide, whereas the other is not.

102 The enhancement of toxicity by cyclothiazide, which alone was not toxic, was concentrat

103 Addition of cyclothiazide, which blocks AMPA receptor desensitizatio

104 Cyclothiazide, which has been shown to prevent desensiti

105 changes evoked by kainate in the presence of cyclothiazide, which inhibits AMPA receptor desensitizat

106 tions of two positive allosteric modulators [cyclothiazide, which modulates desensitization, and 1-(1

107 is critical for directing the interaction of cyclothiazide with AMPA receptors.

108 Coapplication of 10-100 microM cyclothiazide with glutamate, AMPA, or kainate produced

109 The interaction of cyclothiazide with the receptor appears not to be change