ライフサイエンスコーパス: Ca2 current

1 current called ICRAC (Ca2+ release-activated Ca2+ current).

2 rrent called I(CRAC) (Ca2+ release-activated Ca2+ current).

3 ange) rather than in systole (via the L-type Ca2+ current).

4 ts revealed that norepinephrine (NE) reduced Ca2+ current.

5 of these two different Ca2+ release sites by Ca2+ current.

6 ted by 50 microM nickel, a blocker of T-type Ca2+ current.

7 mergence of Ca2+ transients triggered by the Ca2+ current.

8 T-type current and a tetrodotoxin-sensitive Ca2+ current.

9 ormal Ca2+ transients despite reduced L-type Ca2+ current.

10 artially Ca2+-dependent inactivation for the Ca2+ current.

11 PKA effects on RyR, phospholamban (PLB), and Ca2+ current.

12 e amplitudes of twitch shortening and L-type Ca2+ current.

13 d by a decrease in Ca2+ entry via the L-type Ca2+ current.

14 feature of which is a much larger underlying Ca2+ current.

15 re positive voltage dependence of the mature Ca2+ current.

16 al is mediated by a high-threshold sustained Ca2+ current.

17 negative voltage dependence of the immature Ca2+ current.

18 the FMRFamide-induced inhibition of the peak Ca2+ current.

19 change was less than the entry on the L-type Ca2+ current.

20 e mediated by a high-threshold, inactivating Ca2+ current.

21 til it equalled the Ca2+ entry on the L-type Ca2+ current.

22 histograms and to the decaying phase of the Ca2+ current.

23 ET1 inhibited L-type voltage-dependent Ca2+ current.

24 CPA had no effect on inward Ca2+ current.

25 eir abolition by antagonism of inward L-type Ca2+ current.

26 rate of inactivation or facilitation of the Ca2+ current.

27 inhibits RGC firing by decreasing the inward Ca2+ current.

28 racellular Ca2+ release and increased L-type Ca2+ currents.

29 ological properties typical of T- and L-type Ca2+ currents.

30 that differed from dihydropyridine-sensitive Ca2+ currents.

31 eotidases to adenosine, which then inhibited Ca2+ currents.

32 lity in thalamic neurons by potentiating LVA Ca2+ currents.

33 an that obtained by activation of whole-cell Ca2+ currents.

34 ferential expression of voltage-gated K+ and Ca2+ currents.

35 uring stimulus trains, despite inhibition of Ca2+ currents.

36 chronized with measurement of Cd2+-sensitive Ca2+ currents.

37 ytes showed that indomethacin blocked L-type Ca2+ currents.

38 ized by myocytes and had no effect on L-type Ca2+ currents.

39 with the smallest sinusoidal-stimuli-evoked Ca2+ currents.

40 that also expresses a high density of T-type Ca2+ currents.

41 nsistent with the activation kinetics of the Ca2+ current; 3), the voltage dependence of the Ca2+ tra

42 The axonal Ca2+ current activated at potentials positive to -20 mV.

43 s reduced the rise in cAMP levels and L-type Ca2(+) current amplitude, and abolished the inotropic ef

44 inhibitory effects on synaptic transmission, Ca2+ current amplitude and gating and G protein modulati

45 gnificantly altered the relationship between Ca2+ current amplitude and inactivation in ways that wer

46 The Ca2+ current amplitude increased exponentially with dist

47 CGNs, NT and AID peptides reduced whole-cell Ca2+ current amplitude, modified voltage dependence of C

48 , we found that AngII potentiates the L-type Ca2+ currents, an effect mediated by AT1 receptors and a

49 CA shifted the voltage-sensitivities of the Ca2+ current and [Ca2+]i increases in intact guard cells

50 re electrically tuned by a voltage-dependent Ca2+ current and a Ca2+-dependent K+ current (IBK(Ca)).

51 of secretion mirrored that of both the peak Ca2+ current and Ca2+ entry.

52 The time courses of Ca2+ current and Ca2+ spark occurrence were determined i

53 ty, current density increased for the L-type Ca2+ current and decreased for the BK current, consisten

54 ain that is affected by the amplitude of the Ca2+ current and differentially modulated by distinct Ca

55 the persistence of immature features of the Ca2+ current and exocytosis into adulthood.

56 l, which leads to a reduction of presynaptic Ca2+ current and glutamate release.

57 The decreased L-type Ca2+ current and increased Ca2+ efflux on Na+-Ca2+ excha

58 cells was studied at the level of whole-cell Ca2+ current and intramembrane charge movement.

59 receptor agonist decreased voltage-activated Ca2+ current and lowered Ca2+ influx.

60 ue, mimicked the FMRFamide inhibition of the Ca2+ current and occluded any further FMRFamide-induced

61 superimposed upon the relatively slow L-type Ca2+ current and was resistant to conventional Ca2+ chan

62 Each step activated L-type Ca2+ currents and [Ca2+]i transients, but failed to acce

63 tage dependence of the Ca2+ current; and 4), Ca2+ currents and Ca2+ transients were fully blocked by

64 rch has suggested that the interplay between Ca2+ currents and Ca2+-activated K+ channels (KCa channe

65 av2.1 channels modulate presynaptic P/Q-type Ca2+ currents and contribute to activity-dependent synap

66 iological analyses revealed increased inward Ca2+ currents and decreased outward K+ currents, in conj

67 lgesia and allodynia, upregulation of T-type Ca2+ currents and enhanced Ca2+ entry into these cells c

68 ation of RBCs from -60 mV elicited sustained Ca2+ currents and evoked AMPA receptor (AMPAR)-mediated

69 nhances dihydropyridine-sensitive whole-cell Ca2+ currents and increases depolarization-induced incre

70 IP was 27% and was selective for NCX: L-type Ca2+ currents and plasmalemmal Ca2+ pumps were not affec

71 tly inhibits native rat cardiomyocyte L-type Ca2+ currents and the recombinant alpha1C subunit of the

72 oltage (through its influence on sarcolemmal Ca2+ currents) and, therefore, by all ionic currents tha

73 disease (IHD, n=19) on contractility, L-type Ca2+ current, and Ca2+ transients in continuously perfus

74 Action potential duration, L-type Ca2+ current, and Na+ /Ca2+ -exchange current were unalt

75 ted Ca2+ transients, cell shortening, L-type Ca2+ current, and SR volume were not significantly diffe

76 nd beta2a, the kinetics of activation of the Ca2+ current, and the single channel parameters estimate

77 WIN) reversibly inhibited EPSCs, presynaptic Ca2+ currents, and exocytosis.

78 , alter fluo-3 fluorescent responses to RyR2 Ca2+ currents, and for addressing other current research

79 onsistent with the voltage dependence of the Ca2+ current; and 4), Ca2+ currents and Ca2+ transients

80 allowed us to study how immature and mature Ca2+ currents are optimized to their particular function

81 we found that adenosine inhibited an N-type Ca2+ current as well as a further unidentified HVA curre

82 pidermal growth factor still potentiated the Ca2+ currents as determined by the whole-cell patch conf

83 t rate of rise and the magnitude of entering Ca2+ current at positive potentials.

84 sks a dihydropyridine (DHP)-sensitive L-type Ca2+ current at the motor nerve terminal.

85 ite a 2.4-fold difference in the size of the Ca2+ current at the two positions.

86 and the mean time constant for decay of LVA Ca2+ currents at -50 mV was also prolonged.

87 udy represent the first direct recordings of Ca2+ currents at presumed synaptic sites.

88 Whole-cell recordings of Ca2+ currents at Xenopus spinal neuron growth cones indi

89 II loop variant using Cd2+ (10(-4) M) as the Ca2+ current blocker.

90 ne (300 nm) completely suppressed the inward Ca2+ current but had no effect on inward Na+ currents.

91 ignificant effect on the amplitude of L-type Ca2+ current, but a significant reduction in the amplitu

92 ify Ca2+ transients in the absence of inward Ca2+ current, but without changing the external solution

93 We also found that EPA inhibited L-type Ca2+ current by 38.7 +/- 3.9% but this increased to 63.3

94 ontrast, inhibition of the voltage-activated Ca2+ current by CCh was antagonized by 100 nM pirenzepin

95 hanced G-protein-dependent modulation of the Ca2+ current by syntaxin 1A cannot explain the large sup

96 to mu+/+ levels, restored the inhibition of Ca2+ currents by DAMGO, and abolished receptor coupling.

97 periments revealed a reversible reduction of Ca2+ currents by DHPG, with no significant modification

98 sites was affected by increasing the trigger Ca2+ current (by increasing extracellular Ca2+ to 10 mM)

99 L-type Ca2+ currents, [Ca2+]i transient amplitudes, and fractio

100 a2+ entry is manifest as a non-voltage-gated Ca2+ current called ICRAC (Ca2+ release-activated Ca2+ c

101 o fully prevented augmentation of whole-cell Ca2+ currents caused by CH (as monitored using whole-cel

102 e potentials of -60 mV and voltage-dependent Ca2+ currents, characteristic of excitable cells.

103 from five patients inhibited N- and P/Q-type Ca2+ current components to different extents.

104 In most endocardial cells the T-like Ca2+ current comprised two components: a Ni2+-sensitive

105 rtened action potentials, and reduced L-type Ca2+ current contribute to a stunning reduction of intra

106 e presence of a saturating mobile buffer the Ca2+ current cooperativity is greater, and it increases

107 concentration, although vitronectin-induced Ca2+ current could not be detected.

108 ment significantly increased the peak T-type Ca2+ current density by twofold without affecting the ac

109 The developmental increase in Ca2+ current density exactly compensated for decreased s

110 vidual Ca2+ sparks were observed by reducing Ca2+ current density with nifedipine (0.1-8 microM).

111 This compensation was a function purely of Ca2+ current density, not of the transition from immatur

112 hosphorylation, but do show decreased L-type Ca2+ current density.

113 2+-ATPase activity, and a decrease in L-type Ca2+ current density.

114 The density of voltage-activated Ca2+ currents did not change between E8 and E11.

115 to an increased driving force for the L-type Ca2+ current during the action potential, which explains

116 Fluctuations of the L-type Ca2+ current during the AP plateau lead to variability i

117 a2+ in the pipette solution, inactivation of Ca2+ currents during depolarization was about two times

118 hat there was no cumulative change of K+ and Ca2+ currents during the test train.

119 Ca2+/CaM binding and reduces inactivation of Ca2+ currents during trains of repetitive depolarization

120 y, including a slowed inactivation of L-type Ca2+ current, enhanced Ca2+ spark width, duration, and f

121 Ca2+ currents, especially those activated at low voltage

122 % increases in peak current densities of LVA Ca2+ currents evoked at -50 mV from -110 mV in tg, lh, a

123 s by Ca2+-induced Ca2+ release, where L-type Ca2+ current evokes a larger sarcoplasmic reticulum (SR)

124 g rats that two kinetically different T-type Ca2+ currents exist in nRT neurones, with a slowly inact

125 However, Ca2+ current expression levels remained unaltered in sev

126 xpression system completely inhibits de novo Ca2+ current expression.

127 action potential duration shortened, L-type Ca2+ current fast inactivation was more rapid, and sarco

128 owed the current-voltage relationship of the Ca2+ current found in the ganglion cell.

129 Low-threshold Ca2+ currents gate the graded component.

130 ad the following characteristics: 1), L-type Ca2+ currents had a wild-type density; 2), Ca2+ transien

131 Many classes of Ca2+ current have been characterized electrophysiologica

132 However, direct recordings of Ca2+ currents have been limited and the upstream activat

133 luorescence was recorded simultaneously with Ca2+ currents having amplitudes of 0.25-14 pA.

134 ingle-cell level, upregulation of the L-type Ca2+ current I(Ca,L) steepened restitution curves of act

135 itating the activation of the store-operated Ca2+ current I(CRAC).

136 and the underlying calcium release-activated Ca2+ current (I CRAC).

137 Furthermore, feedback inhibition of the Ca2+ current (I(Ca)) by released vesicular protons reduc

138 models of AF implicate a reduction in L-type Ca2+ current (I(Ca)) density in these changes.

139 L-type Ca2+ current (I(Ca)) is reduced in myocytes from cardiac

140 which the two sets of RyRs are controlled by Ca2+ current (I(Ca)) or Ca2+ diffusion remains to be det

141 We found Ca2+ current (I(Ca))-dependent bursting in 7.5% of inspi

142 cated in Ca2+-dependent regulation of L-type Ca2+ current (I(Ca)).

143 L-type Ca2+ current (I(Ca,L)) density measured by whole-cell pa

144 stimulation by phenylephrine (PE) on L-type Ca2+ current (I(Ca,L)) in cat atrial myocytes.

145 L-type Ca2+ current (I(Ca,L)) was measured under basal conditio

146 is a direct regulator of the cardiac L-type Ca2+ current (I(Ca,L)).

147 ystolic Ca2+ transient ([Ca2+]iT) and L-type Ca2+ current (I(Ca,L); P<0.05).

148 sured directly as the Ca2+ release-activated Ca2+ current (I(CRAC)).

149 and I DRK), calcium (Ca2+) release-activated Ca2+ currents (I CRAC) and Ca2+-activated TRPM4-like cur

150 and a possible increase in voltage-sensitive Ca2+ currents (I(Ca)).

151 Whole-cell L-type Ca2+ currents (I(Ca,L)) recorded from single, isolated a

152 cytes despite potently inhibiting the L-type Ca2+ current, I(Ca,L).

153 restingly, the presence of the low-threshold Ca2+ current, I(T) in a postsynaptic neuron allows the r

154 he presence and absence of the low-threshold Ca2+ current, I(T), and the hyperpolarization-activated

155 dominant determinant of inactivation of the Ca2+ current (ICa) and termination of release.

156 of 10 nM endothelin-1 (ET-1) increased peak Ca2+ current (ICa) by 28.2 +/- 2.5 % (n = 13) and slowed

157 L-type Ca2+ current (ICa) density was increased in TG compared

158 Increased L-type Ca2+ current (ICa) density, with unaltered characteristi

159 Activation of Ca2+ current (ICa) failed to produce the typical sarcome

160 nels/ryanodine receptors (RyR) by the inward Ca2+ current (ICa) gives rise to Ca2+-induced Ca2+ relea

161 and isoproterenol (isoprenaline)-stimulated Ca2+ current (ICa) was decreased by 42% and the inactiva

162 Peak L-type Ca2+ current (ICa) was reduced by 62% in KO myocytes com

163 Peak Ca2+ current (ICa) was slightly increased, and action po

164 The isoproterenol-induced increase in L-type Ca2+ current (ICa) was smaller in females versus in male

165 uscarinic M1 ACh receptor suppression of the Ca2+ current (ICa) was temporally correlated with PIP2 h

166 on beta-adrenergic regulation of the L-type Ca2+ current (ICa) were studied in ventricular myocytes

167 for Ca(2+)-CaM-dependent increases in L-type Ca2+ current (ICa), and a CaM-binding IQ domain mimetic

168 examined the respective roles of the L-type Ca2+ current (ICa), SR Ca2+ uptake, storage and release,

169 , 10 mmol/L), there was a decrease in inward Ca2+ current (ICa), the spatially averaged Ca2+ transien

170 e 2 than males, in-part due to higher L-type Ca2+ current (ICa,L) at the base of the heart.

171 es demonstrate an increase in cardiac L-type Ca2+ current (ICa,L) density on sympathetic innervation

172 (beta1-AR) regulation of the cardiac L-type Ca2+ current (ICa,L) was studied using the whole-cell pa

173 the relationship was broader than the L-type Ca2+ current (ICa,L)-voltage relationship.

174 rgic receptor (beta-AR) regulation of L-type Ca2+ current (ICa,L).

175 L-type Ca2+ current (ICa-L) triggers Ca2+ release from the sarc

176 HF, Ca2+ transient amplitude and peak L-type Ca2+ current (ICa-L) were reduced (to 70 +/- 11% and 50

177 ined voltage-clamp recordings of presynaptic Ca2+ currents (ICa(V)) with UV-light flash-induced Ca2+

178 -clamp techniques were used to record L-type Ca2+ currents (ICa) and action potentials, respectively.

179 Ca2+ currents (ICa) and changes in membrane capacitance

180 f overexpression of CYP2J2 on cardiac L-type Ca2+ currents (ICa) in adult transgenic mice.

181 n contraction, [Ca2+]i transient, and L-type Ca2+ currents (ICa) in single ventricular myocytes isola

182 polarization of HF cells to potentials where Ca2+ currents (ICa) were maximal resynchronized SR Ca2+

183 rotein (EGFP)-tagged alpha1sDHPR variants on Ca2+ currents (ICa), charge movements (Q) and SR Ca2+ re

184 c hypertrophy, we measured whole-cell L-type Ca2+ currents (ICa,L), whole-cell Ca2+ transients ([Ca2+

185 ), a blocker of low voltage-activated T-type Ca2+ current ((ICa,T), decreased diastolic depolarizatio

186 al for SR Ca2+ release (voltage-gated L-type Ca2+ current, ICa,L) and SR Ca2+ load during alternans.

187 beta-Adrenergic modulation of the L-type Ca2+ current (ICaL) was characterized for different deve

188 timulation robustly increases cardiac L-type Ca2+ current (ICaL); yet the molecular mechanism of this

189 lamp technique to measure the store-operated Ca2+ current ICRAC and the capacitance method to monitor

190 and amplitude of the Ca2+ release-activated Ca2+ current ICRAC in rat basophilic leukaemia (RBL-1) c

191 gents to activate the Ca2+ release-activated Ca2+ current (ICRAC) in rat basophilic leukaemia (RBL-1)

192 on: (i) the current-voltage relation of the Ca2+ current; (ii) sarcoplasmic reticulum Ca2+ uptake; a

193 hibited high (but not low) voltage-activated Ca2+ current in both DRG and SCG neurons expressing hSNS

194 Peak Ca2+ current in control and IGF-1-treated cells was -7.8

195 s via NOX/ROS signaling and augmented T-type Ca2+ current in IH-treated chromaffin cells.

196 range of experimental data, including L-Type Ca2+ current in response to voltage-clamp stimuli, inact

197 elated to the magnitude of the peak measured Ca2+ current in the presence of Cs+-containing pipette s

198 ion of residues in DRPEER altered fractional Ca2+ currents in a manner consistent with its forming a

199 DPDPE and deltorphin II (1 microM) inhibited Ca2+ currents in both cases.

200 However, in contrast to expectation, L-type Ca2+ currents in cardiac myocytes from DCT-/- mice were

201 We investigated voltage-dependent Ca2+ currents in cultured ICC from the murine colon and

202 dole WIN 55,212-2 (WIN) inhibited whole-cell Ca2+ currents in rat sympathetic neurons previously inje

203 ure rapid and efficient regulation of L-type Ca2+ currents in response to beta-adrenergic stimulation

204 ose of the present study was to characterise Ca2+ currents in smooth muscle cells isolated from biops

205 PCR- and PP2B-mediated suppression of L-type Ca2+ currents in striatal neurons.

206 d biophysical properties of both LVA and HVA Ca2+ currents in thalamic cells of tottering (tg; Cav2.1

207 s, and beta-adrenergic stimulation of L-type Ca2+ currents in the heart.

208 nt proper, contribute to the high fractional Ca2+ currents in these channels under physiological cond

209 a2 agonist clonidine inhibited voltage-gated Ca2+ currents in these neurons.

210 Ca2+ levels affect inactivation of Ca(v)2.1 Ca2+ currents in transfected 293T cells.

211 icked by chronic pharmacological blockade of Ca2+ currents in wild-type neurons.

212 t inhibition of high voltage-activated (HVA) Ca2+ currents in Xenopus laevis embryo spinal neurons.

213 acid (AA) on whole cell and unitary calcium (Ca2+) currents in rat neonatal superior cervical ganglio

214 ibuted and best characterised store-operated Ca2+ current, in a model system, the RBL-1 rat basophili

215 We found that inactivation of Ca(v)2.1 Ca2+ currents increased exponentially with current ampli

216 y attenuate the norepinephrine (NE)-mediated Ca2+ current inhibition by sequestration of Gbeta gamma

217 We find that transient Ca2+ current inhibition is correlated with exocytosis an

218 Ca2+ current inhibition is negligible in acutely dissoci

219 icarbonate) buffering conditions, pronounced Ca2+ current inhibition occurs after exocytosis ( approx

220 The effect of Ca2+ current inhibition on subsequent exocytosis was inv

221 Agonist-mediated Ca2+ current inhibition was blocked by a selective CB1R

222 The Ca2+ current inhibition was concentration dependent and

223 CaV2.1 channels, which conduct P/Q-type Ca2+ currents, initiate synaptic transmission at most sy

224 nhances beta1-AR-induced increases in L-type Ca2+ currents, intracellular Ca2+ transients, and myocyt

225 roximately 2 microm, and that the underlying Ca2+ current is in the range of 10-20 pA.

226 the action-potential threshold, whereas the Ca2+ current is mainly involved, together with the K+ cu

227 Only the Ca2+ current is necessary for spontaneous and induced ac

228 activation indicates that the Cav3.1 T-type Ca2+ current is shifted to a positive potential, at whic

229 to -25 mV) but expressed little or no T-type Ca2+ current (IT).

230 on-induced inactivation of the low-threshold Ca2+ current (IT).

231 dow') component of the low threshold, T-type Ca2+current (IT) and an appropriately large ratio of IT

232 reduced ICaL, whereas IZc showed changes in Ca2+ current kinetics with an acceleration of current de

233 tion, epifluorescence microscopy, and L-type Ca2(+) current measurements were performed in myocardial

234 oncentration changes evoked by low-threshold Ca2+ currents modulate spike-mediated synaptic transmiss

235 In addition, ICRAC, a Ca2+ release-activated Ca2+ current monitored in Jurkat cells by whole-cell pat

236 types which express no or low-density L-type Ca2+ currents, namely beta1 KO and RyR1 KO, beta2a overe

237 However, neither the transient Ca2+ current nor I(A) shows a change in current density,

238 n 1A cannot explain the large suppression of Ca2+ current observed.

239 irst time that the physiologically important Ca2+ current of the TRPV1 receptor is also dynamic and d

240 32A-RyR1-expressing myotubes elicited L-type Ca2+ currents of approximately normal size and myoplasmi

241 sed in HEK293 cells and on native non-L-type Ca2+ currents of cultured hippocampal neurons.

242 nt could be related to changes in whole-cell Ca2+ current or the Ca2+ transient in identified OT or v

243 In addition, increasing the trigger Ca2+ current or the SR Ca2+ load changed the spatial pat

244 causes no significant changes in presynaptic Ca2+ currents or synaptic vesicle exocytosis as measured

245 The sustained kinetics of the mature Ca2+ current permit high-frequency firing during larval

246 ected with Ca(v)1.2, CaBP1 greatly prolonged Ca2+ currents, prevented Ca2+-dependent inactivation, an

247 2+ (25-50 mM) that result in saturating RyR2 Ca2+ currents, proportional fluo-3 fluorescence was reco

248 ials under biionic conditions and fractional Ca2+ currents recorded under physiological conditions.

249 The beta2a-mediated Ca2+ current recovered in beta1 KO myotubes lacking the

250 Concurrent with Ca2+ current recovery, there was a drastic reduction of

251 After this, the Ca2+ current reduced to about 30 % of its maximum size a

252 tors selectively couple to GIRK currents and Ca2+ currents respectively, with negligible cross-talk.

253 The reduction in Ca2+ current resulted in smaller exocytotic responses to

254 Although the rate of Ca2+ current run-down was not affected by 10-15 microM f

255 The inactivation of the immature Ca2+ current serves to limit the frequency and burst dur

256 Maximal Ca2+ influx rates and whole-cell Ca2+ currents showed that both Th1 and Th2 cells express

257 Although the soma of the B cells express two Ca2+ current subtypes, a transient BayK 8644-insensitive

258 there was no detectable voltage-gated inward Ca2+ current, syntilla frequency was increased e-fold pe

259 eshold, fast- and slow-inactivating types of Ca2+ currents, take part in membrane depolarization, and

260 reshold, rapidly activating and inactivating Ca2+ current that resembled the T-type current was prese

261 CaV2.1 channels conduct P/Q-type Ca2+ currents that are modulated by calmodulin (CaM) and

262 an explanation as to why previous whole-cell Ca2+ currents that were recorded in quasi-physiological

263 lished the effect of CaBP4 in prolonging the Ca2+ current through Ca(v)1.3 channel, whereas inactivat

264 kinase A (PKA) greatly increases the L-type Ca2+ current through CaV1.2 channels in isolated cardiac

265 f their NMDA-Rs and the effective fractional Ca2+ current through these receptors.

266 injections proved difficult to quantify, and Ca2+ currents through channels were obscured by K+ curre

267 P/Q-type Ca2+ currents through presynaptic CaV2.1 channels initia

268 els of cardiac Ca2+ sparks have assumed that Ca2+ currents through the Ca2+ release units (CRUs) were

269 Complex modulation of voltage-gated Ca2+ currents through the interplay among Ca2+ channels

270 Thus, by enabling macroscopic store-operated Ca2+ current to activate and then by controlling its ext

271 ing Poisson statistics to relate macroscopic Ca2+ current to the opening of single L-type Ca2+ channe

272 The sensitivity of bipolar cell Ca2+ currents to extracellular pH was assessed: channel

273 ed the increases in contractile response and Ca2+ currents to ISO in WT and to forskolin in both WT a

274 e tested the hypothesis that Rem2 attenuates Ca2+ currents to regulate insulin secretion.

275 ot of the transition from immature to mature Ca2+ current types.

276 Ca(v)2.1 channels, which mediate P/Q-type Ca2+ currents, undergo Ca2+/calmodulin (CaM)-dependent i

277 t rate of rise and the magnitude of the peak Ca2+ current was also found when use of Cs+ was avoided

278 t rate of rise and the magnitude of the peak Ca2+ current was found under a variety of pulse protocol

279 First, the L-type Ca2+ current was larger in endocardial than in epicardia

280 Inhibition of the voltage-gated transient Ca2+ current was lessened after long-term treatment.

281 In voltage clamp, the whole-cell, Ca2+ current was slightly larger during lactation in OT

282 n to TRPV1 responses and discovered that the Ca2+ current was tuned by the mode of activation.

283 L-type Ca2+ current was unaffected by acute exposure to T(3).

284 BAPTA was reduced to 0.5 mm, inactivation of Ca2+ currents was significantly greater than with an equ

285 Inhibition of Ca2+ currents was voltage independent and was largely me

286 In summary, two components of inward Ca2+ current were resolved in ICC of murine small intest

287 The epidermal growth factor-induced Ca2+ currents were completely abolished by a selective p

288 These effects of sorcin on L-type Ca2+ currents were confirmed in Xenopus oocyte expressio

289 voltage-activated (T-type channel-mediated) Ca2+ currents were evident.

290 their somatic counterparts, dendritic N-type Ca2+ currents were hypersensitive to neurotransmitters a

291 found that, in Drosophila cultured neurons, Ca2+ currents were mediated predominantly by the cac cha

292 Sarcolemma voltage-gated Ca2+ currents were not activated following store depleti

293 T-type Ca2+ currents were observed in 47% of distal urethral ne

294 ological properties typical of T- and L-type Ca2+ currents, were present in these cells.

295 CHO-K1 cells reduces native store-activated Ca2+ currents, whereas knock-down of endogenous I-mfa in

296 microM), and baclofen (50 microM) inhibited Ca2+ currents, whereas the -selective ligands [D-Pen2,Pe

297 developed a mathematical model of the L-type Ca2+ current, which is based on data from whole-cell vol

298 tional shortening (video motion), and L-type Ca2+ currents (whole-cell patch clamp) 5 days after tran

299 a wild-type density of nifedipine-sensitive Ca2+ currents with a slow activation kinetics typical of

300 ile lowering extracellular pH suppressed HVA Ca2+ currents, Zn2+ current amplitude was affected oppos