ライフサイエンスコーパス: Ca2 transient

1 responsible for the rapid rise of the normal Ca2+ transient.

2 tes involves a decreased rate of rise of the Ca2+ transient.

3 is a prominent feature of the nucleoplasmic Ca2+ transient.

4 tant combined effects on contraction and the Ca2+ transient.

5 a varying number of points of origin of the Ca2+ transient.

6 cascade, angiotensin II, produced a striking Ca2+ transient.

7 potential, further slowing the decay of the Ca2+ transient.

8 l shock did not affect length shortening and Ca2+ transient.

9 ERCA2a expression restored contractility and Ca2+ transients.

10 e rate of cell movement and the frequency of Ca2+ transients.

11 .1% (P<0.05) with no change in intracellular Ca2+ transients.

12 arinic receptors, did not affect these local Ca2+ transients.

13 lly decreased the amplitude of mitochondrial Ca2+ transients.

14 of these kinases to changes in the frequency Ca2+ transients.

15 ed the half-decay time (t1/2) of IP3-induced Ca2+ transients.

16 ease, nor ryanodine inhibited the purinergic Ca2+ transients.

17 nating Ca2+ transients to stable alternating Ca2+ transients.

18 st, suramin, effectively inhibited the local Ca2+ transients.

19 l Ca2+ flashes', and much smaller, localized Ca2+ transients.

20 icantly reduced the amplitude of IP3-induced Ca2+ transients.

21 AG/L-NIL had no effect on contractility and Ca2+ transients.

22 ress through MI in the absence of detectable Ca2+ transients.

23 he amplitude, duration, and frequency of the Ca2+ transients.

24 ents of the spine (40-50%) but not dendritic Ca2+ transients.

25 tic activation of which summates into global Ca2+ transients.

26 force using simultaneously recorded APs and Ca2+ transients.

27 ide had no effect on either ICa or the local Ca2+ transients.

28 effect on the rate of decay of these larger Ca2+ transients.

29 We monitored effects of the drugs on Ca2+ transients.

30 oupling coefficient and asynchronous APs and Ca2+ transients.

31 as altered to reproduce human atrial myocyte Ca2+ transients.

32 responsible for synchronizing muscle APs and Ca2+ transients.

33 ased prevalence of TTX-sensitive spontaneous Ca2+ transients.

34 he single-channel level and on intracellular Ca2+ transients.

35 ted with a decrease in parallel RyR-mediated Ca2+ transients.

36 as well as Fluo-5F imaging of intracellular Ca2+ transients.

37 age dependency of the amplitude of cytosolic Ca2+ transients.

38 ) synaptic stimulation, augmented AP-induced Ca2+ transients.

39 sessed by the V(m) dependence of current and Ca2+ transients.

40 -0.1 versus 0.7+/-0.03, P<0.05) and systolic Ca2+ transients (1.89+/-0.27 versus 0.80+/-0.08) than GF

41 ing diastole, increases the magnitude of the Ca2+ transient; 3) during prolonged stretching, the X-RO

42 < 0.01) was associated with increased Fura-2 Ca2+ transients (396 +/- 50 versus 250 +/- 24 nmol/liter

43 e Ca2+ currents had a wild-type density; 2), Ca2+ transients activated much slower than controls over

44 induced Ca2+ release, indicated by a smaller Ca2+ transient after FGF13 knockdown.

45 L) in the frequency response of the systolic Ca2+ transient alone and during beta-adrenergic stimulat

46 ECG T-wave alternans (ECG ALT) and Ca2+ transient alternans (Ca2+ALT) were induced by rapid

47 the synchrony of action potentials (APs) and Ca2+ transients among neighboring body wall muscle cells

48 Ca2+ -transient amplitude and sarcoplasmic reticulum Ca2

49 lasmic reticulum Ca2+ load (caffeine-induced Ca2+ -transient amplitude, integrated Na+/Ca2+ -exchange

50 with AdPLB-dn (versus control) had enhanced Ca2+ transient amplitude (2.0+/-0.1 versus 1.6+/-0.05 F/

51 For single APs, the Ca2+ transient amplitude and decay rate were similar at

52 as an inverse relation between frequency and Ca2+ transient amplitude and ICa-L.

53 In HF, Ca2+ transient amplitude and peak L-type Ca2+ current (I

54 significantly attenuated electrically evoked Ca2+ transient amplitude and prolonged the 50% decay tim

55 delling, suggested that low Ko increases the Ca2+ transient amplitude by reducing NKA activity despit

56 Isoproterenol (ISO) increased Ca2+ transient amplitude during systole, sarcoplasmic re

57 by altering the test potential decreased the Ca2+ transient amplitude less than an equivalent reducti

58 en though isoproterenol-induced increases in Ca2+ transient amplitude were similar in both groups.

59 proach resulted in a significant decrease in Ca2+ transient amplitude, but not duration or frequency,

60 timulation with isoprenaline (ISO) increased Ca2+ transient amplitude, ICa-L and SRCa2+ content in bo

61 sponding to moderate hypokalaemia, increased Ca2+ transient amplitude, sarcoplasmic reticulum (SR) Ca

62 Na+ levels sensed by NCX and to increase the Ca2+ transient amplitude.

63 a2+ leak, but did not affect the increase of Ca2+ transient amplitude.

64 sarcolipin resulted in an increase in atrial Ca2+ transient amplitudes, and this resulted in enhanced

65 gic receptor (betaAR)-dependent increases in Ca2+ transient amplitudes, likely accounting for the con

66 ocytes, along with significant depression of Ca2+ transient amplitudes.

67 transgenic mice that displayed normal global Ca2+ transient and cellular contraction levels and reduc

68 lease at the t-tubules; the amplitude of the Ca2+ transient and contraction were also unchanged by 20

69 the lusitropic effect of EPA on the systolic Ca2+ transient and contraction.

70 is required for the initiation of an evoked Ca2+ transient and for spontaneous Ca2+ sparks.

71 M) + acetylcholine (10(-7)M) (to enhance the Ca2+ transient and further shorten the abbreviated actio

72 increasing frequency decreased both systolic Ca2+ transient and ICa-L.

73 ne pulmonary veins, enhanced by an increased Ca2+ transient and increased Na-Ca exchange current.

74 This also explained blunted Ca2+ transient and rate-adaptation of [Ca2+]i and [Na+]i

75 Ca2+ uptake by the SR slows the decay of the Ca2+ transient and reduces SR Ca2+ stores.

76 ion (isoprenaline, 30 nm) increased both the Ca2+ transient and the SR Ca2+ content and removed the d

77 e domains was significantly higher after the Ca2+ transient and was abolished by Wm pretreatment.

78 sence of CPA caused abolition of spontaneous Ca2+ transients and a progressive rise in cytosolic [Ca2

79 body (SSA78) markedly augments intracellular Ca2+ transients and contraction of rat ventricular cardi

80 epletions alternated in phase with cytosolic Ca2+ transients and contractions.

81 ntly perturbed the duration and frequency of Ca2+ transients and disrupted the characteristic shape o

82 In the present study, we compare cellular Ca2+ transients and electrophysiological parameters of 6

83 depolarizations and triggered beats, delayed Ca2+ transients and frequent spontaneous Ca2+ release ev

84 e amplifies the IP3R-induced trigger for the Ca2+ transients and modulates its frequencies, it is not

85 , and rise time of macroscopic I(Ca)-induced Ca2+ transients and of spontaneous Ca2+ sparks were redu

86 ol) could enhance SERCA function and restore Ca2+ transients and positive FFR in ventricular myocytes

87 gendorff model), and in vitro measurement of Ca2+ transients and sarcomere shortening in adult cardio

88 iomyocytes restored diminished intracellular Ca2+ transients and sarcoplasmic reticulum (SR) Ca2+ loa

89 n on NOS inhibition) was mirrored exactly in Ca2+ transients and SR Ca2+ contents.

90 bination of AP remodeling related to altered Ca2+ transients and suppression of IK1.

91 Smaller Ca2+ transients and systolic dysfunction in heart failur

92 (TBS) produced small amplitude postsynaptic Ca2+ transients and triggered long-term potentiation.

93 indicator, Di-8-ANEPPS) simultaneously with Ca2+ transients and/or Ca2+ sparks (fluo-4).

94 y signal both vessel constriction (by global Ca2+ transients) and relaxation (by subsurface Ca2+ spar

95 d Ca2+ current (ICa), the spatially averaged Ca2+ transient, and E-C coupling gain, but no reduction

96 nsPEF caused local anodal Ca2+ waves without Ca2+ transients, and > or =20 nsPEF caused normal transi

97 arcoplasmic reticulum Ca2+ loading, enhanced Ca2+ transients, and augmented contractility, whereas ov

98 nhanced contractility and relaxation, Fura-2 Ca2+ transients, and Ca2+ channel currents.

99 is the major process responsible for global Ca2+ transients, and intracellular variations in sensiti

100 eases in L-type Ca2+ currents, intracellular Ca2+ transients, and myocyte contractility, without alte

101 The magnitude of Ca2+ transients appears to be maintained by an increased

102 ed in RGS2-/- mice, 2) vasopressin-triggered Ca2+ transients are augmented in smooth muscle cells fro

103 nal modeling indicated that the large distal Ca2+ transients are consistent with active, not passive,

104 rsal genes in mutant embryos suggesting that Ca2+ transients are important in mediating dorsal gene e

105 The data also suggest that Ca2+ transients are influenced by additional mechanisms

106 assay were confirmed in the second messenger Ca2+ transient assay.

107 between the BLA assay and the intracellular Ca2+ transient assays in these cells.

108 tentials reproducibly trigger rapidly rising Ca2+ transients at 1-3 local hot spots within the periph

109 esting [Ca2+]i and prolonged the recovery of Ca2+ transients at peak [Ca2+]i C 500 nM.

110 In addition, the raising phase of the Ca2+ transient became biphasic.

111 Verapamil did not affect nsPEF-induced Ca2+ transients, but decreased responses to CP.

112 by increasing the pH slowed the decay of the Ca2+ transient by 2-fold.

113 10 microm) significantly enhanced the spine Ca2+ transients by 40-50%.

114 nd nifedipine (both 10 microm) reduced spine Ca2+ transients by approximately 10%, whereas the L-type

115 ERCA) plays an important role in terminating Ca2+ transients by returning cytosolic Ca2+ to intracell

116 the action potential (AP) and intracellular Ca2+ transient (Ca(i)T) is sometimes altered during vent

117 Localized, brief Ca2+ transients (Ca2+ syntillas) caused by release from

118 d relengthening; and decreased peak systolic Ca2+ transient ([Ca2+]iT) and L-type Ca2+ current (I(Ca,

119 frequency-dependent sarcomere shortening and Ca2+ transients ([Ca2+]i) compared with WT.

120 We evaluated contraction and intracellular Ca2+ transients ([Ca2+]i) in left ventricular (LV) myocy

121 d to investigate ionic mechanisms underlying Ca2+ transient (CaT) and action potential duration (APD)

122 It is widely thought that focal Ca2+ transients cause "spontaneous" exocytosis, although

123 Field-stimulated Ca2+ transients, cell shortening, L-type Ca2+ current, a

124 ease, contributing to the depressed and slow Ca2+ transient characteristic of HF.

125 d development of axon branches revealed that Ca2+ transients coincide spatially and temporally with p

126 igh-frequency stimulation of the ML elicited Ca2+ transients composed of a small-amplitude fast risin

127 Here, differences in the Ca2+ transient could not explain the divergent relaxatio

128 Ca2+ transient data directly paralleled these results, i

129 Ca2+ -transient decay was faster in pAF, but the decay o

130 Ca2+ transients declined faster in AdPLB-dn versus Adbet

131 /- 2.5% to 5.6% +/- 3.4% (p = 0.000) and the Ca2+ transient decreased from 1.15 +/- 0.13 au to 1.08 +

132 : the time constant of decay of the systolic Ca2+ transient decreased to 65.3 +/- 5.0% of control, We

133 ur data reveal the presence of LTS-dependent Ca2+ transients (Delta[Ca2+]) in dendritic spine-like st

134 bit normal resting cytosolic Ca2+ and normal Ca2+ transients despite reduced L-type Ca2+ current.

135 he hypothesis that an increased or prolonged Ca2+ transient during an abbreviated action potential ca

136 d by the sympathetic nervous system, but the Ca2+ transients during neurally stimulated contraction o

137 haffer collateral synapses the magnitudes of Ca2+ transients during plasticity induction do not match

138 olume, and smaller spines experience larger [Ca2+] transients during synaptic transmission.

139 The myoplasmic free [Ca2+] transient elicited by an action potential (Delta[C

140 Our results indicate that purinergic Ca2+ transients evoked by release of ATP from nerve vari

141 ited by cyclosporin A, suggesting that these Ca2+ transients exert their effects via calcineurin.

142 to the behavior of the II-III loop chimera, Ca2+ transients expressed by an alpha1C/alpha1S chimera

143 The Ca2+ transients expressed by the alpha1C(E736K)/alpha1S

144 e of resting [Ca2+]I and in the clearance of Ca2+ transients following activation of voltage-gated Ca

145 S100A1 leads to decreased global myoplasmic Ca2+ transients following electrical excitation.

146 Ca2+ transients from F myocytes were significantly small

147 images of field-stimulated cells, whole-cell Ca2+ transients had two morphologies: 'U-shaped' transie

148 odine was ineffective against the IP3-evoked Ca2+ transient (i.e. when RyRs were not activated, e.g.

149 constant of decline of the caffeine-induced Ca2+ transient, implying impaired sarcolemmal Na+/Ca2+ e

150 not increase the amplitude of the cytosolic Ca2+ transient in CHO-RyR1 cells expressing mAKAP or mAK

151 Ca2+ release slows the rise of the cytosolic Ca2+ transient in failing feline myocytes.

152 in acutely increased cell shortening and the Ca2+ transient in field stimulated guinea-pig ventricula

153 to changes in whole-cell Ca2+ current or the Ca2+ transient in identified OT or vasopressin (VP) neur

154 nied by a 59% reduction (P<0.01) in the peak Ca2+ transient in irregulary paced myocytes compared wit

155 The occurrence of a Ca2+ transient in response to either KCl (25 mM) or caps

156 cutely decreased the amplitude of the evoked Ca2+ transient in small DRG neurons cocultured with fibr

157 ha (PPARalpha), was determined on the evoked-Ca2+ transient in the coculture condition.

158 nsPEF induced Ca2+ transients in 68/104 cells.

159 scular nerves and novel, spatially localized Ca2+ transients in adjacent smooth muscle cells.

160 eptive agonist capsaicin (1 microm) elicited Ca2+ transients in all nerve terminals studied.

161 ker NiCl2 (100 microm) significantly reduced Ca2+ transients in both spines and their parent dendrite

162 Measurements of Ca2+ transients in CA1 pyramidal neurons after weak and

163 intact cohort, was associated with increased Ca2+ transients in cardiac myocytes after isoproterenol

164 Ca2+ transients in cardiomyocytes of KO mice showed a de

165 or decay kinetics of the electrically evoked Ca2+ transients in CNTs.

166 ) on contractility, L-type Ca2+ current, and Ca2+ transients in continuously perfused rat ventricular

167 easurements of agonist-induced intracellular Ca2+ transients in cultured rat hippocampal neurons and

168 Analysis of capsaicin-evoked Ca2+ transients in dissociated mouse dorsal root ganglio

169 e stress-induced TRPM2-mediated currents and Ca2+ transients in DT40 B cells.

170 ced Ca2+ release is the major contributor to Ca2+ transients in ESdCs after 16 days (72%).

171 ye Fluo-4/AM, we determined that spontaneous Ca2+ transients in ESdCs at the onset of beating (day 9)

172 We report that Ca2+ transients in filopodia activate the intracellular

173 he endoplasmic reticulum (ER) contributes to Ca2+ transients in frog sympathetic ganglion neurons.

174 nced the amplitude of store overload-induced Ca2+ transients in HEK293 cells or HL-1 cardiac cells.

175 n of mitral/tufted cells produced stochastic Ca2+ transients in individual granule cell spines.

176 allenge with PAL altered cell shortening and Ca2+ transients in isolated mouse cardiomyocytes but not

177 Spontaneous Ca2+ transients in mdx mouse cells are sensitive to depo

178 ing I(NCX) against reverse-mode NCX-mediated Ca2+ transients in myocytes, we demonstrate that Ca2+-de

179 quency electrical field stimulation revealed Ca2+ transients in perivascular nerves and novel, spatia

180 s in culture and by the presence of abnormal Ca2+ transients in purified cortical oligodendrocytes st

181 as a loss of postsynaptic CP-AMPAR-mediated Ca2+ transients in PYR spines and reduced rectification

182 harmacological agents on electrically evoked Ca2+ transients in rat corneal nerve terminals (CNTs) in

183 ne the frequency and duration of spontaneous Ca2+ transients in single ESdCs.

184 of single Ca2+-permeable channels, miniature Ca2+ transients in single mitochondria ("marks"), and SR

185 nalogs fail to inhibit vasopressin-triggered Ca2+ transients in smooth muscle cells from resistance a

186 Mucosal touch and distention-induced Ca2+ transients in submucous neurons were reduced by apy

187 To quantify Ca2+ transients in the absence of inward Ca2+ current, b

188 cell with a HEL-bearing DC triggered strong Ca2+ transients in the B cells.

189 Ca2+ transients in the dendrites of an individual Oregon

190 migration, whereas it eliminates spike-like Ca2+ transients in the late phase.

191 after neural crest ablation causes depressed Ca2+ transients in the primary heart tube.

192 hich suggests an additional function for the Ca2+ transients in this cellular layer.

193 -R currents at the soma and NMDA-R-mediated [Ca2+] transients in stimulated spines (Delta[Ca2+]).

194 tion among sequential IP3 receptor-mediated [Ca2+] transients in the control of calcium signal propag

195 ation can elicit transient rises in [Ca2+]i (Ca2+ transients) in PSNTs within the corneal epithelium

196 rine similarly enhanced cell contraction and Ca2+ transients, in contrast to anticipated receptor des

197 increases of beta-MyHC expression (18%) have Ca2+ transient-independent physiologically relevant effe

198 Tetrodotoxin inhibited evoked purinergic Ca2+ transients, indicating that they were dependent on

199 IP3R isoforms was correlated with cytosolic Ca2+ transients induced by activation of group I metabot

200 The amplitudes of Ca2+ transients induced by P2Y but not P2X receptor agon

201 Ca2+ transients, induced by the neurotransmitter ATP act

202 Repeating nsPEF increased the likelihood of Ca2+ transient induction (61.8% for <10 nsPEF vs. 80.6%

203 Netrin-1-induced Ca2+ transients involve release from intracellular store

204 The amplitude of the depolarization-evoked Ca2+ transient is larger in dorsal root ganglion (DRG) n

205 tion of the plasma membrane and a whole-cell Ca2+ transient is subsequently induced by voltage-depend

206 patial characteristics of the nucleoplasmic [Ca2+] transient is considered.

207 During this time, junctional Ca2+ transients (jCaTs) were present at relatively high

208 In both cell types, these Ca2+ transients lead to disappearance of phosphorylated

209 Ca2+ transients, measured with multiphoton imaging in in

210 We imaged [Ca2+] transients mediated by synaptically activated NMDA

211 urnover, TRPM2 currents, and TRPM2-dependent Ca2+ transients; no oxidant-induced activation of TRPM2

212 d increase in the frequency of intracellular Ca2+ transients normally present in the enveloping layer

213 Small, local Ca2+ transients occurred spontaneously, and their freque

214 ger (NCX), and Ca2+ buffering in the altered Ca2+ transients of failing human ventricular myocytes.

215 More critically, Ca2+ transients of field-stimulated ventricular I79N-Tg

216 Ca2+ transients of isolated myocytes from knockout mice

217 These changes can explain the defective Ca2+ transients of the failing human ventricular myocyte

218 tamate release driven NMDA receptor mediated Ca2+ transients often occur at the same synapse, these t

219 croM), which did not inhibit the first large Ca2+ transient or subsequent early oscillations but did

220 c nerve stimulation evoked rapid, whole-cell Ca2+ transients, or "Ca2+ flashes," and slowly propagati

221 ze of Ca2+ syntillas, which are brief, focal Ca2+ transients, or an increase in global [Ca2+].

222 nce in length shortening (p = 0.001) but not Ca2+ transient (p = 0.052) was noted.

223 We were able to measure Ca2+ transients produced along terminals by both single

224 isometric force (a surrogate marker for the Ca2+ transient) recordings were obtained from superfused

225 Again, the corresponding Ca2+ transients remained similar.

226 However, both APs and Ca2+ transients remained synchronous after the applicati

227 translocation of SK1 to block the localized Ca2+ transients required for phagosome maturation.

228 Ca2+ sparks are short lived and localized Ca2+ transients resulting from the opening of ryanodine

229 acaine or acidosis, the initial phase of the Ca2+ transient results from Ca2+ release via RyRs direct

230 Ca2+ transients revealed an apparent increase in Ca2+ cl

231 In vivo imaging of muscle Ca2+ transients revealed that cytosolic Ca2+ decay was s

232 g was prevented by either suppression of the Ca2+ transient (ryanodine) or transiently increasing [Ca

233 The [Ca2+] transients showed abnormal 'breaks', decaying phas

234 s were used to measure action potentials and Ca2+ transients simultaneously from hundreds of epicardi

235 adenylyl cyclase with forskolin rescued the Ca2+ transient, SR Ca2+ content and SR Ca2+ uptake rate

236 he antagonist increased the amplitude of the Ca2+ transient, suggesting that PPARalpha receptors are

237 astroglia, which elicits spontaneous somatic Ca2+ transients, synaptogenic thrombospondin 1 (TSP-1) r

238 with field stimulation: large, rapid, global Ca2+ transients termed 'global Ca2+ flashes', and much s

239 erminal, distal boutons had larger single-AP Ca2+ transients than proximal ones, probably attributabl

240 nt pathway cannot be activated by the global Ca2+ transients that cause contraction at each heartbeat

241 om TTX, somatic AP commands evoked dendritic Ca2+ transients that declined steeply with distance.

242 are regulated under conditions of continual Ca2+ transients that mediate cardiac contraction during

243 The model shows how the Ca2+ transients that occur during LTD or LTP induction a

244 ing action potentials, and local, purinergic Ca2+ transients that represent Ca2+ entry through P2X re

245 A 450 mOsm hypertonic stress elicited 2-fold Ca2+ transients that were suppressed by the TRPV1-select

246 lin plus 10 mm caffeine elicited a cytosolic Ca2+ transient, the amplitude of which increased by 22%

247 ines potentially responsible for coordinated Ca2+ transients thought to mediate synaptic plasticity.

248 + loading and the amplitude of the cytosolic Ca2+ transient to enhance cardiac myocyte contractility.

249 ontent and therefore failure of the systolic Ca2+ transient to increase appropriately during beta-AR

250 Isoproterenol increased Ca2+ transients to a comparable amplitude in DM and WT.

251 racellular Ca2+ abolished neuronal cytosolic Ca2+ transients to exogenous glutamate or kainate, this

252 g in a transition from stable nonalternating Ca2+ transients to stable alternating Ca2+ transients.

253 entral nervous system can generate prominent CA2+ transients to various stimuli, a CA2+-dependent K+

254 must be mechanisms that focus intracellular Ca2+ transients towards the ANO1 channels.

255 Ca2+ transients trigger many SNARE-dependent membrane fu

256 LA-peptide did strongly enhance the central Ca2+ transients triggered by ICa at -30 mV (small ICa) b

257 , skeletal-type EC coupling and emergence of Ca2+ transients triggered by the Ca2+ current.

258 This broadening of Ca2+-transient voltage dependence could be prevented by

259 + current; 3), the voltage dependence of the Ca2+ transient was bell-shaped and the maximum was cente

260 onged caffeine exposure, the decrease of the Ca2+ transient was drastically slowed in KO versus WT my

261 either cell type, but the slow decay of the Ca2+ transient was faster in both cell types during lact

262 mulation frequency (1-8 Hz) but the systolic Ca2+ transient was maximal at 6 Hz.

263 bell-shaped voltage dependence of cytosolic Ca2+ transients was dramatically broadened due to activa

264 Also, the amplitude of single-AP Ca2+ transients was inversely correlated with bouton wid

265 er in pAF, but the decay of caffeine-induced Ca2+ transients was unaltered, suggesting increased SERC

266 The frequency of these 'purinergic Ca2+ transients' was increased about 7-fold by a 10 s st

267 Ca2+ transients were activated in rabbit ventricular cel

268 ally dominant negative): 1 microM ATP-evoked Ca2+ transients were augmented, and 100 nM ouabain-induc

269 Capsaicin-evoked Ca2+ transients were completely blocked by the vanilloid

270 (Kd=561 nM), single-action potential-evoked Ca2+ transients were discernable in most neurons with a

271 the spatial spread of the evoked purinergic Ca2+ transients were F/F(o) = 2.4 +/- 0.13, 111.7 +/- 9.

272 Spontaneous, short-lived, focal cytosolic Ca2+ transients were found for the first time and charac

273 the Ca2+ current; and 4), Ca2+ currents and Ca2+ transients were fully blocked by nifedipine.

274 Ca2+ transients were induced by field stimulation, squar

275 Myotubes were voltage-clamped, and Ca2+ transients were measured by confocal line-scan imag

276 Ca2+ transients were measured in ventricular myocytes us

277 In contrast, capsaicin-evoked Ca2+ transients were not attenuated by preincubation wit

278 Purinergic Ca2+ transients were not dependent on VDCC activity.

279 Action potential-dependent Ca2+ transients were recorded in neurons of all six laye

280 ked by brief somatic current injections, and Ca2+ transients were recorded in proximal basal dendrite

281 The contractions and Ca2+ transients were recorded optically with fura-2 load

282 Cytosolic and mitochondrial Ca2+ transients were recorded with digital photometry an

283 Ca2+ transients were significantly blocked by 1 mm lidoc

284 Nevertheless, the corresponding Ca2+ transients were similar, implying an increase in th

285 Cytosolic Ca2+ transients were simultaneously imaged using the flu

286 ration, as evidenced by the observation that Ca2+ transients were suppressed by iodoacetate but unaff

287 Spontaneous Ca2+ transients were suppressed by the inositol-1,4,5-tr

288 unctional conductance (Gj) between them, and Ca2+ transients were synchronous among neighboring muscl

289 In contrast, OAG-induced Ca2+ transients were unaffected by TRPC6 knockdown.

290 urarine decreased the frequencies of APs and Ca2+ transients, whereas blockade of muscle GABAA recept

291 y RNAi also reduced the synchrony of APs and Ca2+ transients, whereas expression of wild-type UNC-9 s

292 the oocyte for the generation of repetitive Ca2+ transients which trigger egg activation at fertilis

293 o alters the myofilament pH response and the Ca2+ transient, which could influence endothelin-mediate

294 s within stratum oriens/alveus elicited fast Ca2+ transients, which showed a steep sigmoidal relation

295 mic reticulum (SR) Ca2+ release by measuring Ca2+ transients with a low affinity indicator in the pre

296 ical field stimulation of the cornea, evoked Ca2+ transients with a magnitude that was proportional t

297 ncy of neuronal stimulation by intracellular Ca2+ transients, with a clear onset of astrocytic activa

298 The magnitudes of the ensuing Ca2+ transients within dendritic spines are thought to d

299 selectively abolished depolarization-evoked Ca2+ transients without affecting chemically induced act

300 and the subsequent increase in intracellular Ca2+ transients, without altering the receptor-mediated