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

11 Tail current activation curves showed that grammotoxin s

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

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

14 Tail currents after depolarizations to potentials betwee

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

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

17 Tail current amplitude had the same dependence on preced

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

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

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

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

22 Tail current analysis of the novel P2Y1 receptor-associa

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

24 Tail current analysis showed that the currents enhanced

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

26 Tail current analysis was used to characterize the kinet

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 644 increased the magnitude of both step and tail currents, but surprisingly failed to slow deactivat

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

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

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

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

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

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

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

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

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

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

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

55 the acidification significantly accelerated tail current deactivation.

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

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

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

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

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

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

62 Tail current experiments showed that the current was cat

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

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

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

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

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

68 +27 mV shifted the reversal potential of the tail currents from 1 +/- 1 to 27 +/- 1 mV (number of cel

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

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

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

72 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 1 potassium channel that promotes an outward tail current of up to 8 s following a depolarizing stimu

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

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

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

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

94 Tail current reversal potentials varied with extracellul

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

121 Tail currents were unaffected by ATP exposure suggesting

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