ライフサイエンスコーパス: voltage-gated

1 channels under strict inhibitory control of voltage-gated A-type K(+) channels.

2 but significant hyperpolarizing shift in the voltage-gated activation kinetics of the channel.

3 of the prokaryotic NaVs NsVBa (nonselective voltage-gated Bacillus alcalophilus) and NaChBac (bacter

4 (Ca(2+)) currents through the regulation of voltage-gated Ca(2+) (CaV) 2.1 channels by Ca(2+) sensor

5 e growth cone, which is mainly controlled by voltage-gated Ca(2+) (Cav) and K(+) (Kv) channels, modul

6 sites on CaV1.2 channels, the most prominent voltage-gated Ca(2+) (CaV) channel type in myocytes in c

7 Voltage-gated Ca(2+) (CaV) channels consist of a pore-fo

8 report the discovery that inhibiting T-type voltage-gated Ca(2+) and KCa channels can effectively in

9 ere, we tested the hypothesis that different voltage-gated Ca(2+) channel densities in presynaptic ac

10 ON-bipolar cells by aligning the presynaptic voltage-gated Ca(2+) channel directing glutamate release

11 cate target cell type-specific modulation of voltage-gated Ca(2+) channel function or different subun

12 rs (GSK7975A and GSK5498A) as well as L-type voltage-gated Ca(2+) channel inhibitors (nifedipine and

13 bunits that is not conserved in CaV2 or CaV3 voltage-gated Ca(2+) channel subunits.

14 and bursts of action potentials evoked fast, voltage-gated Ca(2+) channel-dependent Ca(2+) elevations

15 ht spatial coupling of synaptic vesicles and voltage-gated Ca(2+) channels (CaVs) ensures efficient a

16 -cells depends on Ca(2+) influx through high voltage-gated Ca(2+) channels (HVCCs).

17 Voltage-gated Ca(2+) channels (VGCCs) are important for

18 iting store-operated calcium entry (SOCE) or voltage-gated Ca(2+) channels (VGCCs), we show that SOCE

19 influx through the dendritic high-threshold voltage-gated Ca(2+) channels activates CaCCs, which con

20 were also activated by Ca(2+) influx through voltage-gated Ca(2+) channels and synaptically activated

21 ction potentials, requiring Ca(2+) entry via voltage-gated Ca(2+) channels and transient receptor pot

22 in unmyelinated axons.SIGNIFICANCE STATEMENT Voltage-gated Ca(2+) channels are fulcrums of neurotrans

23 Voltage-gated Ca(2+) channels are involved in numerous p

24 Extracellular Ca(2+) via voltage-gated Ca(2+) channels established a Ca(2+)-depen

25 reases, depolarization increases to activate voltage-gated Ca(2+) channels in the adjacent vascular s

26 the inactivation of heterologously expressed voltage-gated Ca(2+) channels of type 1.3 (CaV1.3) and i

27 t likely by controlling Ca(2+) entry through voltage-gated Ca(2+) channels opened during spike trains

28 Postsynaptic voltage-gated Ca(2+) channels therefore constitute the s

29 relative contributions of store-operated and voltage-gated Ca(2+) channels to this Ca(2+) influx, we

30 L-type voltage-gated Ca(2+) channels were involved in mediating

31 LTP, initially characterized as dependent on voltage-gated Ca(2+) channels, also requires the activat

32 ll to generate large Ca(2+) currents through voltage-gated Ca(2+) channels, and thus have little effe

33 It is generally accepted that voltage-gated Ca(2+) channels, CaV, regulate Ca(2+) home

34 target approach is presented, targeting both voltage-gated Ca(2+) channels, classically studied for n

35 ch is triggered by Ca(2+) influx from L-type voltage-gated Ca(2+) channels, not postsynaptic NMDA rec

36 LTP previously characterized as dependent on voltage-gated Ca(2+) channels.

37 fying potassium current, (2) inhibition of a voltage-gated Ca(2+) current and (3) presynaptic depress

38 letion reduced spike-evoked Ca(2+) entry and voltage-gated Ca(2+) currents.

39 To determine whether voltage-gated Ca(2+) entry is involved in oligodendrocyt

40 ment in the postnatal brain and suggest that voltage-gated Ca(2+) influx in oligodendroglial cells is

41 n in the demyelinated brain and suggest that voltage-gated Ca(2+) influx in OPCs is critical for remy

42 plasticity rely on regulation of presynaptic voltage-gated Ca(2+) type 2.1 (CaV2.1) channels.

43 centration, by varying Ca(2+) influx through voltage-gated Ca(2+)-channels or Ca(2+) uncaging.

44 Voltage gated Ca2+ channels, K(+)ATP channels and the al

45 increase caused by NMDA-receptor (NMDAR) and voltage-gated Ca2+ -channel (VGCC) activation is thought

46 Recombinant voltage-gated calcium (Ca(2+)) channels in heterologous

47 Voltage-gated calcium (Cav) channels contain four homolo

48 lease-activated calcium modulator 1 but also voltage-gated calcium channel (Cav) 1 channels.

49 he final coding exon (exon 47) of the Cav2.1 voltage-gated calcium channel (VGCC) gene produces two m

50 P/Q-type voltage-gated calcium channel (VGCC) puncta colocalized

51 Inborn errors of Cacna1a, the P/Q-type voltage-gated calcium channel alpha subunit gene, expres

52 tors for thymoma (as recognized for neuronal voltage-gated calcium channel autoantibodies).

53 e pore-forming alpha1 subunit of the cardiac voltage-gated calcium channel Cav1.2 at Ser1928, suggest

54 Here we show that the voltage-gated calcium channel CaV1.3 and the big conduct

55 encoding the alpha1A subunit of the P/Q-type voltage-gated calcium channel Cav2.1.

56 des the pore-forming subunit of the neuronal voltage-gated calcium channel Cav2.1.

57 thesis that TSP4 activates its receptor, the voltage-gated calcium channel Cavalpha2delta1 subunit (C

58 Here, we recorded the voltage-gated calcium channel current in nucleated patch

59 requires a physical interaction between the voltage-gated calcium channel dihydropyridine receptor (

60 al muscle excitation-contraction coupling, a voltage-gated calcium channel directly activates opening

61 as used to quantify postsynaptic density and voltage-gated calcium channel protein expression.

62 ched comparison subjects as well as aberrant voltage-gated calcium channel subunit protein expression

63 The effect of increased voltage-gated calcium channel subunit protein expression

64 mechanical allodynia by regulating auxiliary voltage-gated calcium channel subunits alpha2delta-1 and

65 rsed by restoring the expression levels of a voltage-gated calcium channel, cacophony.

66 H caused a reduction in cacophony, a Type II voltage-gated calcium channel, expression and that genet

67 ons in the ryanodine receptor but not in the voltage-gated calcium channel, indicating that these phe

68 ional and mechanical coupling between L-type voltage-gated calcium channels (CaV1.1) and the ryanodin

69 To determine whether L-type voltage-gated calcium channels (L-VGCCs) are required fo

70 L-type voltage-gated calcium channels (LTCCs) are implicated in

71 depend on NMDA receptors (nmdaLTP) or L-type voltage-gated calcium channels (vdccLTP).

72 ddition to Gbetagamma-mediated modulation of voltage-gated calcium channels (VGCC), inhibition can al

73 tivity-dependent potentiation of presynaptic voltage-gated calcium channels (VGCCs) underlies 3,4-dia

74 erties, density, and the spatial location of voltage-gated calcium channels (VGCCs).

75 Voltage-gated calcium channels are essential players in

76 ich includes oscillatory calcium signals via voltage-gated calcium channels as a key component.

77 enes and their implications, with a focus on voltage-gated calcium channels as part of the disease pr

78 , single-channel current amplitude of native voltage-gated calcium channels can be resolved accuratel

79 Voltage-gated calcium channels can coassemble with auxil

80 receptor 2 (mGluR2) signaling, which acts on voltage-gated calcium channels in SACs, selectively rest

81 sential for estimating numbers of functional voltage-gated calcium channels in the membrane and the s

82 y fiber terminals leverage distinct types of voltage-gated calcium channels to mediate short-term fac

83 presynaptic action potentials (APs) activate voltage-gated calcium channels, allowing calcium to ente

84 pha2delta proteins are auxiliary subunits of voltage-gated calcium channels, and influence their traf

85 e proteins that can bind and modulate L-type voltage-gated calcium channels.

86 seases, both genetic and acquired, involving voltage-gated calcium channels.

87 s in a calcium-dependent manner and binds to voltage-gated calcium channels.

88 the transient opening of different types of voltage-gated calcium channels.

89 mutated hippocalcin, mostly driven by N-type voltage-gated calcium channels.

90 This is the case for voltage-gated calcium channels.

91 ABSTRACT: Several studies suggest that voltage-gated calcium currents are involved in generatin

92 The voltage-gated cardiac Na(+) channel (Nav1.5), encoded by

93 4, P = 4 x 10(-14)) in intron 16 of SCN5A, a voltage-gated cardiac sodium channel gene.

94 t for gating currents is well documented for voltage-gated cation channels (VGCC), and it is consider

95 NCE STATEMENT The number and localization of voltage-gated Cav Ca(2+) channels are crucial determinan

96 Voltage-gated Cav1.2 and Cav1.3 (L-type) Ca(2+) channels

97 L-type voltage-gated CaV1.2 calcium channels (CaV1.2) are key r

98 at promotes Ca(2+)-dependent facilitation of voltage-gated Cav1.3 Ca(2+) channels in transfected cell

99 Voltage-gated CaV2.1 channels comprise a pore-forming al

100 stemming from mutations in the KCNE2-encoded voltage-gated channel beta-subunit, is limited.

101 ulopathy caused by mutations of the chloride voltage-gated channel Kb gene (CLCNKB), which encodes th

102 However, voltage-gated channels are also found in thin dendrites

103 The model predicts that voltage-gated channels are less important than store-ope

104 cium oscillations, but calcium entry through voltage-gated channels has much less effect.

105 Ca(2+) entry through voltage-gated channels only becomes important when the c

106 ric ion influxes, preferential activation of voltage-gated channels, and electrophoretic redistributi

107 uced depression depends on calcium entry via voltage-gated channels, is blocked by BAPTA chelation, a

108 o not depend strongly on Ca(2+) entry though voltage-gated channels.

109 ations in the CLCNKB gene encoding the human voltage-gated chloride ClC-Kb (hClC-Kb) channel cause cl

110 sults illustrate how membrane properties and voltage-gated conductances can extract distinct stimulus

111 quency synaptic inputs, so cells with larger voltage-gated conductances prefer higher frequencies.

112 involving recruitment of NMDA receptors and voltage-gated conductances.

113 ent frequencies, due to differences in their voltage-gated conductances.

114 These dimeric voltage-gated ion channel (VGIC) superfamily members hav

115 o acids in the S4 transmembrane segment of a voltage-gated ion channel form ion-conducting pathways t

116 enetic validation for the role of the Nav1.7 voltage-gated ion channel in pain signaling pathways mak

117 They belong to the voltage-gated ion channel superfamily but their activiti

118 ature of the paddle motif in all three major voltage-gated ion channel types (Kv, Nav, and Cav).

119 tifier current (IKs), through the tetrameric voltage-gated ion channel, KCNQ1, and its beta-subunit,

120 Voltage-gated ion channels (VGICs) are outfitted with di

121 Multi-domain voltage-gated ion channels appear to have evolved throug

122 ell as cacophony (cac) and paralytic (para), voltage-gated ion channels central to neuronal excitabil

123 Most small-molecule inhibitors of voltage-gated ion channels display poor subtype specific

124 Rather, it is mediated by voltage-gated ion channels in the cone membrane and acts

125 Voltage-gated ion channels mediate electrical dynamics i

126 Hundreds of mutations in genes encoding voltage-gated ion channels responsible for action potent

127 is composed of diverse animal-specific, non-voltage-gated ion channels that play important roles in

128 Subcellular positioning of voltage-gated ion channels will enable multicompartmenta

129 MDA, GABA-A, mGluR2/3 receptors and Nav, Cav voltage-gated ion channels) and demonstrated the ability

130 regulated by a number of factors, including voltage-gated ion channels, D2-autoreceptors, and nAChRs

131 urrent is reminiscent of an omega current in voltage-gated ion channels.

132 nificantly altered due to changes in several voltage-gated ion channels.

133 hloride ions, and are blocked by blockers of voltage-gated ion channels.

134 ey intermediate position in the evolution of voltage-gated ion channels.

135 ur gating charges commonly found in those of voltage-gated ion channels.

136 ivated state observed in structures of other voltage-gated ion channels.

137 A number of voltage-gated ionic currents can contribute to the gener

138 Voltage-gated K(+) (Kv) channel activation depends on in

139 ) channel blocker, and by 4-aminopyridine, a voltage-gated K(+) (KV) channel blocker.

140 ) channel blocker, and by 4-aminopyridine, a voltage-gated K(+) (KV) channel blocker.

141 Voltage-gated K(+) (Kv) channels are key factors in cont

142 Heterotetramer voltage-gated K(+) (KV) channels KV2.1/KV6.4 display a g

143 rom the symposium on the structural basis of voltage-gated K(+) channel function, as well as the mech

144 The voltage-gated K(+) channel Kv2.1 has been intimately lin

145 molecular methods to determine how Kv3.4, a voltage-gated K(+) channel robustly expressed in dorsal

146 In voltage-gated K(+) channels and the prokaryotic KcsA cha

147 KNIR-1 treatment of cells expressing voltage-gated K(+) channels enabled the visualization of

148 The voltage-gated K(+) channels Kv7.2 and Kv7.3 are located

149 KCNE3 (MiRP2) forms heteromeric voltage-gated K(+) channels with the skeletal muscle-exp

150 assemble with and modulate the properties of voltage-gated K(+) channels.

151 red intrinsic membrane properties, enhancing voltage-gated K(+) currents and increasing intracellular

152 companied by an increase in the amplitude of voltage-gated K(+) currents.

153 oss-of-function or a gain-of-function of the voltage-gated K+ channel Kv1.2, were described to cause

154 ronal excitability through the activation of voltage-gated KCNQ2-5 potassium channels.

155 Less frequent were aquaporin-4, voltage-gated Kv1 potassium channel-complex related prot

156 The human epilepsy gene Kcna1 encodes voltage-gated Kv1.1 potassium channels that act to dampe

157 Voltage-gated Kv1.3 and Ca(2+)-dependent KCa3.1 are the

158 ys implicated in E-T coupling, activation of voltage-gated L-type Ca(2+) channels (LTCCs) in the plas

159 Ca(2+) influx through voltage-gated L-type Ca(2+) channels (LTCCs), in particu

160 neurons, which then pathologically recruits voltage-gated l-type Ca(2+) channels that synergize with

161 Ca2+ entry through voltage-gated L-type Ca2+ channels triggers exocytosis o

162 SNPs) in CACNA1C, the alpha1C subunit of the voltage-gated L-type calcium channel Cav1.2, rank among

163 Voltage-gated L-type calcium channels (VLCC) are distrib

164 Voltage-gated L-type CaV1.2 channels in cardiomyocytes e

165 Voltage-gated L-type CaV1.2 channels in cardiomyocytes e

166 ythmias and can be driven by the kinetics of voltage-gated membrane currents or by instabilities in i

167 Neuronal voltage-gated N-type calcium channels (Cav2.2) are inhib

168 by de novo gain-of-function mutations in the voltage-gated Na channel Nav1.6.

169 Voltage-gated Na(+) (NaV) channels are key regulators of

170 The requirement of voltage-gated Na(+) and Ca(2+) channel activation indica

171 Here we introduce roNaV2, an engineered voltage-gated Na(+) channel harboring a selenocysteine i

172 Thus, influx of Na(+) via voltage-gated Na(+) channels (NaV ) has emerged as an im

173 Voltage-gated Na(+) channels (Nav ) modulate neuronal ex

174 Depolarization leads to the opening of voltage-gated Na(+) channels (Nav) and subsequently volt

175 Neurotransmitter release depends on voltage-gated Na(+) channels (Navs) to propagate an acti

176 BTX targets voltage-gated Na(+) channels and enables them to open pe

177 hich depends on the gating rates of the fast voltage-gated Na(+) current.

178 ched in multimolecular complexes composed of voltage-gated Nav and Kv7 channels associated with cell

179 neuronal excitability whereas Scn2a encodes voltage-gated Nav1.2 sodium channels important for actio

180 overies of AKAP79/150-mediated modulation of voltage-gated neuronal M-type (KCNQ, Kv7) K(+) channels

181 Ion channels, both ligand- and voltage-gated, play fundamental roles in many physiologi

182 re, we show that the transcript for KCNE4, a voltage-gated potassium (Kv) channel beta subunit associ

183 KCNQ1 is a voltage-gated potassium (Kv) channel whose distinctive p

184 Voltage-gated potassium (Kv) channels comprise pore-form

185 Studies of voltage-gated potassium (Kv) channels have identified th

186 s could be ameliorated through modulation of voltage-gated potassium (Kv) channels that regulate temp

187 Cs encoding subunits which resemble metazoan voltage-gated potassium (Kv1-Kv4) channels in assembly a

188 Voltage-gated potassium 7.1 (Kv7.1) channel and KCNE1 pr

189 are studied on the surface of the soma: the voltage-gated potassium and sodium channels Kv1.4 and Na

190 agnetic resonance imaging has linked chronic voltage-gated potassium channel (VGKC) complex antibody-

191 ies against the extracellular domains of the voltage-gated potassium channel (VGKC) complex proteins,

192 ped redefine antigenic components within the voltage-gated potassium channel (VGKC) complex.

193 Antibodies against the voltage-gated potassium channel (VGKC) were first recogn

194 otein-like 2 in 11 patients, uncharacterised voltage-gated potassium channel (VGKC)-complex antigens

195 n 7 patients (6.3%): 3 (2.7%) had TPO-Ab and voltage-gated potassium channel complex (VGKCc) Ab, 2 (1

196 sine RNA editing in transcripts encoding the voltage-gated potassium channel Kv1.1 converts an isoleu

197 4A] is a potent and selective blocker of the voltage-gated potassium channel Kv1.3, which is a highly

198 for conditions treatable by blockade of the voltage-gated potassium channel Kv1.3.

199 this was attributable to interdependence of voltage-gated potassium channel properties.

200 The voltage-gated potassium channel subfamily A member 3 (Kv

201 KCNQ1 is a voltage-gated potassium channel that is modulated by the

202 Kv11.1 (hERG) is a voltage-gated potassium channel that shows very slow ion

203 ction mutations in hERG (encoding the Kv11.1 voltage-gated potassium channel) cause long-QT syndrome

204 e the second transmembrane segment, S2, of a voltage-gated potassium channel, Kv1.3, as a model to pr

205 LGI1-IgG-positive specimens had higher voltage-gated potassium channel-IgG immunoprecipitation

206 hought to be due, in part, to suppression of voltage-gated potassium channels (Kv ) in pulmonary arte

207 FMRP has been confirmed to bind voltage-gated potassium channels (Kv 3.1 and Kv 4.2) mRN

208 -activated potassium (BK) channels and Kv3.3 voltage-gated potassium channels accompanies the inabili

209 EAG-like (ELK) voltage-gated potassium channels are abundantly expresse

210 Kv3.1 and Kv3.2 voltage-gated potassium channels are expressed on parval

211 Oligomers of homomeric voltage-gated potassium channels associate early in biog

212 Voltage-gated potassium channels formed by KCNQ2 and KCN

213 Kv1.2 and related voltage-gated potassium channels have a highly conserved

214 The ether a go-go family of voltage-gated potassium channels is structurally distinc

215 Voltage-gated potassium channels of the KCNQ (Kv7) subfa

216 onstrate a novel mechanism for regulation of voltage-gated potassium currents in the setting of cardi

217 -activated cyclic nucleotide-gated (HCN) and voltage-gated potassium subfamily H (KCNH) channels by p

218 to offer great insight into the mechanism of voltage-gated processes but has been challenging to stud

219 Voltage-gated proton (Hv1) channels are involved in many

220 mutations in previously unreported HVCN1, a voltage-gated proton channel-encoding gene and B-cell re

221 Large-conductance Ca(2+)- and voltage-gated Slo1 BK channels are directly activated by

222 osequencing genotyping and sequencing of the voltage gated sodium channel (VGSC) gene did not detect

223 tiated and propagated by a single isoform of voltage gated sodium channels - SCN5A.

224 ilization within a month, resulting in rapid voltage-gated sodium (NaV) channel and betaIV spectrin l

225 Voltage-gated sodium (Nav) channel inhibitors are used c

226 This voltage-gated sodium (Nav) channel subtype also plays an

227 4) binds to and controls the function of the voltage-gated sodium (Nav) channel with phenotypic outco

228 Voltage-gated sodium (NaV) channels are essential for th

229 Voltage-gated sodium (Nav) channels are responsible for

230 Voltage-gated sodium (NaV) channels are responsible for

231 Voltage-gated sodium (Nav) channels initiate action pote

232 Voltage-gated sodium (Nav) channels play a key role in g

233 in the expected loss of pyramidal neuron AIS voltage-gated sodium and potassium channels.

234 GIC behavior, we addressed how the bacterial voltage-gated sodium channel (BacNa(V)) C-terminal cytop

235 Voltage-gated sodium channel (NaV) mutations cause genet

236 nsfer (LRET) between the rat skeletal muscle voltage-gated sodium channel (Nav1.4) and fluorescently

237 Gain-of-function mutations in the voltage-gated sodium channel (Nav1.5) are associated wit

238 Voltage-gated sodium channel (VGSC) beta subunits signal

239 Veratridine (VTD) is a voltage-gated sodium channel (VGSC) modifier that is use

240 Voltage-gated sodium channel (VGSC) mutations cause seve

241 The prominent role of voltage-gated sodium channel 1.7 (Nav1.7) in nociception

242 The voltage-gated sodium channel 1.7 (Nav1.7) plays an impor

243 , in mice, this effect is mediated solely by voltage-gated sodium channel 1.8 (NaV1.8).

244 However, expression analysis of voltage-gated sodium channel alpha subunits revealed NaV

245 inactivated conformational cycle in a single voltage-gated sodium channel and give insight into the s

246 Mutations in SCN2B, encoding voltage-gated sodium channel beta2-subunits, are associa

247 n Culex quinquefasciatus display CNV for the voltage-gated sodium channel gene (Vgsc), target-site of

248 gous loss-of-function mutations in the brain voltage-gated sodium channel gene SCN1A.

249 caused by de novo missense mutations in the voltage-gated sodium channel gene SCN8A Here, we investi

250 erity have been associated with mutations in voltage-gated sodium channel genes.

251 Although a gate residue in the eukaryotic voltage-gated sodium channel has been identified, the mi

252 The Nav1.1 voltage-gated sodium channel is a critical contributor t

253 The NaV1.7 voltage-gated sodium channel is implicated in human pain

254 Axonal voltage-gated sodium channel mRNA and local trafficking

255 quantify isoflurane binding to the bacterial voltage-gated sodium channel NaChBac.

256 ABSTRACT: Voltage-gated sodium channel NaV 1.7 is required for acu

257 d by loss-of-function mutations in the brain voltage-gated sodium channel NaV1.1.

258 Mutations in SCN2A, a gene encoding the voltage-gated sodium channel Nav1.2, have been associate

259 Therefore, EC cells use Scn3a-encoded voltage-gated sodium channel NaV1.3 for electrical excit

260 ed a critical role for the regulation of the voltage-gated sodium channel NaV1.5 in the heart by the

261 ates that the expression and function of the voltage-gated sodium channel Nav1.7 are increased in a p

262 Human genetic studies have implicated the voltage-gated sodium channel NaV1.7 as a therapeutic tar

263 Trafficking of the voltage-gated sodium channel NaV1.7 is dysregulated in n

264 notoxins MrVIA, MrVIB, and MfVIA inhibit the voltage-gated sodium channel NaV1.8, a well described ta

265 Specifically, voltage-gated sodium channel subtype NaV 1.7 is required

266 c evidence has clearly demonstrated that the voltage-gated sodium channel, Nav1.7, is critical to pai

267 that heterologously expressed human cardiac voltage-gated sodium channel, the principle cardiac sodi

268 n (c.4447G>A; p.E1483K) in SCN8A, encoding a voltage-gated sodium channel.

269 Bacterial voltage-gated sodium channels (BacNavs) serve as models

270 metabotropic glutamate receptor-1 (mGluR1), voltage-gated sodium channels (Nav ) and glutamate trans

271 They are rich in voltage-gated sodium channels (Nav) and thus underpin ra

272 We examined the repertoire of voltage-gated sodium channels (NaV) in fluorescence-sort

273 mans and other vertebrates, target conserved voltage-gated sodium channels (NaV) of nerve and muscle,

274 Voltage-gated sodium channels (NaV) play an important ro

275 ic tension, the thermal random motion of the voltage-gated sodium channels (Nav), which are bound to

276 Cardiac voltage-gated sodium channels (Nav1.5) play an essential

277 Voltage-gated sodium channels (NaVs) are activated by tr

278 Voltage-gated sodium channels (Navs) play crucial roles

279 Voltage-gated sodium channels (Navs) play essential role

280 agnitude shorter than the activation time of voltage-gated sodium channels (VGSC) would evoke action

281 s to efficiently overexpress large mammalian voltage-gated sodium channels (VGSC).

282 ies of myelinated fibres, however, show that voltage-gated sodium channels (VGSCs) aggregate with cel

283 KCNQ2/3 (Kv7.2/7.3) channels and voltage-gated sodium channels (VGSCs) are enriched in th

284 s required for the interaction of FGF14 with voltage-gated sodium channels and neuronal excitability.

285 rs and not through NMDA receptors or through voltage-gated sodium channels and that the spine neck is

286 ABSTRACT: Voltage-gated sodium channels are critical for neuronal

287 Fast opening and closing of voltage-gated sodium channels are crucial for proper pro

288 Voltage-gated sodium channels are essential for electric

289 Voltage-gated sodium channels are responsible for action

290 myelinating Schwann cells, such as clustered voltage-gated sodium channels at the node of Ranvier and

291 deficient for exon 1b, PV interneurons lack voltage-gated sodium channels at their axonal initial se

292 in a reduction in the fraction of available voltage-gated sodium channels due to insufficient recove

293 Slow inactivation of voltage-gated sodium channels has been discussed to be t

294 Mutations in brain isoforms of voltage-gated sodium channels have been identified in pa

295 Inhibition of voltage-gated sodium channels is neuroprotective in prec

296 KEY POINTS: Voltage-gated sodium channels play a fundamental role in

297 ibution from entry through NMDA receptors or voltage-gated sodium channels.

298 of central neurons to hypoxia-an increase in voltage-gated sodium current (INa)-has been unknown.

299 The voltage-gated sodium ion channel (VGSC) belongs to the l

300 ported GpTx-1 analogs that inhibit NaV1.7, a voltage-gated sodium ion channel that is a compelling ta