ライフサイエンスコーパス: voltage-activated

1 vating Kv3.4 channels underlie a robust high voltage-activated A-type K(+) current (I(AHV)) in nocice

2 ll types small voltage steps at subthreshold voltages activated a substantial component of transient

3 ditional calculations performed on the KvAP (voltage-activated) and KirBac1.1 (inward rectifier) chan

4 unknown, although mPanx1 is reported to be a voltage-activated anion-selective channel.

5 the salty receptor, is co-expressed with the voltage-activated ATP release channel CALHM1/3 in a subs

6 e cells of Slo(-/-) mice lacked calcium- and voltage-activated BK currents, whereas local calcium tra

7 The neuronal calcium- and voltage-activated BK potassium channel is modulated by e

8 e the role of large conductance calcium- and voltage-activated (BK) channels in spontaneous and secre

9 High-voltage activated Ca channels participate in multiple ce

10 We show that high-voltage activated Ca(2+) channels are regulated by membr

11 ng Rem2, mediate profound inhibition of high-voltage activated Ca(2+) channels containing intracellul

12 lso find evidence for high expression of low-voltage activated Ca(2+) channels in the same region, in

13 induces rapid Ca(2+) signals mediated by low-voltage activated Ca(2+) channels under strict inhibitor

14 n rearing depressed multiple classes of high-voltage activated Ca(2+) current.

15 aptic mechanism of action, nor did it affect voltage-activated Ca channel currents.

16 cells might trigger Ca(2)(+) influx through voltage-activated Ca(2)(+) channels.

17 The beta subunit of high voltage-activated Ca(2+) (Ca(v)) channels targets the po

18 larly, co-assembly of the BKCa channels with voltage-activated Ca(2+) (Cav) channels, mirroring the n

19 distinct mutations in the gene encoding the voltage-activated Ca(2+) channel alpha(1A) subunit (CACN

20 ansport and physiological properties of high voltage-activated Ca(2+) channel complexes.

21 veral of its analogs directly stimulate high voltage-activated Ca(2+) channels (HVACCs) in acutely di

22 Voltage-activated Ca(2+) channels (VACCs) mediate Ca(2+)

23 Calcium influx through voltage-activated Ca(2+) channels (VACCs) plays a critic

24 e Rem is a potent negative regulator of high voltage-activated Ca(2+) channels and a known interactin

25 th accelerated inactivation kinetics of high-voltage-activated Ca(2+) channels and a modest upregulat

26 role of Ca(v)beta in RGK inhibition of high voltage-activated Ca(2+) channels and prompt a paradigm

27 fects of L-arginine on evoked EPSCs and high voltage-activated Ca(2+) channels expressed in HEK293 ce

28 have shown previously that NO inhibits high voltage-activated Ca(2+) channels in primary sensory neu

29 contrast to the well established function of voltage-activated Ca(2+) channels in the presynaptic mem

30 vated Ca(2+) channels, the inhibition of low-voltage-activated Ca(2+) channels is subtype-dependent a

31 ng the surface expression and gating of high voltage-activated Ca(2+) channels through their interact

32 Unlike high-voltage-activated Ca(2+) channels, the inhibition of low

33 ainly regulated by subtypes of neuronal high-voltage-activated Ca(2+) channels.

34 GTP-binding proteins potently inhibits high voltage-activated Ca(2+) channels.

35 fferent terminals through S-nitrosylation of voltage-activated Ca(2+) channels.

36 hyperpolarization and deinactivation of low-voltage-activated Ca(2+) channels.

37 S-nitrosylation in the NO regulation of high voltage-activated Ca(2+) channels.

38 we show that BPA acts as a potent blocker of voltage-activated Ca(2+) channels.

39 arized level, are further boosted by the low-voltage-activated Ca(2+) conductance.

40 X) rather than presynaptic depolarization or voltage-activated Ca(2+) currents.

41 cellular excitability together with reduced voltage-activated Ca(2+) currents.

42 ich lacks 4D-Ca(v)/Na(v)s, EukCatAs underpin voltage-activated Ca(2+) signaling important for membran

43 ndeed requires activation of Na(v)s and high-voltage-activated Ca(2+)-channels (HVACCs), but also of

44 occur, but there is little evidence that low-voltage-activated, Ca(v)3 ("T-type"), channels take part

45 the membrane and induce Ca2+ influx via high-voltage-activated Ca2+ channels (I(HVA)).

46 tivated by Ca2+ entry through high-threshold voltage-activated Ca2+ channels (L- and N-type), and tog

47 equires proper communication of plasmalemmal voltage-activated Ca2+ channels and Ca2+ release channel

48 High-voltage-activated Ca2+ channels are essential for divers

49 High-voltage-activated Ca2+ channels regulate diverse functio

50 nd their Ca2+ sources through high-threshold voltage-activated Ca2+ channels were studied using whole

51 ts is obligatory for forming functional high-voltage-activated Ca2+ channels, yet the structural dete

52 or a dopamine D1 receptor agonist decreased voltage-activated Ca2+ current and lowered Ca2+ influx.

53 proenkephalin, inhibited high (but not low) voltage-activated Ca2+ current in both DRG and SCG neuro

54 sphatidylinositol 3-kinase/Akt signaling and voltage-activated Ca2+ influx for stimulation of calmodu

55 These data identify a role of low-voltage activated calcium channels in synaptic plasticit

56 Rem2 inhibits high voltage activated calcium channels, is involved in synap

57 ble of acting as a negative modulator of low voltage activated calcium current.

58 anding of gamma(6) subunit modulation of low voltage activated calcium current.

59 High-voltage-activated calcium (Ca(V) 1/Ca(V) 2) channels tra

60 Voltage-activated calcium (Cav) channels couple intracel

61 ample, gabapentin is a ligand of alpha2delta voltage-activated calcium channel subunits that are over

62 The present studies blocked voltage-activated calcium channels (CaV) using the nonse

63 High voltage-activated calcium channels (HVACCs) are essentia

64 Inhibiting high-voltage-activated calcium channels (HVACCs; Ca(V)1/Ca(V)

65 ([Ca(2+)](o)) regulates Ca(2+) entry through voltage-activated calcium channels (VACCs) and consequen

66 CANCE STATEMENT Presynaptic Ca(2+) entry via voltage-activated calcium channels (VACCs) is the major

67 At chemical synapses, voltage-activated calcium channels (VACCs) mediate Ca(2+

68 had lower baclofen-evoked inhibition of high-voltage-activated calcium channels and a defective presy

69 with the alpha1 pore-forming subunit of high voltage-activated calcium channels and modulates several

70 ane protein related to the gamma subunits of voltage-activated calcium channels and the claudin super

71 High-voltage-activated calcium channels are hetero-oligomeric

72 L-type high-voltage-activated calcium channels are involved in the c

73 d the ability of Rem2 to modulate endogenous voltage-activated calcium channels in rat sympathetic an

74 Dihydropyridine-sensitive, voltage-activated calcium channels respond to membrane d

75 These channels are low voltage-activated calcium channels that play a key role

76 Besides opening and closing, high voltage-activated calcium channels transit to a noncondu

77 lcium currents arising from preexisting high-voltage-activated calcium channels without affecting low

78 Rather, by downregulating their voltage-activated calcium channels, vagal motoneurons ac

79 These GTPases also function as regulators of voltage-activated calcium channels, which in turn modula

80 ction site (synprint) found in synaptic high voltage-activated calcium channels.

81 y trigger glutamate release independently of voltage-activated calcium channels.

82 hether CaBP5 can modulate expressed Ca(v)1.2 voltage-activated calcium channels.

83 vated calcium channels without affecting low-voltage-activated calcium channels.

84 de of currents arising from preexisting high-voltage-activated calcium channels.

85 (I(h)), persistent Na+ current (I(NaP)), low-voltage-activated calcium current (I(L/T)) mediated by T

86 ardly rectifying current I(h), low-threshold voltage-activated calcium current I(t), and activity at

87 This glycine response reduced high voltage-activated calcium current.

88 further, we show that baclofen inhibits high-voltage-activated calcium currents in granule cells.

89 Ghrelin significantly increased voltage-activated calcium currents in isolated single DM

90 selective effect of gamma(6) on LVA and high voltage-activated calcium currents in vivo.

91 reases in C(m), which were correlated to the voltage-activated calcium currents.

92 s, it has been reported to block T-type (low-voltage activated) calcium channels.

93 on (Hv1) channels are relatives of classical voltage-activated cation channels.

94 might have been augmented by three types of voltage-activated cationic currents known to increase ne

95 Like other high voltage-activated Cav channels, Cav1.4 channels are comp

96 ted from a transcriptional downregulation of voltage-activated (Cav) calcium channels in DMV neurons,

97 n for activation of co-expressed BK and high-voltage activated CaV2.2 channels.

98 Mitral cells express low-voltage activated Cav3.3 channels on their distal apical

99 ls coimmunoprecipitate and interact with low voltage-activated Cav3.2 Ca(2+) channels at the nanodoma

100 eceptor activation was found to regulate low-voltage-activated CaV3.2 calcium channels localized to t

101 a(6) calcium channel subunit to modulate low voltage activated (Cav3.1) calcium current density.

102 The dendritic arborization and voltage-activated channel complement of rat neocortical

103 Cardiac mitoBK(Ca) is a calcium- and voltage-activated channel that is sensitive to paxilline

104 e cardiac L-type voltage-gated calcium (high voltage-activated) channel with accessory proteins beta

105 brake and its function to maintain these low voltage-activated channels closed at resting membrane po

106 R-type high voltage-activated channels inactivate fully in a few hun

107 amma-dependent inhibition of non-L-type high-voltage-activated channels of the Ca(v)2 family.

108 uring (P7-P9) type I hair cells acquired low-voltage-activated channels that shortened the rise time

109 pithelial tissues, whereas KCNQ1 function as voltage-activated channels with very slow kinetics in ca

110 r-ear mechanisms (transducer adaptation, low-voltage-activated channels, nonquantal transmission, and

111 e interaction with the external potential in voltage-activated channels.

112 which usually permit Ca influx through high-voltage-activated channels.

113 GTPase, between the N-cadherin JMD and these voltage-activated channels.

114 showing that MDIMP preferentially blocks low-voltage-activated channels.

115 As previously reported for voltage-activated conductances, none of these currents w

116 r results suggest alteration in subthreshold voltage-activated currents might be the mechanism underl

117 .1 and other Ca(V)2 channels, including high voltage-activated currents that are larger in external B

118 v3.1b subunits, which mediate high-threshold voltage-activated currents.

119 Voltage-activated human ether-a-go-go-related gene (hERG

120 was attributable to calcium influx via high-voltage-activated (HVA) (N- and P/Q-type) calcium channe

121 GnRH neurons express prominent high-voltage-activated (HVA) and small low-voltage-activated

122 While both ON and OFF cells express high-voltage-activated (HVA) Ca(2+) channels, only OFF RGCs a

123 GTP-binding proteins potently inhibits high voltage-activated (HVA) Ca(2+) channels, providing a pow

124 arizing steps (> or =20 ms) that evoked high-voltage-activated (HVA) Ca(2+) currents (I(Ca)) and elev

125 d that the current density of high threshold voltage-activated (HVA) calcium (Ca(2+)) channels was ma

126 ed both low-voltage-activated (LVA) and high-voltage-activated (HVA) calcium current (I(Ca)).

127 rease in the amplitude of the high-threshold voltage-activated (HVA) calcium current.

128 ltage-gated Ca2+ channel subunits alter high-voltage-activated (HVA) calcium currents, impair neurotr

129 on between -60 mV and -70 mV as well as high voltage-activated (HVA) current with an activation volta

130 rolled by calcium (Ca(2)(+)) influx via high-voltage-activated (HVA), Ca(v)2, channels ("N-, P/Q-, or

131 The characteristics of voltage-activated I(Na) and I(K) in the GnRH-containing

132 itability, in part by enhancing subthreshold voltage-activated inward currents.

133 location-specific interactions of IPSPs with voltage-activated ion channels are likely to influence t

134 re simply on the selective expression of low-voltage-activated ion channels by irregular afferents.

135 Voltage-activated ion channels contain S1-S4 domains tha

136 The properties of the voltage-activated ion channels that regulate synaptic in

137 Cortical axons contain a diverse range of voltage-activated ion channels, including Ca(2+) current

138 data suggest that Kv3.4 and Cav1.2, two high-voltage-activated ion channels, may act together to cont

139 In voltage-activated ion channels, voltage sensor (VSD) act

140 For voltage-activated ion channels, X-ray structures suggest

141 pid bilayer are critical for the function of voltage-activated ion channels.

142 a notable example being the S1-S4 domains of voltage-activated ion channels.

143 we report a study on the characterization of voltage-activated ionic currents in GnRH-containing TN c

144 pore domain govern the mammalian Ca(2+)- and voltage-activated K(+) (BK) channel opening.

145 adipose tissue expression of the Ca(2+)- and voltage-activated K(+) (BK) channel was identified in mo

146 ASIC1a and the high-conductance Ca(2+)- and voltage-activated K(+) (BK) channel.

147 Large-conductance Ca(2+)- and voltage-activated K(+) (BK) channels are involved in a l

148 Large-conductance Ca(2+)- and voltage-activated K(+) (BK) channels are well known for

149 Large-conductance Ca(2+) and voltage-activated K(+) (BK) channels control membrane ex

150 muscle cells, large-conductance Ca(2+)- and voltage-activated K(+) (BK) channels provide a critical

151 Large conductance Ca(2+)- and voltage-activated K(+) (BK) channels, composed of pore-f

152 amples from calcium-activated K(+) (BK(Ca)), voltage-activated K(+) (K(v)) and Ca(2+) channel (L-type

153 as 4-aminopyridine (4-AP) are widely used as voltage-activated K(+) (Kv) channel blockers and can imp

154 mia impairs vascular reactivity and inhibits voltage-activated K(+) (Kv) channels.

155 High-conductance Ca(2+)- and voltage-activated K(+) (Slo1 or BK) channels (KCNMA1) pl

156 The large-conductance Ca(2+)- and voltage-activated K(+) channel (BK(Ca), MaxiK), which is

157 Slo1 is a Ca(2+)- and voltage-activated K(+) channel that underlies skeletal a

158 nel, which is a large-conductance Ca(2+) and voltage-activated K(+) channel, is involved in the hypox

159 In particular, the KCNQ (Kv7) family of voltage-activated K(+) channels functions to stabilize n

160 nal with temporal precision depends on a low-voltage-activated K(+) conductance (gKL) and a hyperpola

161 nces are relatively small, in particular low-voltage-activated K(+) conductances (K(LVA)).

162 The large-conductance, calcium- and voltage-activated K(+)(BK) channel consists of the pore-

163 Large-conductance, Ca2+- and voltage-activated K+ (BK) channels are broadly expressed

164 NMA1 encodes the large-conductance Ca2+- and voltage-activated K+ (BK) potassium channel alpha-subuni

165 ental question about the gating mechanism of voltage-activated K+ (Kv) channels is how five positivel

166 Reductions in voltage-activated K+ (Kv) currents may underlie arrhythm

167 Large conductance Ca(2+)- and voltage-activated K+ (maxi-K) channels modulate human my

168 Large-conductance Ca2+-voltage-activated K+ channels (BK channels) control many

169 plicating slow inactivation of low-threshold voltage-activated K+ channels as its mechanism.

170 tsynaptic sites suggests that this family of voltage-activated K+ channels may have additional roles

171 rent (I(M)), comprised of Kv7 channels, is a voltage-activated K+ conductance that plays a key role i

172 s were unchanged in TASK-1/3 KO mice as were voltage-activated K+ currents, including the non-inactiv

173 a1 subunit of BK (large conductance Ca2+ and voltage-activated K+) channels is essential for many key

174 present study tested the hypothesis that low-voltage activated Kv1 channels affect threshold dynamics

175 Low-voltage-activated Kv1-type (dendrotoxin-I sensitive) K+

176 These immature nodal structures lacked low-voltage-activated KV1.1 which was not enriched at juxtap

177 Voltage-activated Kv2.1 channels have properties commens

178 High-voltage-activated KV3.1b and KV2.2 were expressed in mut

179 us, endogenous membrane PIP(2) supports high-voltage activated L-, N-, and P/Q-type Ca(2+) channels,

180 n by SSRIs was mediated by a direct block of voltage-activated L-type Ca(2+) channels and was indepen

181 (2+) channels (Ca(v)1.3) responsible for low voltage-activated L-type Ca(2+) current.

182 cellular calcium transients mediated by high-voltage-activated L-type calcium channels.

183 herapeutic effect primarily by blocking high-voltage-activated L-type calcium channels.

184 Thus, potentiation of a low-voltage-activated L-type current by synaptically release

185 Among these conductances, the Ca(2+)- and voltage-activated large conductance Ca(2+)-activated K(+

186 ls, we examine regulation of the Ca(2+)- and voltage-activated large conductance Ca(2+)-activated K(+

187 ning TN cells examined, we recorded both low-voltage-activated (LVA) and high-voltage-activated (HVA)

188 We have tested the hypothesis that low voltage-activated (LVA) and nonvoltage-gated (NVG) chann

189 2+) channels, only OFF RGCs also express low-voltage-activated (LVA) Ca(2+) channels.

190 Low-voltage-activated (LVA) Ca2+ channels are widely distrib

191 on and responsiveness of high (HVA)- and low-voltage-activated (LVA) Ca2+ channels to IGF-1, using th

192 fier toxins have been reported to target low-voltage-activated (LVA) calcium channels, and the struct

193 lcium channel gamma(6) subunit modulates low voltage-activated (LVA) calcium current in both human em

194 ealed that MDIMP binds preferentially to low-voltage-activated (LVA) channels.

195 nsmitter release, and stimulate thalamic low-voltage-activated (LVA) currents that contribute to a co

196 tage clamp recordings revealed transient low voltage-activated (LVA) currents with activation between

197 ated via dendrotoxin-sensitive low-threshold voltage-activated (LVA) K(+) channels.

198 t high-voltage-activated (HVA) and small low-voltage-activated (LVA) macroscopic (whole-cell) Ca curr

199 Ca(v)3.x gene family members, encoding low voltage-activated (LVA) or T-type channels, were first i

200 Low voltage-activated (LVA), T-type, calcium channels mediat

201 In contrast, voltage-activated M-type K(+) current (I(M)) improved sp

202 A voltage-activated molecular-plasmonics device was create

203 tor (nAChR) subtype and an inhibitor of high-voltage-activated N-type calcium channel currents.

204 al output reflects a progressive decrease in voltage-activated Na(+) and K(+) currents, which occurs

205 The roles of oligodendroglial voltage-activated Na(+) channels (Nav) and electrical ex

206 receptors, l-calcium channels, nitric oxide, voltage-activated Na(+) channels, or intracellular calci

207 of the fast inactivation phase of mammalian voltage-activated Na(+) channels.

208 SCs generated a TTX (1 microm)-resistant voltage-activated Na(+) current (I(Na)) that had a peak

209 Voltage-activated Na+ channels in the primary sensory ne

210 The peak of transient component (NaT) of the voltage-activated Na+ current is also filtered more than

211 The opening and closing of voltage-activated Na+, Ca2+ and K+ (Kv) channels underli

212 ltage ramps revealed a non-inactivating, low-voltage-activated, nimodipine-sensitive current that was

213 itude and that they display distinct linear, voltage-activated or rectified current-voltage character

214 d inhibitory because of this increase in low-voltage activated outward currents.

215 type I hair cells is the expression of a low-voltage-activated outward rectifying K(+) current, IK,L

216 ed the calyx, and by the expression of a low-voltage-activated outward rectifying K(+) current, IK,L

217 In spinal motoneurons, dendrites have voltage-activated persistent inward currents that are fa

218 The large conductance Ca(2+)-and-voltage activated potassium channel (BK) is well-suited

219 elegans slo-1 large-conductance calcium and voltage-activated potassium (BK) channel gene, which con

220 a-subunits of large conductance calcium- and voltage-activated potassium (BK) channels are potently m

221 Large conductance calcium- and voltage-activated potassium (BK) channels are widely exp

222 e the role of large conductance calcium- and voltage-activated potassium (BK) channels in spontaneous

223 a-subunits of large conductance calcium- and voltage-activated potassium (BK) channels play an import

224 Here we use four-fold symmetric voltage-activated potassium (K(v)) channels as reporters

225 Voltage-activated potassium (K(v)) channels contain a ce

226 end of pore, as it has been established for voltage-activated potassium (K(V)) channels.

227 In voltage-activated potassium (Kv) channels, basic residue

228 rly understood when compared to those of the voltage-activated potassium (Kv) channels.

229 ssion of the large-conductance, calcium- and voltage-activated potassium (MaxiK) channel in the corti

230 The large conductance calcium- and voltage-activated potassium channel (BK channel) and its

231 The large conductance calcium- and voltage-activated potassium channel (BK(Ca)) is widely e

232 The large-conductance calcium- and voltage-activated potassium channel (BK) is a well-estab

233 in, the human large-conductance calcium- and voltage-activated potassium channel (BK), in a lipid env

234 on when transplanted from an archaebacterial voltage-activated potassium channel (KvAP) or voltage-se

235 rminus of the large conductance calcium- and voltage-activated potassium channel is an important dete

236 ifically in this area, including a number of voltage-activated potassium channel subunits.

237 The large conductance, calcium- and voltage-activated potassium channel, known as the BK cha

238 Calcium- and voltage-activated potassium channels (BK) are regulated

239 Large conductance Ca(2+)- and voltage-activated potassium channels (BKCa) shape neuron

240 unanticipated action of COX-2 inhibitors on voltage-activated potassium channels and their physiolog

241 calcium-activated potassium channels and Kv2 voltage-activated potassium channels both regulate actio

242 amplitudes were mediated extensively by low voltage-activated potassium channels containing the Kv1.

243 The Kv7 family (Kv7.1-7.5) of voltage-activated potassium channels contributes to the

244 ch residues are involved in this process for voltage-activated potassium channels, several different

245 Using available structures of TRPV1 and voltage-activated potassium channels, we engineered chim

246 smooth muscle cells express Kv7.4 and Kv7.5 voltage-activated potassium channels, which contribute t

247 ion is associated with altered physiology of voltage-activated potassium channels.

248 lancing the suppression of EPSP peaks by low voltage-activated potassium channels.

249 in proteins (Hv1 and Ci-VSP) into eukaryotic voltage-activated potassium channels.

250 A strong, low-voltage-activated potassium conductance (g(KL)) at the c

251 Interestingly, we also found a low-voltage-activated potassium conductance present at E18,

252 low input resistance and activation of a low-voltage-activated potassium conductance that are charact

253 uronal excitability is governed primarily by voltage-activated potassium conductances (K(VA)).

254 ing subthreshold synaptic integration: a low-voltage-activated potassium current (I(K-LVA)) and a hyp

255 The M-current is a low voltage-activated potassium current generated by neurona

256 A low voltage-activated potassium current, IKL, is found in au

257 rpolarization-activated cation current (Ih), voltage-activated potassium current, large-conductance c

258 ion potential firing by suppression of a low voltage-activated potassium current, M-current.

259 SP (1 to 25 microM) also suppressed voltage-activated potassium currents (IK+) and calcium c

260 ligand for 30 min increased the amplitude of voltage-activated potassium currents 2-fold on average.

261 was accompanied by consistent reductions in voltage-activated potassium currents near the action pot

262 gular firing phenotype, due to different low-voltage-activated potassium currents.

263 re associated with increased inactivation of voltage-activated potassium currents.

264 Voltage-activated proton (Hv1) channels are relatives of

265 tified in voltage-sensitive phosphatases and voltage-activated proton channels, both of which lack as

266 The voltage-activated rGO was highly sensitive to NO2 with a

267 e development of chemiresistive sensors with voltage-activated sensitivity for the detection of CO co

268 Voltage-activated sodium (Na(v)) channels are crucial fo

269 s and is a vital step in the biosynthesis of voltage-activated sodium (Nav) channels.

270 ations of the SCN1A gene encoding a neuronal voltage-activated sodium channel.

271 high-frequency action potentials by blocking voltage-activated sodium channels in a use-dependent fas

272 te the action potential is conducted through voltage-activated sodium channels, and mutations of thes

273 1-Ca(v)3.3 constitute the T-type, or the low-voltage-activated, subfamily, the abnormal activities of

274 cologically, revealing all of the major high-voltage activated subtypes: L-, N-, P/Q-, and R-type Ca(

275 indicated that T-type calcium channels (low-voltage activated T-channels) are potently inhibited by

276 molecule that has been shown to inhibit low-voltage activated T-type Ca(2+) channels (TCCs).

277 We found that the increased activity of low voltage activated T-type calcium channels induced by the

278 All three forms of recombinant low voltage-activated T-type Ca(2)(+) channels (Ca(v)3.1, Ca

279 has been considered electrically silent, low voltage-activated T-type Ca(2+) channels are assumed to

280 ent evidence that H2 S is a modulator of low voltage-activated T-type Ca(2+) channels, and discrimina

281 Low voltage-activated T-type Ca(v)3.2 calcium channels are e

282 enetic data indicate a prominent role of low-voltage-activated T-type calcium channels (T-channels) i

283 nd in mice, secondarily elevate neuronal low-voltage-activated T-type calcium currents.

284 r calcium entry into T cells-through the low-voltage-activated T-type CaV3.1 calcium channel.

285 Calcium currents via low-voltage-activated T-type channels mediate burst firing,

286 between P/Q channels and Gem-insensitive low voltage-activated T-type channels, we identify a region

287 depolarized from -100 mV, inactivating, low voltage-activated (T-type channel-mediated) Ca2+ current

288 Although the presence of low-voltage-activated (T-type) Ca channels in nuclear neuron

289 (2+) channel subunit Ca(V)3.2 mediates a low voltage-activated (T-type) Ca(2+) current (I(CaT)) that

290 Low voltage-activated (T-type) Ca2+ channels are responsible

291 Low-voltage-activated (T-type) calcium channels are responsi

292 s oxide's selective inhibition of CaV3.2 low-voltage-activated (T-type) calcium channels in pain path

293 ACNA1H is a human gene encoding Ca(v)3.2 low-voltage-activated, T-type calcium channels associated wi

294 s wherein redox active recognition units are voltage-activated to give enhanced and highly specific r

295 After 24 h in NA, additional low-voltage activated transient Ca(2+) current developed who

296 ytes in noradrenaline for 24 h induced a low-voltage activated transient Ca(2+) current whose pharmac

297 In cac neurons, unexpectedly, voltage-activated transient K+ current I(A) is upregulat

298 -driven action potentials, because they lack voltage-activated transient Na(+) currents.

299 d and CF-EPSPs activate P/Q-type VGCCs, high-voltage activated VGKCs, and BK channels, leading to Ca(

300 at 23 A resolution, for a member of the low voltage-activated voltage-gated calcium channel family,