ライフサイエンスコーパス: tail current

1 the AP was interrupted to produce an I(NCX) tail current).

2 uring the initial depolarizing pulse and the tail current.

3 ons is mediated by an Ni2+-sensitive calcium tail current.

4 ng the first millisecond of an evoked Ca(2+) tail current.

5 om the time constant of the decay (tau D) of tail currents.

6 ck only the fast relaxation component of the tail currents.

7 aline or forskolin caused an increase in IKr tail currents.

8 determined from the monoexponential decay of tail currents.

9 ding potential of -80 mV evoked large inward tail currents.

10 -fold in SY/YY cells compared with SS cells (tail current: 0.66+/-0.1 versus 1.2+/-0.1 pA/pF; P<0.001

11 conductance-voltage (G-V) relationship, and tail current acceleration as the number of nonactivatabl

12 Magnetopause and tail currents account for part of the high-order field,

13 Tail current activation curves showed that grammotoxin s

14 P currents were measured in voltage clamp as tail currents after 2 ms voltage pulses that triggered a

15 large depolarizing pulse, and the other uses tail currents after a very strong activating pulse.

16 Tail currents after depolarizations to potentials betwee

17 netic components contributed equally to peak tail current amplitude (measured at -35 mV) after a sing

18 dependence of activation was determined from tail current amplitude at -50 mV.

19 Tail current amplitude had the same dependence on preced

20 fluxes were no different when normalized to tail current amplitude measured upon repolarization from

21 For protons, the Kd values for the effect on tail current amplitude versus kinetics were, respectivel

22 g a 300 ms depolarising step to +20 mV, mean tail current amplitude was increased 47 +/- 12% by isopr

23 ramembrane gating charge movements and ionic tail current amplitudes indicated that the reduction in

24 lcium channel activation, as determined from tail current analyses, was similar when the entire prepa

25 Tail current analysis of the novel P2Y1 receptor-associa

26 ctivation of around 220 ms (at -130 mV), and tail current analysis revealed a half-activation voltage

27 Tail current analysis showed that the currents enhanced

28 Reversal of tail current analysis showed this current was due to a C

29 Tail current analysis was used to characterize the kinet

30 rsal potential of SV currents (determined by tail current analysis) passed through maximum or minimum

31 produces a significant decrease in the I(h) tail current and a hyperpolarizing shift in the activati

32 pmental shortening of APs ensures I(Ca) as a tail current and faithful synaptic delay, which is parti

33 Slow tail currents and [Ca2+]i decay following 0.2 - 2 s depo

34 ts and abolished the effects of CO on Kv11.1 tail currents and APs in guinea pig myocytes.

35 Cocaine reduces both the peak tail currents and the instantaneous currents measured by

36 (based on biexponential fits to deactivating tail currents) and a pharmacological approach approach (

37 tant of deactivation of open channels (ionic tail current), and both are strongly voltage dependent o

38 ss-crossing kinetics, its slow deactivation (tail current), and its small (11 pS) conductance in 110

39 he muscle action potential produced a sodium tail current, and thus slowed deactivation opposes repol

40 In the meanwhile, the resurgent hERG tail currents are dose-dependently inhibited by AMD with

41 ail phenotype, whereby large decaying inward tail currents are elicited upon spermine unbinding.

42 The subsequent tail currents at -40 mV displayed an initial rising phas

43 he effects of pHo on permeation, we measured tail currents at 0 mV, following steps to + 120 mV to ma

44 The decay of tail currents at potentials between -80 and -30 mV was a

45 after deltamethrin treatment, the resultant "tail" currents being used to quantify the effects of thi

46 block of both IKr and IKs, with an IC50 for tail current block of 0.14+/-0.01 micromol/L for IKr and

47 ltiple channel subtypes contribute to Ca(2+) tail current, but the need for an action potential to pr

48 644 increased the magnitude of both step and tail currents, but surprisingly failed to slow deactivat

49 ments revealed that PD-307243 increased hERG tail currents by 2.1 +/- 0.6 (n = 7) and 3.4 +/- 0.3-fol

50 n of PKC by phorbol dibutyrate increased IKr tail currents by 24 +/- 5%.

51 l(-) with gluconate(-) diminishes the inward tail current (Cl(-) efflux) at a membrane potential of -

52 The time course of the tail current closely matched the fast component of the f

53 ng the contribution of a slowly deactivating tail current component.

54 In ventricular myocytes, two exponential tail current components were distinguished; these compon

55 in the patch pipette solution eliminated the tail current, consistent with this current reflecting Ca

56 y near the soma, and the amplitude of Ca(2+) tail currents correlates with the strength of bursting a

57 zation to -140 mV, the amplitude of the slow tail current corresponded to less than 3% of total Na(+)

58 bine was associated with a slowing of M-like tail current deactivation in these cells.

59 rse of current activation was unchanged, but tail current deactivation was dramatically accelerated.

60 the acidification significantly accelerated tail current deactivation.

61 tivation was 4.0 times faster, deactivation (tail current decay) was 5.4 times slower, the H+ conduct

62 current with instantaneous onset and slowed tail current decay, sensitive to the I (Ks) blocker (3R,

63 Activation of SK tail currents depended on the duration of the depolarizi

64 he release was submaximal (e.g., at +30 mV), tail currents did activate additional Ca2+ spikes; confo

65 n washout (with 0.1% DMSO present), the slow tail current disappeared monophasically (exponential tau

66 In the present study, we show that a Ca(2+) tail current drives bursting in subicular pyramidal neur

67 o cells with TTX-R Na(+) channels, the Na(+) tail current during repolarization developed a large slo

68 Tail current experiments showed that the current was cat

69 These properties suggest the tail current flows through a Ca(2+)-activated K+ channel

70 polarising steps, slowed the kinetics of the tail current following repolarisation, and induced a neg

71 urations, whereas 2 mM cobalt reduced the SK tail current for pulses greater than 80 ms, demonstratin

72 n the range -10 to +50 mV and found that the tail currents for IKr do not activate with the same time

73 Tail currents for the wild-type channel and L1014F chann

74 +27 mV shifted the reversal potential of the tail currents from 1 +/- 1 to 27 +/- 1 mV (number of cel

75 The mean time constant of slow deactivating tail currents generated by a preceding 20 mV pulse was 2

76 ing and non-inactivating components, and the tail currents had both a fast component (IKf) with a tim

77 and induction of a slow poststimulus inward tail current (I(ADP)) (measured under voltage clamp at -

78 n of WT-Kv11.1 or T421M-Kv11.1 produced peak tail current (I(Kv11.1)) of 8.78+/-1.18 and 1.91+/-0.22

79 e describe a slow (tau approximately 350 ms) tail current in voltage-clamped light responses and show

80 ad no effect on the reversal potential of SV tail currents in the presence of Ca2+ and a K+ gradient,

81 ecreased and that of the Na(+)-Ca2+ exchange tail current increased.

82 f extracellular Eosin of La3+ prolonged slow tail currents, indicating a contribution of plasma membr

83 about one order of magnitude lower than for tail current inhibition.

84 n external medium with no added calcium, INa tail current initially increases in amplitude severalfol

85 ncurrently with progressive loss of slow AHP tail current (IsAHP) evoked by brief depolarizations.

86 time constant (tau) of Ca(2+)-activated Cl- 'tail' currents (Itail) evoked by Ca2+ influx through vol

87 Cl- currents (STICs) and Ca2+-activated Cl- 'tail' currents (Itail) was described by a single exponen

88 ed by depolarization were followed by inward tail currents lasting several hundred milliseconds.

89 From tail current measurements, the current was maximal at -5

90 A magnetopause and tail-current model was defined by using 332 magnetopause

91 imilar kinetics also described the decay of 'tail currents' observed on repolarization.

92 (SK) current was measured by subtraction of tail currents obtained before and after treatment with a

93 HERG current with half-maximal block of peak tail current of 7.2 microM.

94 n-CaMKII interaction gave rise to an outward tail current of up to 8 s duration following a depolariz

95 1 potassium channel that promotes an outward tail current of up to 8 s following a depolarizing stimu

96 endent but time-dependent increase in a slow tail current, providing an unexpected mechanism by which

97 Ionic substitution and relaxation (tail) current recordings showed that outward IAP was mai

98 Exponential fits to deactivating tail currents revealed a fast and a slow component.

99 Analysis of the tail currents revealed rapidly and slowly deactivating c

100 Tail current reversal potentials varied with extracellul

101 extracellular K+ was replaced with Cs+, IPO tail current reversal potentials were dependent upon the

102 lity being associated with KORC (analysis of tail current reversal potentials), there is no correlati

103 Ih,slow tail currents reversed between -65.3 and -56.6 mV (with

104 a including ionic currents, gating currents, tail currents, steady-state inactivation, recovery from

105 hair cells, prolonged the time course of the tail current, supporting the idea that the channel monit

106 ization elicited a calcium-dependent outward tail current that reversed near E(K).

107 adrenal chromaffin cells, by measuring slow tail currents through small-conductance Ca(2+)-activated

108 s using pharmacological channel block or the tail current titration probes the cooperativity between

109 DT caused a slowly rising and slowly falling tail current to be developed in tetrodotoxin-sensitive s

110 ion with the slope of the linear part of the tail current to calculate the single channel conductance

111 allowed us to convert the peak inward I(NCX) tail currents to [Ca(2+)](sm).

112 We used tail currents to distinguish effects of pHo on channel g

113 Conductance/voltage curves obtained from tail currents together with kinetics analysis reveal tha

114 current deactivation, causing a crossover of tail current traces recorded before and after drug treat

115 rons demonstrated that ethanol inhibited the tail current triggered by release from hyperpolarization

116 eriotoxin-insensitive current, detected as a tail current upon repolarization, in fibres from denerva

117 fenvalerate, generated a large and prolonged tail current upon repolarization.

118 Persistent I(f) "tail" current upon release of the hyperpolarization driv

119 The tail current was carried by K+ and Cs+ (relative permeab

120 The envelope of SK tail currents was diminished by 10 microM ryanodine for

121 The activation time course determined from tail currents was relatively voltage insensitive over th

122 Both the Ca2+ current and slow tail current were abolished by nifedipine.

123 a slow, (+)-202-791-induced component of the tail current were inhibited by 67 +/- 6 and 60 +/- 10 %,

124 When hERG tail currents were analyzed upon -50 mV repolarization a

125 The decays of permethrin-induced tail currents were exclusively monophasic.

126 Tail currents were linear in the range between -60 and +

127 Bay K-enhanced tail currents were slowed by R528H and accelerated by R1

128 Tail currents were unaffected by ATP exposure suggesting

129 After recording tail currents with an amphotericin-perforated patch, the