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1 ation at -40 mV, coinciding with the rise of resurgent current.
2  of persistent current and a slowed decay of resurgent current.
3 ystems, however, Na(V)beta4 fails to produce resurgent current.
4 rst blocking protein that is responsible for resurgent current.
5 d endogenous block, beta4(154-167) generated resurgent current.
6 etics of NaV1.6 appear well adapted to carry resurgent current.
7 e Na(V)1.6 subunit may lead to production of resurgent current.
8 ent current, and step repolarizations evoked resurgent current.
9  neurons that produce tetrodotoxin-resistant resurgent currents.
10 oportion of the neurons that generate Nav1.8 resurgent currents.
11  SI in order to investigate their effects on resurgent currents.
12  hitherto been considered a prerequisite for resurgent currents.
13 rated by the same mechanism underlying TTX-S resurgent currents.
14 v1.6 is the major contributor to these TTX-S resurgent currents.
15 the three drugs on Navbeta4 peptide-mediated resurgent currents.
16 andamide, exhibit differential inhibition of resurgent currents.
17 induce nociceptor hyperexcitability increase resurgent currents.
18 , the non-NaV1.6 subunits can produce robust resurgent currents.
19 ation from positive potentials, producing a "resurgent" current.
20 tions elicit slower channel reopening, or a 'resurgent' current.
21 e electrophysiological phenotypes: a loss of resurgent current, a reduction of persistent current, a
22 pen-channel blocking protein responsible for resurgent current acts as a natural antagonist of lidoca
23 R1872Q, identifies one common dysfunction in resurgent current, although these mutations alter distin
24 ugh carbamazepine did not selectively target resurgent currents, anandamide strongly inhibited resurg
25  inherited spinocerebellar ataxias, controls resurgent current and repetitive firing in Purkinje neur
26  channel inactivation rate, thereby reducing resurgent current and repetitive spiking.
27 pplication of alkaline phosphatase abolished resurgent current and significantly slowed inactivation
28 ical, molecular and structural mechanisms of resurgent current and their relation to the normal funct
29 ed proexcitatory increases in persistent and resurgent currents and rightward shifts in inactivation
30             Thus, the presence or absence of resurgent current, and of persistent sodium current, app
31                  The G1662S mutation doubled resurgent currents, and the T790A mutation increased the
32                                              Resurgent current appears to depend primarily on NaV1.6
33                    Our results indicate that resurgent currents are associated with multiple channelo
34 t kinetics, although the mechanisms by which resurgent currents are augmented remain unclear for all
35                                      Because resurgent currents are evoked during action potential re
36                    Therefore, persistent and resurgent currents are likely to determine whether a mut
37                                    The TTX-R resurgent currents are similar to classic TTX-S resurgen
38                                              Resurgent currents arise after relief of ultra-fast open
39 ptide, can block open Na channels and induce resurgent current as channels unblock upon repolarizatio
40  the necessity of this subunit in generating resurgent current, as well as its influence on Na channe
41 ntial firing in nociceptive neurons and that resurgent currents associated with the Nav1.5 mutation c
42          Computer simulations indicated that resurgent currents associated with the Nav1.7 mutation c
43                                       Inward resurgent currents at strongly negative potentials, howe
44 urrent; Purkinje cells without Na(V)1.6 lack resurgent current, but resurgent current is absent from
45 ion, and conventional inactivation regulates resurgent current by controlling the extent of open-chan
46 0A current density but reduces TTX-resistant resurgent currents by 56%.
47 itions and that enhancement of both types of resurgent currents by inflammatory mediators could contr
48 nsient current amplitude, demonstrating that resurgent currents can be selectively targeted.
49 stent current, while Patient 3 had increased resurgent current compared to controls.
50        Trypsin and chymotrypsin each removed resurgent current, consistent with established roles for
51             We propose that these slow TTX-R resurgent currents contribute to the membrane excitabili
52     Additionally, in control gradients, peak resurgent currents decreased linearly with driving force
53                            The generation of resurgent current depends on a factor in the Na(+) chann
54 n mutation L955 (DeltaL955) fails to produce resurgent currents despite enhanced persistent currents,
55  resurgent Na(+) and K(+) currents, Kv3.1b's resurgent current does not originate from recovery of ch
56                           However, the TTX-R resurgent currents exhibit much slower kinetics, occur a
57                    Na channels that generate resurgent current express an intracellular endogenous op
58 ntal studies have led to the hypothesis that resurgent current flows upon repolarization when an endo
59 damide and cannabidiol on peak transient and resurgent currents from wild-type and mutant channels.
60 erlying molecular components contributing to resurgent current have not been fully identified.
61               Tetrodotoxin-sensitive (TTX-S) resurgent currents have been described in many different
62                                              Resurgent currents (I(NaR)) produced by voltage-gated so
63 current clamp to investigate the role of the resurgent current in action potential formation.
64 ent current in wild-type neurons and induced resurgent current in med neurons.
65 rom five species have the capacity to induce resurgent current in mouse hippocampal neurons, which la
66                          beta-PMTX increased resurgent current in wild-type neurons and induced resur
67 en observed to mediate unique persistent and resurgent currents in cerebellar Purkinje cells.
68       We also show that both TTX-S and TTX-R resurgent currents in DRG neurons are enhanced by inflam
69        These results suggest that slow TTX-R resurgent currents in DRG neurons are mediated by Nav1.8
70      Our data indicate that increased Nav1.8 resurgent currents in DRG neurons greatly prolong action
71 hannel opening, and increased persistent and resurgent currents in large-diameter dorsal root ganglio
72 urgent currents are similar to classic TTX-S resurgent currents in many respects, but not all.
73  Reduced fast inactivation without increased resurgent currents induces symptoms of IEM, not PEPD, in
74            We observed a correlation between resurgent current inhibition and a drug-mediated increas
75 without Na(V)1.6 lack resurgent current, but resurgent current is absent from many other Na(V)1.6-exp
76                                          The resurgent current is associated with recovery of transie
77 es more rapidly than in wild-type cells, and resurgent current is nearly abolished.
78              Emerging research suggests that resurgent current is preferentially increased in a varie
79 ality that we discovered is an alteration of resurgent current kinetics, although the mechanisms by w
80 ctions on voltage-gated sodium channels, and resurgent current may be a promising therapeutic target
81 inactivation, leading to the hypothesis that resurgent current may facilitate high-frequency firing.
82                                 Neurons with resurgent current may therefore be less susceptible to u
83                      As such, enhancement of resurgent currents may constitute a pathological mechani
84  that selective attenuation of PEPD-enhanced resurgent currents might contribute to this therapeutic
85  ZL0177 not only decreases the transient and resurgent currents of Nav1.8 and Nav1.9 but also reduces
86 t (Patient 1) and the patient with increased resurgent current (Patient 3).
87                             At -40 mV, this "resurgent" current peaked in 8 msec and decayed with a t
88        The macroscopic voltage dependence of resurgent current raises the question of whether the blo
89  found that P10-P14 Purkinje cells exhibited resurgent current (ranging from -3.6 to -15.4 pA/pF in 1
90 Here we report a novel TTX-resistant (TTX-R) resurgent current recorded from rat DRG neurons.
91  molecular mechanism underlying these unique resurgent currents represents a novel therapeutic target
92                                              Resurgent current results from unbinding of a blocking p
93                                As with TTX-S resurgent currents, they are activated by membrane repol
94 n endogenous particle whose unbinding allows resurgent current to flow.
95 trast, IEM mutations, whenever tested, leave resurgent currents unchanged.
96  disease-causing mutations lead to increased resurgent currents, unusual sodium currents that have no
97 t current upon depolarization, but also pass resurgent current upon repolarization.
98   With 50 mM sodium as a charge carrier, the resurgent current was on average approximately 120 pA.
99 r insight into the potential mechanism(s) of resurgent currents, we examined whether these inhibitors
100 missense mutation in Scn8a, steady-state and resurgent current were also reduced, with altered voltag
101 d the voltage dependence of block, such that resurgent currents were evoked even after conditioning a
102          The amplitudes of the transient and resurgent currents were highly correlated across patches
103                In reverse gradients, outward resurgent currents were tiny or absent, suggesting that
104 nnels in Purkinje cells produce an unusual, "resurgent" current when the cells are repolarized to int
105 of block, beta4(154-167) fully reconstituted resurgent current, whereas scrambled or point-mutated pe
106 pen-state inactivation) and did not increase resurgent currents, which have been suggested to contrib
107                 PEPD mutations also increase resurgent currents, which involve the voltage-dependent
108  that enhanced SI is accompanied by impaired resurgent currents, which suggests that SI may interfere
109 ated in part by a voltage-gated Na(+) (NaV) 'resurgent' current, which allows renewed Na(+) influx du
110 h mutations in Nav1.6 dramatically increased resurgent currents while mutations in Nav1.1 did not.
111 nje cells isolated from embryonic chick have resurgent currents with kinetics and amplitudes indistin
112 gent currents, anandamide strongly inhibited resurgent currents with minimal effects on the peak tran
113 sodium channels of Purkinje neurons produce "resurgent" current with repolarization, which results fr
114 ge-clamp that R185H variant channels enhance resurgent currents within dorsal root ganglion neurons a

 
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