ライフサイエンスコーパス: resurgent current

1 ystems, however, Na(V)beta4 fails to produce resurgent current.

2 rst blocking protein that is responsible for resurgent current.

3 d endogenous block, beta4(154-167) generated resurgent current.

4 etics of NaV1.6 appear well adapted to carry resurgent current.

5 e Na(V)1.6 subunit may lead to production of resurgent current.

6 ent current, and step repolarizations evoked resurgent current.

7 ation at -40 mV, coinciding with the rise of resurgent current.

8 rated by the same mechanism underlying TTX-S resurgent currents.

9 v1.6 is the major contributor to these TTX-S resurgent currents.

10 SI in order to investigate their effects on resurgent currents.

11 the three drugs on Navbeta4 peptide-mediated resurgent currents.

12 andamide, exhibit differential inhibition of resurgent currents.

13 , the non-NaV1.6 subunits can produce robust resurgent currents.

14 hitherto been considered a prerequisite for resurgent currents.

15 ation from positive potentials, producing a "resurgent" current.

16 tions elicit slower channel reopening, or a 'resurgent' current.

17 e electrophysiological phenotypes: a loss of resurgent current, a reduction of persistent current, a

18 pen-channel blocking protein responsible for resurgent current acts as a natural antagonist of lidoca

19 ugh carbamazepine did not selectively target resurgent currents, anandamide strongly inhibited resurg

20 inherited spinocerebellar ataxias, controls resurgent current and repetitive firing in Purkinje neur

21 channel inactivation rate, thereby reducing resurgent current and repetitive spiking.

22 pplication of alkaline phosphatase abolished resurgent current and significantly slowed inactivation

23 ical, molecular and structural mechanisms of resurgent current and their relation to the normal funct

24 ed proexcitatory increases in persistent and resurgent currents and rightward shifts in inactivation

25 Thus, the presence or absence of resurgent current, and of persistent sodium current, app

26 Resurgent current appears to depend primarily on NaV1.6

27 Our results indicate that resurgent currents are associated with multiple channelo

28 Therefore, persistent and resurgent currents are likely to determine whether a mut

29 The TTX-R resurgent currents are similar to classic TTX-S resurgen

30 Resurgent currents arise after relief of ultra-fast open

31 ptide, can block open Na channels and induce resurgent current as channels unblock upon repolarizatio

32 the necessity of this subunit in generating resurgent current, as well as its influence on Na channe

33 ntial firing in nociceptive neurons and that resurgent currents associated with the Nav1.5 mutation c

34 Computer simulations indicated that resurgent currents associated with the Nav1.7 mutation c

35 Inward resurgent currents at strongly negative potentials, howe

36 urrent; Purkinje cells without Na(V)1.6 lack resurgent current, but resurgent current is absent from

37 ion, and conventional inactivation regulates resurgent current by controlling the extent of open-chan

38 itions and that enhancement of both types of resurgent currents by inflammatory mediators could contr

39 nsient current amplitude, demonstrating that resurgent currents can be selectively targeted.

40 Trypsin and chymotrypsin each removed resurgent current, consistent with established roles for

41 We propose that these slow TTX-R resurgent currents contribute to the membrane excitabili

42 Additionally, in control gradients, peak resurgent currents decreased linearly with driving force

43 The generation of resurgent current depends on a factor in the Na(+) chann

44 n mutation L955 (DeltaL955) fails to produce resurgent currents despite enhanced persistent currents,

45 resurgent Na(+) and K(+) currents, Kv3.1b's resurgent current does not originate from recovery of ch

46 However, the TTX-R resurgent currents exhibit much slower kinetics, occur a

47 Na channels that generate resurgent current express an intracellular endogenous op

48 damide and cannabidiol on peak transient and resurgent currents from wild-type and mutant channels.

49 erlying molecular components contributing to resurgent current have not been fully identified.

50 Tetrodotoxin-sensitive (TTX-S) resurgent currents have been described in many different

51 current clamp to investigate the role of the resurgent current in action potential formation.

52 ent current in wild-type neurons and induced resurgent current in med neurons.

53 rom five species have the capacity to induce resurgent current in mouse hippocampal neurons, which la

54 beta-PMTX increased resurgent current in wild-type neurons and induced resur

55 en observed to mediate unique persistent and resurgent currents in cerebellar Purkinje cells.

56 We also show that both TTX-S and TTX-R resurgent currents in DRG neurons are enhanced by inflam

57 These results suggest that slow TTX-R resurgent currents in DRG neurons are mediated by Nav1.8

58 urgent currents are similar to classic TTX-S resurgent currents in many respects, but not all.

59 Reduced fast inactivation without increased resurgent currents induces symptoms of IEM, not PEPD, in

60 We observed a correlation between resurgent current inhibition and a drug-mediated increas

61 without Na(V)1.6 lack resurgent current, but resurgent current is absent from many other Na(V)1.6-exp

62 es more rapidly than in wild-type cells, and resurgent current is nearly abolished.

63 Emerging research suggests that resurgent current is preferentially increased in a varie

64 ctions on voltage-gated sodium channels, and resurgent current may be a promising therapeutic target

65 inactivation, leading to the hypothesis that resurgent current may facilitate high-frequency firing.

66 Neurons with resurgent current may therefore be less susceptible to u

67 As such, enhancement of resurgent currents may constitute a pathological mechani

68 that selective attenuation of PEPD-enhanced resurgent currents might contribute to this therapeutic

69 At -40 mV, this "resurgent" current peaked in 8 msec and decayed with a t

70 The macroscopic voltage dependence of resurgent current raises the question of whether the blo

71 found that P10-P14 Purkinje cells exhibited resurgent current (ranging from -3.6 to -15.4 pA/pF in 1

72 Here we report a novel TTX-resistant (TTX-R) resurgent current recorded from rat DRG neurons.

73 Resurgent current results from unbinding of a blocking p

74 As with TTX-S resurgent currents, they are activated by membrane repol

75 n endogenous particle whose unbinding allows resurgent current to flow.

76 trast, IEM mutations, whenever tested, leave resurgent currents unchanged.

77 disease-causing mutations lead to increased resurgent currents, unusual sodium currents that have no

78 With 50 mM sodium as a charge carrier, the resurgent current was on average approximately 120 pA.

79 r insight into the potential mechanism(s) of resurgent currents, we examined whether these inhibitors

80 missense mutation in Scn8a, steady-state and resurgent current were also reduced, with altered voltag

81 d the voltage dependence of block, such that resurgent currents were evoked even after conditioning a

82 The amplitudes of the transient and resurgent currents were highly correlated across patches

83 In reverse gradients, outward resurgent currents were tiny or absent, suggesting that

84 nnels in Purkinje cells produce an unusual, "resurgent" current when the cells are repolarized to int

85 of block, beta4(154-167) fully reconstituted resurgent current, whereas scrambled or point-mutated pe

86 pen-state inactivation) and did not increase resurgent currents, which have been suggested to contrib

87 PEPD mutations also increase resurgent currents, which involve the voltage-dependent

88 that enhanced SI is accompanied by impaired resurgent currents, which suggests that SI may interfere

89 ated in part by a voltage-gated Na(+) (NaV) 'resurgent' current, which allows renewed Na(+) influx du

90 h mutations in Nav1.6 dramatically increased resurgent currents while mutations in Nav1.1 did not.

91 nje cells isolated from embryonic chick have resurgent currents with kinetics and amplitudes indistin

92 gent currents, anandamide strongly inhibited resurgent currents with minimal effects on the peak tran

93 sodium channels of Purkinje neurons produce "resurgent" current with repolarization, which results fr

94 ge-clamp that R185H variant channels enhance resurgent currents within dorsal root ganglion neurons a