ライフサイエンスコーパス: calcium current

1 sult in an overall reduction in the P/Q-type calcium current.

2 n of the nifedipine-sensitive, voltage-gated calcium current.

3 ntial for its inhibition of the Cav3.1 (LVA) calcium current.

4 cine response reduced high voltage-activated calcium current.

5 negative modulator of low voltage activated calcium current.

6 subunit modulation of low voltage activated calcium current.

7 t hairpin RNA partially inhibited the L-type calcium current.

8 C with only a small contribution from L-type calcium current.

9 ading to potassium efflux that increases the calcium current.

10 f the high-threshold voltage-activated (HVA) calcium current.

11 with no significant AON effect on the L-type calcium current.

12 o calcium-induced inactivation of the L-type calcium current.

13 and mimicked inhibition of the voltage-gated calcium current.

14 higher than those found to affect the L-type calcium current.

15 be entirely due to inhibition of the L-type calcium current.

16 n that DLAMOs depend on post-synaptic L-type calcium current.

17 oride-sensitive portion of the transient LVA calcium current.

18 bbons had larger global and ribbon-localized calcium currents.

19 of CaV2.2, alpha2delta-1 and the associated calcium currents.

20 and a poorly understood increase of cardiac calcium currents.

21 levate neuronal low-voltage-activated T-type calcium currents.

22 Arsenic may act on QT by increasing cardiac calcium currents.

23 GCs demonstrated that (+)-SKF10047 inhibited calcium currents.

24 synaptic action potential or the presynaptic calcium currents.

25 polarity development that is driven by polar calcium currents.

26 ynaptic cleft pH that modulate photoreceptor calcium currents.

27 for the first time-by an increase in cardiac calcium currents.

28 hERG) trafficking and an increase of cardiac calcium currents.

29 terval, compared with the h-current (Ih) and calcium currents.

30 activating GIRK conductances and depressing calcium currents.

31 bitory effect of adenosine on nerve terminal calcium currents.

32 g requirement for induction of intracellular calcium currents.

33 resulting in maintained depolarizing L-type calcium currents.

34 motif in Rem2 did not affect suppression of calcium currents.

35 but unlike CaV1.1a it also conducts sizable calcium currents.

36 e voltages the onset and trough (maximum) of calcium currents.

37 itive pacemakers depend on the activation of calcium currents.

38 perfusion of roscovitine failed to modulate calcium currents.

39 L-type and the low voltage-activated T-type calcium currents.

40 in part mediated by L- and P- but not T-type calcium currents.

41 the effect of changing pH on isolated T-type calcium currents.

42 v1.2, they lack detectable voltage-dependent calcium currents.

43 abidiol, also failed to induce inhibition of calcium currents.

44 ffect adrenergic regulation of voltage-gated calcium currents.

45 activity and activation of L-type and Q-type calcium currents.

46 ha and PKCbeta do not facilitate presynaptic calcium currents.

47 ich were correlated to the voltage-activated calcium currents.

48 M)] potassium currents and N-type (Ca(V)2.2) calcium currents.

49 TIM2-induced CRAC (calcium release-activated calcium) currents.

50 lack functional flagellar alkaline-activated calcium currents, 50 microM thimerosal raised the flagel

51 It is suggested that increased calcium currents accompany calcium inflow in glomus cell

52 Calcium currents across the plasma membrane of plant cel

53 calcium stores and modulation of the L-type calcium current activity.

54 ng the shoulder, with high voltage-activated calcium current also contributing significantly (39%).

55 red neurite outgrowth, neuronal survival and calcium current amplitude and subtype distribution to th

56 with a decrease of the voltage-gated L-type calcium current amplitude.

57 evels are kept low by PTEN and do not affect calcium current amplitudes.

58 e was upregulation of both T-type and P-type calcium current and a change in the balance of calcium c

59 gation was mediated by an increase of L-type calcium current and a decrease of transient outward pota

60 lcium current and a change in the balance of calcium current and calcium-activated potassium current

61 Here we have studied the regulation of calcium current and cell contraction of cardiomyocytes i

62 teepened APD restitution by increased L-type calcium current and decreased activation latency via enh

63 nt potassium channels (K(Ca)) by the smaller calcium current and in vitro can be pharmacologically re

64 In silico, L-type calcium current and Na(+)/Ca(2+) exchanger current deter

65 We propose that an increase in cardiac calcium current and reduced trafficking of hERG channels

66 hannel accessory beta-subunit would modulate calcium current and suppress cardiac hypertrophy.

67 d that drugs that suppress the low-threshold calcium current and the hyperpolarization-activated cati

68 that controls the inward/depolarizing L-type calcium current and the inactivation gate that controls

69 xpressed voltage-gated sodium, potassium and calcium currents and calcium-dependent potassium current

70 Calcium currents and exocytosis (measured as membrane ca

71 alpha2delta2 protein is necessary for normal calcium currents and exocytosis in inner hair cells.

72 ric dilator (PD) neuron, in part by reducing calcium currents and increasing outward potassium curren

73 e important modulatory subunits that enhance calcium currents and may also have other roles in synapt

74 By measuring calcium currents and membrane capacitance during depolar

75 allow simultaneous recording of presynaptic calcium currents and postsynaptic responses.

76 term exposure to As(2)O(3) increases cardiac calcium currents and reduces surface expression of the c

77 nd a mixture of calcium channel blockers for calcium currents) and ionic substitution (TTX-resistant

78 ium current, peak sodium current, and L-type calcium current, and exhibits antiadrenergic effects.

79 ctifying K+ channel) current, and attenuated calcium current, and indirectly by reducing excitatory s

80 tifying K(+) channel current, and attenuated calcium current, and indirectly through reducing excitat

81 result of reduced calcium release activated calcium currents, and independently of potassium channel

82 activation of a GIRK current, depression of calcium currents, and indirectly through increased inhib

83 ted cation currents and low threshold T-type calcium currents, and tonic- or initial bursting firing

84 scular KCNQ5 currents, suppression of L-type calcium currents, and vasodilation.

85 he delayed rectifier current, and the L-type calcium current are modified to represent human data at

86 : Several studies suggest that voltage-gated calcium currents are involved in generating high frequen

87 No calcium currents are recorded from human embryonic kidne

88 Thus, calcium currents are selectively coupled to the calcium-

89 , we find that both N-type and DHP-sensitive calcium currents are sensitive to this toxin.

90 Ca(v)3), but the commonly held view that LVA calcium currents are usually mediated by Ca(v)3 rather t

91 rologous expression of Rem2 nearly abolished calcium currents arising from preexisting high-voltage-a

92 s in control conditions that elicit the same calcium current as in EPA also activate the same level o

93 rvical ganglion and inhibition of the native calcium currents as an assay for receptor activation, a

94 Analysis of calcium currents associated with the AP waveform indicat

95 Maximal increases in calcium current at nearly saturating concentrations of i

96 s not contribute to regulation of whole-cell calcium currents at basal calcium levels.

97 of adenosine is associated with decreases in calcium currents at mouse motor nerve endings.

98 ased delayed rectifier K+ current and L-type calcium current but decreased the transient outward K+ c

99 on GPR18-expressing neurons did not inhibit calcium currents but instead potentiated currents in a v

100 s in BDNF mutant VMH neurons revealed normal calcium currents but reduced frequency of EPSCs.

101 to 10 Torr, also increased the amplitude of calcium currents, but shifted to more positive voltages

102 ivated cation current (I(h)) or blocking all calcium current by Mg(2+) replacement of Ca(2+).

103 ovel pharmacological inhibitor of the Cav3.1 calcium current by performing whole-cell electrophysiolo

104 on of hERG-chaperone complexes and increases calcium currents by a faster cellular process.

105 f the SNARE complex, such that modulation of calcium currents by a G-protein coupled receptor cannot

106 (syntaxin or SNAP-25) prevents modulation of calcium currents by A(1) adenosine receptors at mammalia

107 ersibly reduced the voltage-gated sodium and calcium currents by approximately one third of their pea

108 GBP produces a chronic inhibitory effect on calcium currents by causing a reduction in the total num

109 nsitive potassium (K(ATP)) and inhibition of calcium currents by galanin were disrupted by anti-G(o)2

110 The potentiation of tail calcium currents caused by roscovitine and by the L-chan

111 Large L-type calcium current conductance is responsible for RA disapp

112 e sympathetic nervous system increase L-type calcium currents conducted by Ca(V)1.2a channels in the

113 L-type calcium currents conducted by CaV1.2 channels initiate e

114 ycine 12 to valine) markedly increased basal calcium current density by 41 % compared with control ce

115 downstream effectors), significantly reduced calcium current density by 47 %.

116 ming subunit of L-type channels and augments calcium current density by facilitating channel opening

117 ed delivery of Gem markedly decreased L-type calcium current density in ventricular myocytes, resulti

118 Calcium current density was significantly increased in d

119 ooligomerization significantly increases the calcium current density, while heterooligomerization may

120 t to modulate low voltage activated (Cav3.1) calcium current density.

121 Inhibition of this calcium current directly or indirectly involves calmodul

122 Calcium current during the interspike interval was, on a

123 Inward calcium currents elicited by voltage ramps (0.24 V/s) or

124 rane anchoring of alpha(2)delta subunits for calcium current enhancement.

125 The cardiac-specific L-type calcium current enhancer Bay Y5959 prevented initiation

126 NE and clonidine decreased calcium currents evoked by depolarizing voltage steps.

127 In order to examine the robustness of L-type calcium current expression, the response to changes in C

128 h may reflect an indirect effect of abnormal calcium current fluxes during development.

129 on of roscovitine markedly enhanced the tail calcium current following repolarization from depolarize

130 ium channels (CaV) enable the inward flow of calcium currents for a wide range of cells.

131 We propose that the increase in calcium currents from -3.2 +/- 0.3 to -5.1 +/- 0.3 pA/pF

132 ntrations of 0.3 microM PAT increase cardiac calcium currents from -4.8 +/- 0.7 to -7.3 +/- 0.5 pA/pF

133 -sensitive sodium current, P-type and T-type calcium current, hyperpolarization-activated cation curr

134 urrent I(h), low-threshold voltage-activated calcium current I(t), and activity at rest.

135 m S218L KI mice showed a strong shift of the calcium current I-V curve to more negative potentials, l

136 rs and computational modeling show that both calcium currents I(Ca) and the hyperpolarization-activat

137 Crude oil exposure also decreased calcium current (I(Ca)) and calcium cycling, which disru

138 We have tested the alterations of L-type calcium current (I(Ca)) and cardiac function in CaMKIIde

139 Both calcium current (I(Ca)) and DeltaC(m) were reversibly bl

140 Block of calcium current (I(Ca)) and rapid component of the delay

141 ation of events was due to increased trigger calcium current (I(Ca)) as well the enhanced ability of

142 p studies revealed that ISO increases L-type calcium current (I(Ca)) faster than I(Ks) (time constant

143 acitance (DeltaC(m)) as a function of inward calcium current (I(Ca)) follows the linear relationship

144 dependence on membrane potential (V(m)) and calcium current (I(Ca)) of calcium-induced calcium relea

145 m HCs to cones involves small changes in the calcium current (I(Ca)) that do not always generate dete

146 The L-type calcium current (I(Ca)), however, was larger in LDLr(-/-

147 vated (LVA) and high-voltage-activated (HVA) calcium current (I(Ca)).

148 ig heart cells dramatically depresses L-type calcium current (I(Ca,L)) ( approximately 90% inhibition

149 n cardiomyocytes dramatically blocked L-type calcium current (I(Ca,L)) and inhibited Ca(2+)-induced C

150 on (AF) is characterized by decreased L-type calcium current (I(Ca,L)) in atrial myocytes and decreas

151 The L-type calcium current (I(Ca,L)) is another determinant of acti

152 xpression of Cav-3 inhibited the peak T-type calcium current (I(Ca,T)) and adenovirus (AdCa(v)3.2)-me

153 rs (beta-ARs), which leads to an increase in calcium current (I(Ca-L)) density through cardiac Ca(v)1

154 L-type calcium current (I(Ca-L)) density was greater in beta2a-

155 calcium entry and calcium release-activated calcium current (I(crac)) in lacrimal acinar cells, rat

156 Na+ current (I(NaP)), low-voltage-activated calcium current (I(L/T)) mediated by T- and/or L-type Ca

157 n of Ca(v)3.1 channels conducting the T-type calcium current (I(T)) contributed to I(tail), but ethan

158 The low-threshold transient calcium current (I(T)) plays a critical role in modulati

159 opyridine were applied to inhibit the L-type calcium current (I:(Ca)) and the transient outward curre

160 LTCCs, and subsequent increases in GABAergic calcium currents (I(Ca(2+))) that can be reversed by rei

161 mu-Opioid agonists have no effect on calcium currents (I(Ca)) in neurohypophysial terminals w

162 native properties of unitary cardiac L-type calcium currents (i(Ca)) measured with physiological cal

163 by monitoring mGluR8a-mediated inhibition of calcium currents (I(Ca)) using whole-cell voltage-clamp

164 inase A (PKA)-mediated enhancement of L-type calcium currents (I(Ca,L)) is essential for sympathetic

165 agonist carbachol (CCh) on the basal L-type calcium current, I(Ca,L), in ferret right ventricular (R

166 tial, input resistance, or the low-threshold calcium current, I(T).

167 dependence and increase in amplitude of the calcium current (ICa) in cones that is induced by change

168 from a shift in activation of voltage-gated calcium currents (ICa) to more negative potentials.

169 MPR is sensitive to blockers of H- (IH) and calcium-currents (ICa).

170 ther, we investigated the role of the L-type calcium current, ICa-L, in the restitution portrait.

171 ltage-activated potassium currents (IK+) and calcium currents (ICa2+).

172 DCK/VLO neurons revealed that low threshold calcium currents, Ih currents, and subthreshold oscillat

173 subunits alter high-voltage-activated (HVA) calcium currents, impair neurotransmitter release, and s

174 ubunit modulates low voltage-activated (LVA) calcium current in both human embryonic kidney (HEK) cel

175 ABAergic pathway that directly modulates the calcium current in cones.

176 uscle cells, but had no effect on the T-type calcium current in either type of dissociated heart musc

177 represent a minor fraction of the whole-cell calcium current in most neurons.

178 lock of conduction caused by enhanced L-type calcium current in reentrant circuits may result from a

179 Additionally, recordings of calcium current in response to a command waveform based

180 al adhesion proteins in regulation of L-type calcium current in single vascular myocytes.

181 d an increase in the amplitude of the L-type calcium current in the type II heart muscle cells, but h

182 put of about two-thirds of bipolar cells and calcium current in two-thirds of ganglion cells are sens

183 fic activator of cdk5, roscovitine regulated calcium currents in a manner similar to that observed in

184 ents and suppressed L-type voltage-sensitive calcium currents in A7r5 rat aortic smooth muscle cells

185 decreased the amplitude of voltage-dependent calcium currents in almost all tested neurons.

186 tu patch clamp recordings of somatodendritic calcium currents in an identified adult Drosophila moton

187 rs, including Akt, on sodium, potassium, and calcium currents in cardiac myocytes.

188 hat baclofen inhibits high-voltage-activated calcium currents in granule cells.

189 ransmission in vivo and potentiated synaptic calcium currents in isolated bipolar cells.

190 in significantly increased voltage-activated calcium currents in isolated single DMNV neurones from a

191 th an increase in steady-state voltage-gated calcium currents in LH neurons and a CB1R-mediated depol

192 ndeed, uncleaved alpha2delta inhibits native calcium currents in mammalian neurons.

193 attenuation of the MCH-induced inhibition of calcium currents in most neurons.

194 induced by 100% N(2) significantly increased calcium currents in normal bathing solutions and during

195 sed to analyze the effect of (+)-SKF10047 on calcium currents in primary RGCs.

196 It is generally accepted that to generate calcium currents in response to depolarization, Ca(v)1.2

197 Depolarizing steps evoked sustained calcium currents in rods and cones that in turn produced

198 chronic ethanol self-administration reduces calcium currents in thalamic relay cells without alterin

199 oked by current injection at the soma causes calcium currents in the apical shaft whose amplitudes de

200 ion of the free PUFAs to modulate sodium and calcium currents in the myocytes.

201 Calcium currents in the photoreceptors were observed to

202 leted layer VI neurons was unaltered, T-type calcium currents in the postsynaptic thalamic relay and

203 mca1A, underlies HVA and LVA somatodendritic calcium currents in the same neuron.

204 osphatase PTEN by As(2)O(3) enhances cardiac calcium currents in the therapeutic concentration range

205 granule cells (CGCs) and modulates P/Q-type calcium currents in tsA201 cells and CaV2.1 surface expr

206 f gamma(6) on LVA and high voltage-activated calcium currents in vivo.

207 hat Dmca1A underlies the HVA somatodendritic calcium currents in vivo.

208 Xu and Wu show that, under some conditions, calcium current inactivation explains stimulus-dependent

209 tial, decreasing input resistance and inward calcium currents, increasing G-protein-gated inwardly re

210 a pig ventricular myocytes, PIP(3) regulates calcium currents independently of the protein kinase Akt

211 CaV1.2DeltaDCT neurons have reduced L-type calcium current, indicating that the distal C-terminal d

212 ctivate receptors, did not tonically inhibit calcium currents, indicating a lack of GPR18 activation

213 Calcium current inhibition after short-term exposure to

214 ependent facilitation (CDF) of voltage-gated calcium current is a powerful mechanism for up-regulatio

215 For instance, an increase in L-type calcium current is FRD when this is accompanied by indir

216 Indeed, the L-type calcium current is larger in the soma of dopamine neuron

217 No change in voltage-dependent calcium current is observed, suggesting that the decreas

218 Voltage-dependent calcium current is small at all subthreshold voltages.

219 The attenuation of calcium currents is consistent with an inhibitory action

220 ential and the availability of the transient calcium current IT, a hallmark of thalamic excitability.

221 ly of ion channels, and the transient inward calcium current, IT .

222 functional scaling is achieved by different calcium current kinetics that compensate for the smaller

223 The contributions of T- and P/Q-type calcium current, large (BK) and small (SK) conductance c

224 rest of voltage-dependent transient (T-type) calcium currents [low-threshold spike (LTS)].

225 NPY attenuated voltage-dependent calcium currents mainly via a Y1 receptor subtype.

226 An increase in L-type calcium current may improve conduction of premature impu

227 esults demonstrate novel mechanisms by which calcium currents may control the electrophysiological pr

228 ysiological or pharmacological modulation of calcium currents may have a greater impact in CaV1.1e ex

229 to normal sleep patterns is a low-threshold calcium current mediated by T-type calcium channels.

230 ly described a model of plasticity that uses calcium currents mediated by N-methyl-D-aspartate recept

231 pression of VGCCs and enhanced voltage-gated calcium currents, mitochondrial dysfunction and cell dea

232 ent reversed the decrease in mGluR1-mediated calcium current modulation associated with Homer 2b expr

233 otein Rab3A greatly enhances the efficacy of calcium current modulation.

234 alpha(q/11)-coupled receptor, resulted in VI calcium current modulation.

235 y near threshold, and high voltage-activated calcium currents much less (approximately 2%).

236 armacological differences were found between calcium currents obtained from high- and low-frequency c

237 Reducing the presynaptic calcium current or buffering the intracellular calcium w

238 y, presynaptic afterpotentials did not alter calcium current or neurotransmitter release.

239 These mutations predict reduced calcium currents, particularly in cerebellar Purkinje ce

240 s compacta (SNc) neurons, where subthreshold calcium current plays a dominant role.

241 However, peak calcium current plays a role only at small values of BCL

242 Thus, calcium current plays only a minor role in pacemaking of

243 voltage-dependent calcium channels influence calcium current properties and may be involved in other

244 Calcium currents, recorded simultaneously with the trans

245 of myoblasts were impaired while the L-type calcium current remained unaffected.

246 pport repetitive spiking is due to unopposed calcium currents resulting from a reduction in large-con

247 nd that in the majority of cells blockade of calcium currents results in avid high-frequency bursting

248 sly implicated in DM1, regulating sodium and calcium currents, Scn5a, Junctin, Junctate, Atp2a1, Atp1

249 g sodium currents sensitive to tetrodotoxin, calcium currents sensitive to nifedipine and omega-conot

250 Upon removal of ghrelin, calcium currents slowly returned to baseline.

251 nt substitution in CaV1.1a had abolished the calcium currents, substitution of the II-III loop in CaV

252 anges exceeded depression of the presynaptic calcium current, suggesting that it is primarily caused

253 experiments, MCH depressed the amplitude of calcium currents, suggesting that a mechanism of inhibit

254 comitant increase in the amplitude of T-type calcium currents (T-currents) in neurons of the nucleus

255 Blocking calcium currents terminated firing by preventing repolar

256 implicated in the facilitation of an inward calcium current that could enhance release.

257 inal cone horizontal cells contain an L-type calcium current that has been proposed to be involved in

258 enosine caused a prominent inhibition of the calcium current that was totally blocked by pretreatment

259 a(2a) produced holding potential-independent calcium currents that closely mimicked native non-inacti

260 In contrast to neuronal N-type calcium currents that inactivate during long depolarizat

261 m channel, Ca(V)2.1, which conducts P/Q-type calcium currents that initiate neurotransmitter release.

262 ndogenous alpha(1S)), alpha(1S)-scr restored calcium currents that were indistinguishable, in current

263 t to account for the observed attenuation in calcium current; the remaining gating current was no dif

264 HEK cells lack calcium currents, thereby circumventing the need for pha

265 cardiac plasma membrane, and thus the inward calcium current, through a complex pathway involving red

266 ization-activated cation current (I(h)), and calcium current to pacemaking by using the cell's own fi

267 experimental traces by analyzing macroscopic calcium-current traces elicited by membrane depolarizati

268 Calcium currents travel in rostro-caudal waves with moto

269 Unlike calcium current, TTX-resistant sodium current is not acc

270 The T-type calcium current underlies burst responses in thalamic nu

271 rmining the time course of the modulation of calcium current via tyrosine phosphorylation.

272 Calcium currents via low-voltage-activated T-type channe

273 gest that MCH exerts an inhibitory effect on calcium currents via PTX-sensitive G-protein pathways, p

274 ssium (GIRK) and depression of voltage-gated calcium currents via Y1 and Y2 receptor subtypes.

275 We investigated potassium and calcium currents, voltage responses and synaptic activit

276 rried the largest inward current, and T-type calcium current was also substantial.

277 PTA demonstrated that 98% of the increase in calcium current was attributable to beta1-adrenergic rec

278 Kainate-induced inhibition of the calcium current was diminished when intracellular calciu

279 were recorded in both regions, but the Cav3 calcium current was expressed at a substantially higher

280 entration-dependent inhibition of whole-cell calcium current was observed in the presence of chloroqu

281 Except immediately before spikes, calcium current was outweighed by calcium-activated pota

282 Caffeine-induced modulation of the calcium current was reduced in the presence of ruthenium

283 ot altered by Rem2 expression at a time when calcium current was totally abolished.

284 charge carried by the late sodium and L-type calcium currents was evaluated as a potential metric for

285 Roscovitine-induced potentiation of tail calcium currents was significantly blocked by the P/Q-ch

286 l DeltaC(m), but not the maximal size of the calcium current, was significantly reduced by 45% in bas

287 tial approached threshold, while both Ih and calcium current were minimal.

288 sing the whole-cell recording technique, and calcium currents were characterized based on activation,

289 Galanin actions on K(ATP) and calcium currents were completely lost in G(o)2(-/-) beta

290 H2) on the L-type (ICa,L) and T-type (ICa,T) calcium currents were investigated in muscle cells disso

291 Consistent with this idea, L-channel calcium currents were reduced by Ha-Ras(V12), which also

292 However, both cardiac sodium and calcium currents were significantly increased on long-te

293 Calcium currents were significantly smaller in cells exp

294 this phenotype demonstrated that presynaptic calcium currents were unaffected.

295 s different affinities for Cav3.1 and Cav1.2 calcium currents, which is consistent with the selective

296 ancing KCNQ5 currents and suppressing L-type calcium currents, which ultimately reduces vascular tone

297 ruited proportional to the whole cell L-type calcium current, with the total release of calcium from

298 whole cell, high-threshold voltage-dependent calcium currents, with a larger proportion of L-type cur

299 e-wave models increased low-threshold T-type calcium currents within postsynaptic thalamic relay and

300 ited the amplitude of Ca(v)3.3-evoked T-type calcium current without altering other biophysical prope