ライフサイエンスコーパス: potassium current

1 voltage-dependent contribution to ACh-evoked potassium current.

2 -dependent changes in slow delayed rectifier potassium current.

3 arybdotoxin-sensitive (BK) calcium-dependent potassium current.

4 fied potassium current and transient outward potassium current.

5 equired for generating the transient outward potassium current.

6 which leads to an increase in voltage-gated potassium current.

7 that is mediated by a slow calcium-activated potassium current.

8 hat are mediated by a slow calcium-activated potassium current.

9 ch dictated by a different calcium-dependent potassium current.

10 cardiac rapidly activating delayed rectifier potassium current.

11 id not influence the PMA-induced increase of potassium current.

12 A, neurons of the VTA by inducing an outward potassium current.

13 current and a decrease of transient outward potassium current.

14 s that underlie dendrotoxin-sensitive D-type potassium current.

15 xpressions and attenuated the peak of inward potassium current.

16 ontributions to the depolarization-activated potassium current.

17 east in part, by decreased Kv7.2/3 (KCNQ2/3) potassium currents.

18 d by an increase in the amplitude of several potassium currents.

19 type, due to different low-voltage-activated potassium currents.

20 ntrast, NRG1 had minor effects on whole-cell potassium currents.

21 nd the acquisition of mature inner hair cell potassium currents.

22 increased inactivation of voltage-activated potassium currents.

23 r6.2 (I(KATP)) and reducing inward rectifier potassium currents.

24 pe, delayed rectifier, and calcium-dependent potassium currents.

25 tivation include regulation of voltage-gated potassium currents.

26 cing calcium currents and increasing outward potassium currents.

27 nel gating kinetics of the calcium dependent potassium currents.

28 on as wild-type channels but fail to conduct potassium currents.

29 the fast-inactivating and calcium-activated potassium currents.

30 nce, depolarisation block, and low-threshold potassium currents.

31 slowly rising and falling calcium-dependent potassium currents.

32 DHPG also decreased potassium currents.

33 sion, increased degradation and smaller Kir3 potassium currents.

34 failed to alter holding or voltage-dependent potassium currents.

35 her mechanisms may also lead to reduction of potassium currents.

36 d by calcium-activated, cyclic AMP-sensitive potassium currents.

37 e) cause compensatory decreases in postspike potassium currents.

38 sociated with two distinct calcium-activated potassium currents.

39 bility by reducing BK-type calcium-activated potassium currents.

40 increasing sodium currents and reducing fast potassium currents.

41 n of a G protein-coupled inwardly rectifying potassium current, (2) inhibition of a voltage-gated Ca(

42 ory processing and that changes in levels of potassium currents across the nuclei, by mechanisms such

43 rane potential hyperpolarized due in part to potassium current activation.

44 d docking simulations we show that the novel potassium current activator, NS5806, binds at a hydropho

45 M-current is a slowly activating potassium current, active at subthreshold potentials.

46 The transient outward potassium current agonist NS5806 (5 muM) and the Ca(2+)-

47 rkably, daily antiphase cycles of sodium and potassium currents also drive mouse clock neuron rhythms

48 ting from reduction of the transient outward potassium current, alters properties of EC coupling.

49 associated with decreased transient outward potassium current and Kv4.2 and KChIP2 protein expressio

50 the Drosophila brain reveal that whole-cell potassium current and properties of single dSlo channels

51 ons express the fast delayed rectifier (FDR) potassium current and raise questions about the function

52 ation via normalization of transient outward potassium current and sarcoplasmic reticulum Ca(2+) cont

53 pposing effects: the rapid delayed rectifier potassium current and the L-type calcium current.

54 ion of a large conductance calcium-dependent potassium current and the opening of a transient outward

55 ns across models identified inward rectifier potassium current and the sodium-potassium pump as the t

56 ith blockade of ultrarapid delayed rectified potassium current and transient outward potassium curren

57 v4.2 is a major constituent of A-type (I(A)) potassium currents and a key regulator of neuronal membr

58 2.1 and SK, which underlie delayed rectifier potassium currents and afterhyperpolarization respective

59 are responsible for distinct types of native potassium currents and are associated with several human

60 alretinin cells (85%) exhibited large A-type potassium currents and delayed firing action potential d

61 cells that include inhibition of KIR and KV potassium currents and elevations of intracellular calci

62 used in cancer can prolong QT by inhibiting potassium currents and increasing late sodium current (I

63 toplasmic calcium activated Ca(2+) dependent potassium currents and led to neuronal apoptosis in KO h

64 heir stimulation inhibits M-type [Kv7, K(M)] potassium currents and N-type (Ca(V)2.2) calcium current

65 , enDUB treatment restored delayed rectifier potassium currents and normalized action potential durat

66 clofenac, dramatically enhanced KCNQ (K(v)7) potassium currents and suppressed L-type voltage-sensiti

67 In na mutants, expression of potassium currents and the key neuropeptide PDF are elev

68 o fourfold interanimal variability for three potassium currents and their mRNA expression.

69 and chronically inhibited delayed rectifier potassium current, and chronically enhanced late sodium

70 capacitance, reduced transient and sustained potassium currents, and altered voltage dependence and k

71 delayed firing discharge, large rapid A-type potassium currents, and central, radial or vertical cell

72 rrents, depressed the slow delayed rectifier potassium currents, and increased the resting membrane p

73 elayed repolarization from downregulation of potassium currents, and multiple reentry circuits during

74 POSH decreased potassium currents, and the inhibitory effect of POSH on

75 es in the leak, sodium and calcium-activated potassium currents are central to these two developmenta

76 ased in pathological situations where A-type potassium currents are decreased.

77 A-type potassium currents are important determinants of neurona

78 ons, we have now found that sodium-dependent potassium currents are increased several-fold in neurons

79 rom differential expression of voltage-gated potassium currents, as tufted cells exhibited faster act

80 dominant-negative reduction of the resulting potassium current at subthreshold membrane potentials.

81 rrent (I(M)), and may also underlie the slow potassium current at the node of Ranvier, I(Ks).

82 did not affect hERG/IKr or any other cardiac potassium current at therapeutic concentrations.

83 urve (2 voltage sensor mutations) decreasing potassium currents at the subthreshold level at which th

84 In addition to modulating sodium and potassium currents, beta subunits play nonconducting rol

85 e between inward sodium currents and outward potassium currents, but mechanisms establishing this cri

86 We observed large voltage-dependent potassium currents, but only a small chromanol sensitive

87 ly because of lack of inhibition of the I(A) potassium current by ERK.

88 gets, including the I(Ks) (slowly activating potassium current) channel.

89 y (HEK) 293 cells produced a noninactivating potassium current characteristic of M current.

90 GS and GLAST expressions and enhanced inward potassium currents compared with those in the COH rats w

91 dy, we show that IK(Na) , a sodium-activated potassium current, contributes a major portion of macros

92 igher amplitudes and faster kinetics of fast potassium currents correlated with this hyperexcitabilit

93 positive membrane potential, the ACh-evoked potassium current decayed exponentially over approximate

94 We observed reduced sodium and potassium current densities in ventricular myocytes, as

95 The balance between two particular potassium currents dictates how heart cells respond to p

96 Individual neurons with different levels of potassium currents differ in their ability to follow spe

97 ings are consistent with the hypothesis that potassium current downregulation leads to abnormal repol

98 esults from frequency-dependent reduction of potassium current during spike repolarization.

99 Inactivation of potassium currents during maintained firing results in a

100 e M-current, a low-threshold noninactivating potassium current, during seizures.

101 from OVX than OVX+E mice; blocking transient potassium currents eliminated this difference.

102 the G protein-activated inwardly-rectifying potassium current evoked by receptor-saturating concentr

103 ting the duration of the AP, the BK-mediated potassium current exerts control over the frequency of A

104 ll-cell coupling lead to regional changes in potassium current expression, which in this case facilit

105 Reduced inward potassium current following nerve ligation would increas

106 Noninactivating potassium current formed by KCNQ2 (Kv7.2) and KCNQ3 (Kv7

107 They are responsible for background leak potassium currents found in many cell types.

108 patch-clamp techniques, recordings of either potassium current from rat posterior taste receptor cell

109 contact sites and has been shown to regulate potassium current gating kinetics as well as channel tra

110 The M-current is a low voltage-activated potassium current generated by neuronal Kv7 channels.

111 non-inactivating low-threshold voltage-gated potassium current generated by the M-channel.

112 Potassium currents generated by voltage-gated potassium

113 Although several potassium currents have been reported to play a role in

114 , we evaluated whether the transient outward potassium current I(A) is expressed in PVN-RVLM neurones

115 often caused by direct block of the cardiac potassium current I(Kr)/hERG, which is crucial for termi

116 ed most often by direct block of the cardiac potassium current I(Kr)/hERG.

117 Apamin sensitive potassium current (I KAS), carried by the type 2 small c

118 A-type potassium current (I(A)) both activates and inactivates

119 med to address whether the transient outward potassium current (I(A)) in identified rostral ventrolat

120 hat DA could immediately alter the transient potassium current (I(A)) of identified neurons in the st

121 dine and 0.5 mM Ba2+, consistent with A-type potassium current (I(A)).

122 n activated current (I(h)) and the transient potassium current (I(A)).

123 n the time course of acetylcholine-activated potassium current (I(K)(ACh)) activation and deactivatio

124 a(2+) current (I(CaL)) and delayed rectifier potassium current (I(K)) in guinea pig SAN pacemaker cel

125 (I(Na)) and 4AP-sensitive and TEA-resistant potassium current (I(K)).

126 a)) and to suppress a delayed rectifier-like potassium current (I(K)).

127 ynaptic integration: a low-voltage-activated potassium current (I(K-LVA)) and a hyperpolarization-act

128 n important role for the inwardly rectifying potassium current (I(K1)) in controlling the dynamics of

129 rrent mechanisms are the inwardly rectifying potassium current (I(K1)), which is important for mainte

130 ductance differences in the inward rectifier potassium current (I(K1)).

131 ally depended on the expression of an A-type potassium current (I(KA)), which when active attenuated

132 of the rapidly activating delayed rectifier potassium current (I(Kr)) important for repolarization o

133 cts the rapidly activating delayed rectifier potassium current (I(Kr)) in the heart.

134 hrough the blocking of the delayed rectifier potassium current (I(Kr)).

135 es an increase of the slow delayed rectifier potassium current (I(Ks)).

136 Kv1.5 mediates the ultrarapid potassium current (I(Kur)) that controls atrial action p

137 nnels contributing to the ultrarapid outward potassium current (I(Kur)).

138 pression would predict different patterns of potassium current (I(Kv)) regulation.

139 maturing VGNs also acquire low-voltage-gated potassium currents (I (KL)), whose inhibitory influence

140 rrelated to the density of low-voltage-gated potassium currents (I (KL)).

141 sed the inward and delayed outward rectifier potassium currents (I IRK and I DRK), calcium (Ca2+) rel

142 neurons, the amplitude of rapid inactivating potassium currents (I(A)) was significantly increased at

143 ge-dependent activation of voltage-sensitive potassium currents (I(K)).

144 treatment with blockers of calcium-activated potassium currents (I(KCa)) reproduced this shift and bl

145 t a novel coupled system of sodium-activated potassium currents (I(KNa)) and persistent sodium curren

146 that contribute to cardiac transient outward potassium currents (I(to)).

147 sing cultured DRG neurons, that of the total potassium current, I(K), the K(Na) current is predominan

148 the rapid delayed rectifier potassium current, I(Kr), which flows through the human

149 pid compensatory interaction among a pair of potassium currents, I(A) and I(KCa), that stabilizes bot

150 ltage-clamp experiments, 2-AG reduced A-type potassium current (IA) through a cannabinoid receptor-in

151 GxTX-1E also reduced A-type potassium current (IA), but much more weakly.

152 by the opposing actions of the fast outward potassium current, IA , mediated by alpha subunits of th

153 system underlying the ultra-rapid rectifying potassium current (Ik(ur)), a major repolarizing current

154 solated CB preparation and decreased outward potassium current (Ik) in CB glomus cells to levels simi

155 pendent, time-independent rectifying outward potassium current (IK).

156 In each neuron, voltage-dependent potassium currents (IK) were evaluated and, in represent

157 We report that a sodium-activated potassium current, IK(Na) , has been inadvertently overl

158 lum Ca2+ concentrations, inwardly rectifying potassium current (IK1) density, and gap junction conduc

159 ssium current (IKr) and the inward rectifier potassium current (IK1) were also downregulated (P<0.05)

160 Delayed excitation, caused by A-type potassium current (IKA), was observed in most of NTS neu

161 armacological tools, acetylcholine-regulated potassium current (IKACh) with patch clamp recording, me

162 paper unveils the critical role of the brake potassium current IKD in damage-triggered cold allodynia

163 utational modeling, that a low-voltage-gated potassium current, IKLT, underlies the resonance.

164 nt with rapid inactivation and low-threshold potassium current, IKLT.

165 he rapid components of the delayed rectifier potassium current (IKr) and the inward rectifier potassi

166 Drugs are screened for delayed rectifier potassium current (IKr) blockade to predict long QT synd

167 ition of the cardiac rapid delayed rectifier potassium current (IKr).

168 and KCNE1 protein coassembly forms the slow potassium current IKS that repolarizes the cardiac actio

169 KCNE1, Kv7.1 conducts the slowly activating potassium current IKs, which is one of the major current

170 Effects on the slow delayed rectifier potassium current (IKs) are less recognized.

171 ate the slowly activating, voltage-dependent potassium current (IKs) in the heart that controls the r

172 The slow delayed rectifier potassium current (IKs) is a key repolarizing current du

173 tion, which increases slow-delayed rectifier potassium current (IKs).

174 l, IKr, and the adrenergic-sensitive cardiac potassium current, IKs, are two primary contributors to

175 potassium channel and its associated cardiac potassium current, IKur.

176 that SNX-482 dramatically reduced the A-type potassium current in acutely dissociated dopamine neuron

177 ac arrhythmias that can arise from increased potassium current in cardiomyocytes.

178 res based on the properties of the transient potassium current in cells from OVX or OVX+E mice were c

179 Dysfunction of the fast-inactivating Kv3.4 potassium current in dorsal root ganglion (DRG) neurons

180 Moreover, POSH still decreased the potassium current in oocytes injected with a ROMK1 mutan

181 (rs1805128), known to modulate an important potassium current in the heart, predicted diLQTS with an

182 esemble rapidly activating delayed rectifier potassium current in the human heart, are blocked by fen

183 Estradiol reduced both potassium current in the membrane potential range typica

184 nd TREK-2 provide the predominant background potassium current in the primary sensory neurons of the

185 The largest outward potassium current in the soma of neocortical pyramidal n

186 tamine produced a dose-dependent increase in potassium currents in a subset of bipolar cells.

187 n resulted in lack of time-dependent outward potassium currents in guard cells, higher rates of water

188 n previously shown to modulate voltage-gated potassium currents in heterologous expression systems.

189 results indicated that the voltage dependent potassium currents in hippocampal neurons were different

190 ion potential waveforms, and reduced outward potassium currents in isolated cardiac myocytes.

191 ression of CD63 had no significant effect on potassium currents in oocytes injected with ROMK1; howev

192 strated MYOCD-induced, iberiotoxin-sensitive potassium currents in porcine coronary SMCs.

193 d by reductions in BK-type calcium-activated potassium currents in spontaneously firing neurons, is e

194 e data support two highly novel conclusions: potassium currents in taste receptor cells are significa

195 we investigated Kv3.1b immunoreactivity and potassium currents in the auditory brainstem sound local

196 Leak potassium currents in the nervous system are often carri

197 By enhancing potassium currents in the ON bipolar cells, histamine is

198 H at 5 microM increased the amplitude of the potassium currents in the ON bipolar cells.

199 el mechanism for regulation of voltage-gated potassium currents in the setting of cardiac pathology a

200 NTS: Kv2 channels underlie delayed-rectifier potassium currents in various neurons, although their ph

201 Kv2 channels underlie delayed-rectifier potassium currents in various neurons, although their ph

202 ) was employed to block Kv3-mediated outward potassium currents in voltage- and current clamp experim

203 al evidence that the mutant protein disrupts potassium current inactivation, strongly supports KCND2

204 In voltage clamp mode, the sodium and potassium currents increased significantly at higher [Na

205 regulated Kcna2, reduced total voltage-gated potassium current, increased excitability in DRG neurons

206 neurons in the locus ceruleus to measure the potassium current induced by morphine.

207 the first explanation for how this increased potassium current induces hyperexcitability, which could

208 ctions) does not affect the extent of M-type potassium current inhibition produced by either receptor

209 at, at the cellular level, delayed-rectifier potassium current is a main contributor of KECG correlat

210 evidence that opposite regulation of A-type potassium current is an important factor in this bidirec

211 er, a mutation that impairs Shaker-dependent potassium current, is an allele of sleepless.

212 bunit in somatodendritic subthreshold A-type potassium current (ISA) channels.

213 gnificant reduction of the transient outward potassium current (Ito) in EPI but not in endocardial (E

214 The fast transient outward potassium current (Ito,f) plays a critical role in the e

215 revealed downregulation of transient outward potassium current (Ito; P<0.05).

216 tagonized by activators of the ATP-sensitive potassium current (K(ATP)).

217 h inhibition of a tonic, inwardly rectifying potassium current (K(IR) ).

218 the supernormal phase results from a reduced potassium current Kdr as a result of accumulation of per

219 genes (hERG), which encode two repolarizing potassium currents known as I(Ks) and I(Kr).

220 Thus, a potassium current, likely mediated through BK channels,

221 n in rat neurons depresses delayed rectifier potassium currents, limits the magnitude of the K+ curre

222 ctive" mutations affecting calcium-dependent potassium currents localized to the C-domain of CaM.

223 BA(A) current and an intrinsic membrane slow potassium current (M-current).

224 ng by suppression of a low voltage-activated potassium current, M-current.

225 Thus, the sodium-activated potassium current may serve to moderate blood pressure i

226 hrough G-protein coupled inwardly rectifying potassium currents mediated by delta and mu opioid recep

227 e rat hippocampal slices we show that D-type potassium current modulates the size of the ADP and the

228 tside-out recordings of dendritic sodium and potassium currents, morphological reconstructions and mu

229 y consistent reductions in voltage-activated potassium currents near the action potential threshold a

230 lective, as NS5A1a does not depress neuronal potassium currents nor inhibit Src phosphorylation of Kv

231 led that the isoflurane-activated background potassium current observed in cortical pyramidal neurons

232 ion was mediated by activation of an outward potassium current or blockade of a tonically active inwa

233 tes, the slowly activating delayed rectifier potassium current, or IKs, is believed to be a heteromul

234 e two calcium channels and acting on the two potassium currents, or with differences in channel gatin

235 ation of the MOR and reduced activation of a potassium current over the same time course.

236 CHO-K1 cells line produces highly selective potassium current, overexpression of R162W mutant Kir7.1

237 In the evening, basal potassium currents peak to silence clock neurons.

238 tassium current, the acetylcholine activated potassium current, peak sodium current, and L-type calci

239 le (CG) cells and many other neurons, A-type potassium currents play an important role in regulating

240 the major cause of ischemic cell death, and potassium currents play important roles in regulating th

241 Neuron models that included a low-threshold potassium current present in a subset of CM neurons show

242 Importantly, A-type potassium currents recorded in mesoaccumbal neurons disp

243 t reduction, but the contribution to overall potassium current reduction was almost always much small

244 KS) (slow component of the delayed rectifier potassium current) remained intact.

245 ng value, mediated by an inwardly rectifying potassium current, resulting in reduced neuronal excitab

246 age dependence of acetylcholine (ACh)-evoked potassium currents reveal a more complex relationship be

247 pression of KCNQ1-S140G with KCNE1 generated potassium currents (S140G-IKs) that exhibited greater se

248 -calcium exchanger activity, reduced outward potassium currents, sarcoplasmic reticulum Ca2+ defects,

249 ation of ALD increased outward voltage-gated potassium currents significantly, and simultaneously upr

250 ese is an apamin-sensitive calcium-dependent potassium current (SK).

251 nvolving small conductance calcium-dependent potassium currents (SK).

252 n of the small conductance calcium-activated potassium current, SK.

253 idal neurones we studied the modulation of a potassium current (slow AHP current, I(sAHP)) known to b

254 nce of calcium current and calcium-activated potassium current such that their net influence shifted

255 lasma membrane where their voltage-dependent potassium currents suppress neuronal excitability.

256 ent is a slowly activating, non-inactivating potassium current that has been shown to be present in n

257 , there was a component of calcium-dependent potassium current that showed frequency-dependent reduct

258 Since Hodgkin and Huxley discovered the potassium current that underlies the falling phase of ac

259 These channels produce background leak type potassium currents that act to regulate resting membrane

260 ype specific with the involvement of altered potassium currents that allow for a sustained, continued

261 also evokes non-synaptic activity-dependent potassium currents that are amplified by gap junction-me

262 licited increases of the inwardly rectifying potassium currents that could be blocked by the GABA(B)

263 fier potassium current, the inward rectifier potassium current, the acetylcholine activated potassium

264 ent, the slowly activating delayed-rectifier potassium current, the inward rectifier potassium curren

265 ing the rapidly activating delayed-rectifier potassium current, the slowly activating delayed-rectifi

266 Expression of one important potassium current, the transient outward current (I(to))

267 ny medications inadvertently block the KCNH2 potassium current, these novel findings seem to have cli

268 The ability of crotamine to inhibit the potassium current through K(V) channels unravels it as t

269 Potassium currents through SK channels demonstrate inwar

270 channel 3, where SP enhances M-channel-like potassium currents through the NK1 receptor in a G prote

271 A-type and delayed-rectifier (DR) potassium currents, two putative transcriptional targets

272 fort, a molecular-level understanding of the potassium current underlying the slow afterhyperpolariza

273 Little is known about the voltage-dependent potassium currents underlying spike repolarization in mi

274 selectively coupled to the calcium-dependent potassium currents underlying the AHPs, thereby creating

275 molecular correlate of the transient outward potassium current up-regulated by Abeta peptide, conside

276 specifically enhances an inwardly rectifying potassium current via NPY-Y1 receptors.

277 naptic efficacy, inhibiting postsynaptic Kv3 potassium currents (via phosphorylation), reducing EPSCs

278 Reduction of potassium current was also seen with multimeric G85R SOD

279 Although this potassium current was described two decades ago, the mec

280 dent reduction of overall spike-repolarizing potassium current was identified as Kv3 current by its s

281 The potassium current was inhibited by 4-AP and by Heteropod

282 ion of G protein-coupled inwardly rectifying potassium current was measured using whole-cell voltage-

283 The effect of cross-linked 300 kDa on potassium current was reduced by removing Na(+) from the

284 tivation kinetics of D(2) receptor-dependent potassium current was studied using outside-out patch re

285 ution of afferent neuronal voltage-dependent potassium currents was a prominent feature of urethral a

286 Further supporting the involvement of potassium currents, we observed an overexpression of KCN

287 Whole-cell recordings of potassium currents were made from bipolar cells in slice

288 The major potassium currents were not different in LDLr(-/-) and A

289 Potassium currents were recorded using 2-microelectrode

290 In 10 mM TEA, potassium currents were reduced in all the bipolar cells

291 In contrast, outward potassium currents were significantly reduced by microin

292 ntrast, depolarization-activated calcium and potassium currents were unaffected, thus supporting the

293 his current matched that of the native Slack potassium current, which was identified using an siRNA a

294 with specific ionic currents, such as A-type potassium currents, which can linearize the frequency-in

295 ity may be limited by the presence of A-type potassium currents, which limit the effectiveness of the

296 d of SK (small-conductance calcium-activated potassium) currents, which were essential for a wide lin

297 KCNQ channels might also contribute to this potassium current whose molecular identity is unknown.

298 ive rise to the M-current, a noninactivating potassium current with slow kinetics.

299 mulation, which regulate cardiac calcium and potassium currents with differential kinetics.

300 ffect of POSH on ROMK1 channels, we measured potassium currents with electrophysiological methods in