ライフサイエンスコーパス: sodium current

1 imal inhibitory concentration, fast and late sodium current).

2 ng the amplitude of voltage-gated persistent sodium current.

3 es and prolonged inactivation of the cardiac sodium current.

4 the effect of BjIP on calcium transients and sodium current.

5 ovary cells transfected with SCN5A, encoding sodium current.

6 creased the transient outward K+ current and sodium current.

7 tment with ranolazine, a blocker of the late sodium current.

8 cardiomyopathy phenotype by reducing cardiac sodium current.

9 enlarged window current, and huge sustained sodium current.

10 FA modulation of TTX-sensitive voltage-gated sodium current.

11 y sodium cyanide to activate this persistent sodium current.

12 NTA1 in cardiac myocytes also increased late sodium current.

13 , which also markedly reduced the persistent sodium current.

14 ls, and neither mutation affected persistent sodium current.

15 t contribution of subthreshold TTX-sensitive sodium current.

16 ssium current, and chronically enhanced late sodium current.

17 V1.2 mutation displaying enhanced persistent sodium current.

18 tion of its recovery or increased persistent sodium current.

19 tributed to preferential suppression of late sodium current.

20 ersely affecting the transient voltage-gated sodium current.

21 ns from all three patients displayed altered sodium currents.

22 tude of tetrodotoxin-sensitive and resistant sodium currents.

23 beta-III spectrin complexes fail to enhance sodium currents.

24 in excitability resulted from inhibition of sodium currents.

25 Cells with AHP expressed greater density of sodium currents.

26 nactivation of Nav1.7 and enhanced resurgent sodium currents.

27 of inactivation and inhibition of persistent sodium currents.

28 s caused use- and voltage-dependent block of sodium currents.

29 and Fyn enhancement of fast inactivation of sodium currents.

30 selective Nav1.7 channel blocker)-sensitive sodium currents.

31 tion so that depolarizing steps evoke larger sodium currents.

32 in the pipette solution to induce resurgent sodium currents.

33 ring action potentials and also "persistent" sodium current, a noninactivating TTX-sensitive current

34 d with a reduction in tetrodotoxin-sensitive sodium current, a requirement for much larger depolarizi

35 Riluzole, a blocker of the persistent sodium current, abolished the effect of PGE2 on sigh act

36 ity was caused by a drastic reduction in the sodium current, accompanied by an increase in the amplit

37 potency and selectivity for inhibiting late sodium current across a panel of 7 LQT3 sodium channel v

38 tion increases channel availability and late sodium current activity, leading to enhanced cardiac exc

39 ombin amplifies the persistent voltage-gated sodium current affecting resting membrane potential and

40 ity-dependent potentiation of the persistent sodium current altering intrinsic firing properties of d

41 eir excitability with small changes to their sodium currents, alternating between hyperexcitable and

42 The reduction of sodium current amplitude by estradiol suggests a negativ

43 PHN-associated VZV significantly increased sodium current amplitude in the cell line when compared

44 t studies show that voltage-gated persistent sodium current amplitude is regulated by alternative spl

45 Estradiol decreased the persistent sodium current amplitude, and induced a significant nega

46 radiol significantly decreased the transient sodium current amplitude, but prolonged the sodium curre

47 ed sodium channel protein abundance and peak sodium current amplitudes (H/H, 41.0+/-2.9 pA/pF at -30

48 ting of sodium channels to produce resurgent sodium current, an unusual form of gating in which sodiu

49 -L precipitate a marked decrease in the peak sodium current and a potentially lethal BrS-like proarrh

50 to this property: a persistent TTX-sensitive sodium current and a ruthenium red-sensitive, TRP-like c

51 Both TipE and TEH1 enhanced the amplitude of sodium current and accelerated current decay of all thre

52 This regulation led to a decreased sodium current and action potential upstroke velocity an

53 this variant with mexiletine restored their sodium current and administration of mexiletine to 1 car

54 substantial augmentation of persistent late sodium current and an increase in ramp current.

55 e findings correlated with larger persistent sodium current and depolarized inactivation in neurons f

56 have altered action potential, reduced peak sodium current and diminished conduction velocity.

57 odels of Dravet syndrome (DS) reveal reduced sodium current and excitability in GABAergic interneuron

58 this disease is caused by selective loss of sodium current and excitability of GABAergic inhibitory

59 The mutation results in increased persistent sodium current and hyperactivity of transfected neurons.

60 arkedly augments an inward voltage-sensitive sodium current and inhibits the outward nonselective cur

61 rations of A-803467 selectively block "late" sodium current and shorten action potentials in mouse an

62 palmitoylation-null beta1-p.C162A modulated sodium current and sorted to detergent-resistant membran

63 plex attached to SCN5A as a key regulator of sodium current and suggest that SNTA1 be considered a ra

64 of at least four voltage-gated currents: the sodium current and the M-type, delayed rectifier, and ca

65 Mexiletine is used to block late sodium current and to shorten QT interval in LQT3 patien

66 to peak, persistent, and resurgent forms of sodium current and to sustained action potential firing.

67 bility is mediated in part by an increase in sodium currents and a reduction in the fast-inactivating

68 on with loss of planarity, reduced resurgent sodium currents and abnormal glutamatergic neurotransmis

69 Similarly, the sodium currents and action potential firing are also imp

70 ns in NaV1.1 channels have severely impaired sodium currents and action potential firing in hippocamp

71 Dravet inhibitory neurons showed deficits in sodium currents and action potential firing, which were

72 halenyl)-2,4-hexadienamide (BTG 502) reduces sodium currents and antagonizes the action of BTX on coc

73 s using a mouse model of DS revealed reduced sodium currents and impaired excitability in GABAergic i

74 FGF13 increased Nav1.7 sodium currents and maintained the membrane localization

75 The Possum mutation enhanced Na(v)1.8 sodium currents and neuronal excitability and heightened

76 r with even a small imbalance between inward sodium currents and outward potassium currents, but mech

77 ved from lithium responders while increasing sodium currents and reducing fast potassium currents.

78 trodotoxin (TTX)-resistant, SCN10A-dependent sodium currents and response to nociceptive stimuli such

79 egrees C, the mutant channel did not produce sodium current, and function was not restored by coexpre

80 tylcholine activated potassium current, peak sodium current, and L-type calcium current, and exhibits

81 e clusters are major contributors to cardiac sodium current, and that loss of NaV1.5 expression reduc

82 PKP2 expression alters the properties of the sodium current, and the velocity of action potential pro

83 t, without change to transient voltage-gated sodium current, and to rescue of seizure in this model i

84 xhibited robust tetrodotoxin (TTX)-sensitive sodium currents, and acute infection significantly reduc

85 ata supporting the hypothesis that the TTX-R sodium currents are similarly distributed between nodose

86 av3 mutations, F97C and S141R, increase late sodium current as a potential mechanism to prolong actio

87 om an adaptation current and the receptor or sodium current as main sources for the colored and white

88 tivated a substantial component of transient sodium current as well as persistent current.

89 ctivation of transient as well as persistent sodium current at subthreshold voltages produces amplifi

90 arameters between V232I+L1308F and wild-type sodium currents at baseline, use-dependent inhibition of

91 activation rate to severely suppress cardiac sodium currents at elevated temperatures.

92 and known to block persistent and resurgent sodium currents, at pharmacologically relevant concentra

93 saicin induces in small DRG neurons a robust sodium current block within 30 s.

94 e same cell line all four WNKs also increase sodium current blocked by the ENaC inhibitor amiloride.

95 Consistent with increased sodium currents, both types of patient-derived neurons s

96 lso activated a large component of transient sodium current, but IPSP-like waveforms engaged primaril

97 Unexpectedly, it also reduced the peak sodium current by 80%.

98 esulted in a decrease of amiloride-sensitive sodium current by approximately 60% and ciliary length b

99 We moreover assessed T-tubules sodium current by recording whole-cell sodium currents i

100 ding of Fyn kinase and mediate inhibition of sodium currents by enhancing fast inactivation.

101 sion of Fyn with Na(V)1.2 channels decreases sodium currents by increasing the rate of inactivation a

102 determined that the increase in a persistent sodium current causes heterogeneously prolonged action p

103 3 results in a 2- to 3-fold increase in late sodium current compared with wild-type caveolin-3.

104 n heterologous cells increased peak and late sodium current compared with WT-SNTA1, and the increase

105 a2+ influx, as well as reduced voltage-gated sodium currents, consistent with compromised neurite int

106 Resurgent sodium currents contribute to the regeneration of action

107 A T-tubules sodium current could, however, not be demonstrated.

108 ate a natural temperature-dependent shift in sodium current deactivation (exacerbated by mutation) ma

109 nic Kidney-293 cells, showing a reduction in sodium current densities similar to typical BrS mutation

110 underlying mechanism by which MOG1 increased sodium current densities.

111 f MOG1 with Nav1.5 in HEK293 cells increased sodium current densities.

112 s increase was accompanied by an increase in sodium current density and a leftward shift in the sodiu

113 PSC-derived neurons also displayed increased sodium current density and increased excitatory and decr

114 Sodium current density and intrinsic neuronal excitabili

115 ) mice exhibited normalized pyramidal neuron sodium current density and reduced hippocampal NaV1.6 pr

116 ed correction of the mutation re-establishes sodium current density and SCN5A expression.

117 n downregulating SCN5A, leading to decreased sodium current density and slower conduction velocity.

118 Scn2b null atria had normal levels of sodium current density compared with wild type.

119 drome, we found no measurable differences in sodium current density in acutely dissociated CA3 hippoc

120 Sodium current density was half that of wild-type muscle

121 d neuronal hyperexcitability, suppressed the sodium current density, and right-shifted the V1/2 of th

122 t excessive cleavage of Navbeta2 and reduced sodium current density, but the phenotype associated wit

123 on slowing in the BZ was modeled by reducing sodium current density, whereas structural conduction sl

124 and was associated with significantly lower sodium current density.

125 type TRPV1, despite similar or even reduced sodium current density.

126 ng behaviour was both voltage and persistent sodium current dependent and could be stimulated by sodi

127 nts, albeit all neurons presented persistent sodium current-dependent intrinsic pacemaker properties

128 t widths slows conduction because of reduced sodium current driving force, termed "self-attenuation."

129 me type III (LQT3) is an excessive inflow of sodium current during phase 3 of the action potential ca

130 We quantified these two components of sodium current during the pacemaking trajectory using ac

131 Sodium currents elicited from a holding potential of -60

132 C, but lamotrigine also increased persistent sodium current evoked by this mutation.

133 sult from increased voltage-gated persistent sodium current expression.

134 gical mechanism whereby calcium ions promote sodium current facilitation due to Ca(2+) memory at high

135 gy, as prolonged pharmacological blockade of sodium current failed to phenocopy channel knockdown.

136 neuronal biophysical mechanisms-a persistent sodium current ([Formula: see text]) and a calcium-activ

137 need for a high-fidelity technique to record sodium currents from intact mouse muscle fibres.

138 ned the effects of cannabidiol on endogenous sodium currents from striatal neurons, and similarly we

139 ated the ability of cannabinoids to modulate sodium currents from wild-type and epilepsy-associated m

140 Whereas TTX-R sodium currents have been documented in lung vagal senso

141 ulted in a complete disruption of the normal sodium current heterogeneity that exists between atrial,

142 he density of Nav1.5-generated voltage-gated sodium current I (Na) and Nav1.5 surface protein levels

143 of the tetrodotoxin-resistant, voltage-gated sodium current I(Na) in alphaMyHC-FKBP12 ventricular car

144 tributed to preferential suppression of late sodium current (I (NaL)).

145 harmacology of GS-967 and eleclazine on peak sodium current (I (NaP)) recorded from human induced plu

146 The persistent sodium current (I(Na(P))) has been implicated in the reg

147 In addition, we characterized TTX-sensitive sodium current (I(Na)) and 4AP-sensitive and TEA-resista

148 bserved that loss of Pum2 leads to increased sodium current (I(Na)) and action potential firing, mimi

149 al repressor Pumilio (Pum) as a regulator of sodium current (I(Na)) and excitability in Drosophila mo

150 (0.5-2 mumol/L) had no effect on either mean sodium current (I(Na)) density or I(Na) gating kinetics

151 sma membrane (PM) expression of Na(v)1.5 and sodium current (I(Na)) density, thus we hypothesize that

152 ffects on Na(v) inactivation ensure adequate sodium current (I(Na)) reserve to safeguard against nume

153 tress has been shown to increase late inward sodium current (I(Na)), reducing the net cytosolic Ca(2+

154 the cell resting membrane potential, and the sodium current (I(Na)), which provides a rapid depolariz

155 Suppressing the late sodium current (I(NaL)) may counterbalance the reduced r

156 variable, whereas blockade of the persistent sodium current (I(NaP)) abolished them.

157 s also demonstrate an increase in persistent sodium current (I(NaP)) and a hyperpolarizing shift in t

158 Up-regulation of the persistent sodium current (I(NaP)) and down-regulation of the potas

159 dominated by inward TTX-sensitive persistent sodium current (I(NaP)) that activated near -75 mV and i

160 ting activity that depends upon a persistent sodium current (I(NaP)).

161 We compared sodium currents (I(Na)) in small DRG neurons from beta2+

162 d potassium currents (I(KNa)) and persistent sodium currents (I(NaP)), the components of which are wi

163 Resurgent sodium currents (I(NaR)) are atypical currents believed

164 that CaMKII-mediated modulation of neuronal sodium current impacts neuronal excitability in Scn2a(Q5

165 isplaying lower amplitudes of a "persistent" sodium current important for such pacemaking.

166 We examined gating of subthreshold sodium current in dissociated cerebellar Purkinje neuron

167 c insights into the central role of the late sodium current in HCM, and introduce the scientific rati

168 Scn10a expression contributes to late sodium current in heart and represents a new target for

169 Electrophysiological analysis of sodium current in HEK293 cells stably expressing hNa(v)1

170 estradiol modulated a tetrodotoxin-sensitive sodium current in isolated GnRH neurons from both young

171 only approximately 20% of the TTX-resistant, sodium current in mouse dorsal root ganglion neurons.

172 ls was specific because POSH did not inhibit sodium current in oocytes injected with ENaC-alpha, beta

173 Nonlinear loss of sodium current in Purkinje neurons from heterozygous and

174 channels a capacity to serve as a pacemaking sodium current in the primitive heart and brain in lieu

175 ing site of Na(v)1.6 prevented generation of sodium current in transfected cells.

176 n potential firing by blocking voltage-gated sodium currents in a subset of somatosensory neurons, wh

177 ntially increased the amplitude of resurgent sodium currents in an optimized adult rat-derived dorsal

178 mpal mossy fibers of adult mice, we recorded sodium currents in axonal and somatic membrane patches.

179 DS patient-derived neurons show increased sodium currents in both bipolar- and pyramidal-shaped ne

180 bules sodium current by recording whole-cell sodium currents in control (N=5) and detubulated (N=5) w

181 oxin-sensitive (TTX-S) and resistant (TTX-R) sodium currents in dorsal root ganglion neurons followin

182 ontrast, Ae1a failed to significantly affect sodium currents in dorsal unpaired median neurons from t

183 l administered to the female mouse modulates sodium currents in fluorescently-labeled GnRH neurons.

184 Here we show that FFA inhibits voltage-gated sodium currents in hippocampal pyramidal neurons; this e

185 , flagellin/QX-314 co-application suppressed sodium currents in large-diameter human DRG neurons.

186 and modulate the expression of TTX-resistant sodium currents in medium-sized muscle nociceptors.

187 biophysical properties of VGSCs, we isolated sodium currents in MSO principal neurons in gerbil brain

188 eceptors, was found to inhibit voltage-gated sodium currents in N1E-115 neuroblastoma cells.

189 onsequence, reduce voltage-gated calcium and sodium currents in primary sensory neurons.

190 f whole-cell peak, persistent, and resurgent sodium currents in Purkinje neurons were reduced by 58-6

191 atives, such as 7 and 27, also blocked TTx-r sodium currents in rat dorsal root ganglia (DRG) neurons

192 his study was to examine the contribution of sodium currents in the negative feedback action of estra

193 uced sensitization of tetrodotoxin-resistant sodium current, in small-diameter dorsal root ganglion n

194 the early (peak) and late components of the sodium current (INa and INaL), but ranolazine preferenti

195 pH 7.4, VCL-M94I caused 30% decrease in peak sodium current (INa) amplitude compared to WT; under aci

196 1768D/+) mice showed increases in persistent sodium current (INa) density in CA1 pyramidal but not bi

197 Whole-cell patch-clamp was used to measure sodium current (INa) density in isolated cardiomyocytes.

198 h was paralleled by a higher Ito and a lower sodium current (INa) density in subepicardium versus sub

199 regulatory proteins that reduce or eliminate sodium current (INa) have been linked to BrS.

200 cardiac sodium channel, NaV1.5, carries the sodium current (INa) that provides a rapid depolarizing

201 mice displayed reduced NaV1.5 expression and sodium current (INa), specifically at the lateral myocyt

202 rons to hypoxia-an increase in voltage-gated sodium current (INa)-has been unknown.

203 oke velocity because of a 2-fold increase in sodium current (INa).

204 iting potassium currents and increasing late sodium current (INa-L) in cardiomyocytes.

205 polarization additionally by increasing late sodium current (INa-L) via inhibition of phosphoinositid

206 To determine whether increased sodium current(INa) would promote EADs, we employed aden

207 odels incorporate a formulation of the rapid sodium current, INa, based on 30 year old data from chic

208 sodium current amplitude, but prolonged the sodium current inactivation time constant.

209 o inactivate, contributing to increased late sodium current (INaL), which is directly responsible for

210 tiple ion currents, including the persistent sodium current INaP.

211 cal cable theory predictions, the persistent sodium current (INaP), a non-inactivating mode of the vo

212 d that riluzole, a blocker of the persistent sodium current (INap), abolished the modulatory effect o

213 We simulate the blockade of a persistent sodium current (INaP), proposed to underlie rhythm gener

214 ability through regulation of the persistent sodium current (INaP).

215 monstrated a dramatic increase in persistent sodium current, incomplete channel inactivation, and a d

216 PHN-associated VZV sodium current increases were therefore mediated in part

217 These sodium current increases were unaffected by acyclovir pr

218 ationale and execution of the Impact of Late Sodium Current Inhibition on Exercise Capacity in Subjec

219 ty in L-cells was due to large voltage gated sodium currents, inhibition of which by tetrodotoxin red

220 Resurgent sodium current is an atypical near threshold current pre

221 ly, pharmacological induction of a transient sodium current is capable of restoring regeneration even

222 Exaggerated late sodium current is known to mediate arrhythmogenic early

223 found that non-voltage-dependent background sodium current is much smaller in SNc neurons than VTA n

224 A subthreshold sodium current is necessary for a continuous frequency d

225 current, in combination with the persistent sodium current, is essential to respiratory rhythm in vi

226 Diminution of sodium currents, largely NaV1.7, was recapitulated in se

227 a inhibition of the late phase of the inward sodium current (late I(Na)) during cardiac repolarizatio

228 Late sodium current (late INa) is enhanced during ischemia by

229 a marked increase in both the peak and late sodium currents leading to prolongation of the action po

230 isolated CAR(+)/(-) myocytes showed reduced sodium current magnitude specifically at the intercalate

231 as AP maximum upstroke velocity, whole-cell sodium current magnitude/properties, and mRNA levels of

232 ological targeting of the physiological late sodium current may provide added therapeutic efficacy to

233 , and that enhanced resurgent and persistent sodium currents may provide a general mechanistic basis

234 + neurons, brought about in part by enhanced sodium currents, may contribute to the spontaneous itch-

235 transcripts, Na(V)1.5 protein abundance, and sodium current measured in isolated ventricular myocytes

236 However, sodium currents measured in the Orai3-expressing HEK293

237 a(+)](o) modulate neuronal excitability by a sodium current mechanism and that excessively altered ne

238 gnificantly increase TTX-resistant resurgent sodium currents mediated by Nav1.8.

239 In contrast, Dc1a has little effect on sodium currents mediated by PaNav1 channels from the Ame

240 mutation has been shown to disrupt both the sodium-current-modulatory and cell-adhesive functions of

241 dings revealed that two currents, persistent sodium current (NaP) and K(+)-dominated leak current (Le

242 leptic drugs target voltage-gated persistent sodium current, none exclusively repress this current wi

243 -E did not prevent heptanol-induced block of sodium currents, nor did it alter voltage dependence or

244 oncentrations, KIIIA incompletely blocks the sodium current of Na(V)1.2, leaving a 5% residual curren

245 effects of the novel analogs were tested on sodium currents of native myofibers.

246 substantial contribution from the transient sodium current or bulk [Na(+)](i).

247 ent had no effect on either pyramidal neuron sodium current or hippocampal NaV1.6 levels.

248 nabidiol can preferentially target resurgent sodium currents over peak transient currents generated b

249 natal mouse myocytes markedly attenuated the sodium current (P<0.01).

250 s HEK cells produced a significantly reduced sodium current (P<0.01).

251 n-inactivating mode of the voltage-dependent sodium current, paradoxically increases Rin and taum whe

252 ne of the patients with increased persistent sodium current (Patient 1) and the patient with increase

253 und that the activity of a persistent inward sodium current (persistent I(Na)) is highly effective at

254 These results suggest that the persistent sodium current plays a major role in determining firing

255 X-314, leading to TLR5-dependent blockade of sodium currents, predominantly in A-fiber neurons of mou

256 butes to QT prolongation by altering cardiac sodium current properties (INa).

257 s and mouse models have demonstrated altered sodium current properties.

258 exhibited significantly increased persistent sodium currents (range, 0.5% to 1.7% of peak current) ty

259 ects of GS967 on peak (INaP) and late (INaL) sodium current recorded from cells that heterologously e

260 from the Na(V)1.8 WW binding motif decreased sodium currents, reduced Na(V)1.8 protein expression, an

261 eads to conduction slowing, especially after sodium current reduction.

262 alcn, a unique channel that generates "leak" sodium currents, regulates excitability and neuromodulat

263 s: the deactivation threshold for persistent sodium currents reversibly shifts to a more negative vol

264 ificant reduction in L-type calcium and peak sodium current, shortening of action potential duration

265 icular excitability via 20% reduction of the sodium current should increase vulnerability to life-thr

266 mp experiments showed an increased sustained sodium current, suggesting a mechanistic overlap between

267 e that lack Na(v)1.6, reduces tetrodotoxin-S sodium currents, suggesting isoform-specific modulation

268 model, which has no axon or spike-generating sodium currents, suggests that MSO spikes do not contrib

269 nd discusses BACE physiological functions in sodium current, synaptic transmission, myelination, and

270 The sodium current that initiates the nerve action potential

271 otype by reducing the driving force and late sodium current that produces early afterdepolarizations

272 ead to increased resurgent currents, unusual sodium currents that have not previously been implicated

273 Voltage-gated sodium channels (Nav) produce sodium currents that underlie the initiation and propaga

274 The sensitivity of the sodium current to shaking was dependent on intact cilia.

275 of BDNF to enhance a tetrodotoxin-resistant sodium current (TTX-R I(Na)) and to suppress a delayed r

276 stradiol did not significantly attenuate the sodium current underlying the action potential in cells

277 The amplitude of the sodium current underlying the action potential was signi

278 Persistent tetrodotoxin-resistant (TTX-r) sodium currents up-regulated by intracellular GTP have b

279 Importantly, this reduction in sodium current was also seen when the atypical mutations

280 Previously unobtainable robust sodium current was demonstrated through 38 passages, sui

281 Persistent sodium current was found to account for most of the PIC

282 Sodium current was lower when NaV1.5 was coexpressed wit

283 However, for narrow clefts, late sodium current was reduced via self-attenuation, a prote

284 TTX-sensitive sodium current was substantial throughout the entire int

285 The hypothesis that a persistent sodium current was the predominant determinant of cell f

286 in a computational model when voltage-gated sodium currents were impaired in basket cells (BCs).

287 Whole-cell sodium currents were measured in tsA201 cells transientl

288 Only L263V and Q1489K generated quantifiable sodium currents when coexpressed in tsA201 cells with th

289 pical mutations could lead to a reduction in sodium currents when coexpressed with WT to mimic the he

290 CN5A, and was associated with increased late sodium current, which is the characteristic biophysical

291 d slows down the inactivation process of the sodium current, while shifting the inactivation curve ~1

292 utant channel revealed significantly delayed sodium current with a dominant negative effect.

293 -like waveforms engaged primarily persistent sodium current with only a small additional transient co

294 tive feedback in subthreshold voltage range: sodium current with rapid inactivation and low-threshold

295 mutations in SCN5A result in a reduction of sodium current with some mutations even exhibiting a dom

296 ithin all models, the combination of reduced sodium current with structural remodeling more often deg

297 t channel generated voltage-dependent inward sodium currents with an average peak current density com

298 isoforms produce a multiplicity of distinct sodium currents with different time-dependent characteri

299 -cell configuration, carbamazepine inhibited sodium current within seconds when applied externally, b

300 ficant reduction in voltage-gated persistent sodium current, without change to transient voltage-gate