ライフサイエンスコーパス: membrane depolarization

1 entry (SOCE) pathway and accompanied plasma membrane depolarization.

2 outer-membrane permeability and to determine membrane depolarization.

3 ted with increased incidence of CF EPSPs and membrane depolarization.

4 eads to prolonged Ca(2+) responses evoked by membrane depolarization.

5 ns to phenylephrine, accompanied by enhanced membrane depolarization.

6 itical for coupling glucose stimulation with membrane depolarization.

7 and then transduced to the beating cilia by membrane depolarization.

8 ses and behaviours associated with prolonged membrane depolarization.

9 sure ATP efflux and fluorescence to evaluate membrane depolarization.

10 on Ca(2+) influx rather than Na(+) influx or membrane depolarization.

11 ch mouse muscle cells subjected to depleting membrane depolarization.

12 l insulin amounts in response to K(+)-evoked membrane depolarization.

13 )-dependent process triggered in response to membrane depolarization.

14 ns through cellular membranes in response to membrane depolarization.

15 (2+) and K(+) channels that are activated by membrane depolarization.

16 d genes, where it promotes H3.3 loading upon membrane depolarization.

17 ncreased intracellular Na(+) and cell plasma membrane depolarization.

18 A-LTx was followed by a strong mitochondrial membrane depolarization.

19 channels conduct Ca(2+) ions in response to membrane depolarization.

20 bination of intracellular Ca(2+) release and membrane depolarization.

21 r activation potentiated Ca(2+) influx after membrane depolarization.

22 ed by reactive oxygen species generation and membrane depolarization.

23 ion, cytochrome c release, and mitochondrial membrane depolarization.

24 ore the channel can be opened in response to membrane depolarization.

25 um under physiological conditions leading to membrane depolarization.

26 nal plasticity, on the level and duration of membrane depolarization.

27 induced Ca(2+) release and its dependence on membrane depolarization.

28 ivation of a slowly developing and sustained membrane depolarization.

29 (v)1.2 and RyR2 to enhance responsiveness to membrane depolarization.

30 etrusor muscle to muscarinic stimulation and membrane depolarization.

31 ithin the voltage sensor domain (VSD) during membrane depolarization.

32 sport affects the duration of TPC1-dependent membrane depolarization.

33 th ER Ca(2+) leakage from the RyR and plasma membrane depolarization.

34 eostasis in excitable cells following plasma membrane depolarization.

35 leading to voltage sensor stabilization upon membrane depolarization.

36 croscopic calcium-current traces elicited by membrane depolarization.

37 ng gene induction, growth arrest, and plasma membrane depolarization.

38 taline-induced PH and correlated with plasma-membrane depolarization.

39 then release them in response to appropriate membrane depolarization.

40 pplication to the inhibition of subthreshold membrane depolarizations.

41 ants, environmental stressors trigger plasma membrane depolarizations.

42 ose-excited neurons, elevated glucose evoked membrane depolarization (11 mV) and an increase in membr

43 hila Schneider cells exhibited mitochondrial membrane depolarization, a 60% decrease in ATP levels, i

44 these 5 lncRNAs are closely associated with membrane depolarization, action potential conduction, co

45 an important way to the dominantly inherited membrane depolarization, action potential failure, flacc

46 )](i) induced by NMDA receptor activation or membrane depolarization activates AMPK in a CAMKK2-depen

47 Membrane depolarization activates voltage-dependent Ca(2

48 The resulting membrane depolarization activates voltage-dependent Ca(2

49 ivated glutamate receptors was the result of membrane depolarization activating voltage-dependent Ca2

50 centration- and time-dependent mitochondrial membrane depolarization, activation of caspases-3 and -7

51 uate the efficiency of the passive spread of membrane depolarization along TATS.

52 rom a resting to an active conformation upon membrane depolarization, altering the activity of the pr

53 lease (DCR) can induce arrhythmogenic plasma membrane depolarizations, although the mechanism respons

54 dow for postsynaptic excitation, controlling membrane depolarization amplitude and timing via subthre

55 dependent proton conductance is activated by membrane depolarization, an alkaline extracellular envir

56 chanisms, induced by transient mitochondrial membrane depolarization and activation of the metallopro

57 Inhibition of SLO2.1 leads to membrane depolarization and activation of voltage-depend

58 evoked [Ca2+]i transients in SCN neurons via membrane depolarization and activation of voltage-depend

59 of residual K(ATP) channel activity leads to membrane depolarization and an increase in action potent

60 Furthermore, Glu induced a plasma membrane depolarization and an intracellular Ca(2+) incr

61 Stimulation with NE induced membrane depolarization and an intracellular Ca2+ ([Ca2+

62 ndrial respiration and induced mitochondrial membrane depolarization and apoptosis in a subset (7/11,

63 cell lines and induced potent mitochondrial membrane depolarization and apoptosis when combined with

64 We conclude that TRPM7 influences diastolic membrane depolarization and automaticity in SAN indirect

65 in the brain, activates receptors coupled to membrane depolarization and Ca(2+) influx that mediates

66 can be dynamically regulated in response to membrane depolarization and Ca(2+)/calmodulin-dependent

67 Because mitochondrial membrane depolarization and calcium are known to activat

68 Increased secretion does require membrane depolarization and calcium influx but appears t

69 Exposure to 30 mm KCl to induce membrane depolarization and calcium influx increased exp

70 Experience-driven synaptic activity causes membrane depolarization and calcium influx into select n

71 ltimately led to apoptosis via mitochondrial membrane depolarization and caspase activation in endoth

72 , and Cav3.3) are activated by low threshold membrane depolarization and contribute greatly to neuron

73 nnels whose inhibition by cAMP is coupled to membrane depolarization and cortisol secretion through c

74 nnels, closing the conduction pathway during membrane depolarization and dynamically regulating neuro

75 in glucose leads to K(ATP) channel closure, membrane depolarization and electrical activity that cul

76 Changes in plasma membrane depolarization and elevated intracellular Na(+)

77 of BK channels typically requires coincident membrane depolarization and elevation in free cytosolic

78 tivation, leading to increased mitochondrial membrane depolarization and excitotoxic cell death.

79 ationship and antimicrobial mechanisms using membrane depolarization and fluorescent microscopy assay

80 o hydrogen peroxide, contributes to cellular membrane depolarization and HPV.

81 , which results in reduced responsiveness to membrane depolarization and in the other state H1a uncou

82 erol and thereby activates PKC, resulting in membrane depolarization and increased action potential f

83 ncy to the first evoked spike in response to membrane depolarization and increased the total number o

84 o the surface membrane of neurons can induce membrane depolarization and initiate an action potential

85 atio that blocks the KATP channel leading to membrane depolarization and insulin exocytosis.

86 nel activation, typically necessitating both membrane depolarization and interaction with membrane li

87 Membrane depolarization and intracellular Ca(2+) promote

88 K(+) channels (BK(Ca)) are activated by both membrane depolarization and intracellular Ca(2+).

89 in slices with Shiga toxin 2 evoked a strong membrane depolarization and intracellular calcium accumu

90 ented CaCC activity in PASMCs may potentiate membrane depolarization and L-type channel activation in

91 ochondrial fusion, is induced by Parkin upon membrane depolarization and leads to their degradation i

92 wever, SCN rhythmicity depends on sufficient membrane depolarization and levels of intracellular calc

93 normal beta cells, ETV4 was stabilized upon membrane depolarization and limited insulin secretion un

94 ctance K+ channels, which respond jointly to membrane depolarization and micromolar concentrations of

95 tivates closure of K(+) channels, leading to membrane depolarization and neuronal firing.

96 tivates closure of K(+) channels, leading to membrane depolarization and neuronal firing.

97 TNL1 KO mice to phenylephrine, KCl-dependent membrane depolarization and phorbol 12,13-dibutyrate (PD

98 PBCV-1 infection results in rapid host membrane depolarization and potassium ion release.

99 Surfactin treatment of these cells led to membrane depolarization and reduced ATP production.

100 e in a dose-dependent manner in part through membrane depolarization and rupture.

101 ons were not necessary to cause postsynaptic membrane depolarization and spiking.

102 ck the K(ATP) channel K(ir)6.2/Sur1, causing membrane depolarization and stimulating insulin secretio

103 GABA-induced membrane depolarization and the resulting activation of

104 gated potassium channels open in response to membrane depolarization and then inactivate within milli

105 ne proteins that results in endothelial cell membrane depolarization and then the activation of speci

106 where they contribute to local subthreshold membrane depolarization and thereby influence action pot

107 nferred by NO occurred through mitochondrial membrane depolarization and through a caspase-independen

108 SK-like potassium channel (K(B)) they induce membrane depolarization and thus neurosecretion.

109 rterial myocyte TMEM16A channels, leading to membrane depolarization and vasoconstriction.

110 by agonist-induced Ca(2+) release results in membrane depolarization and vasoconstriction.

111 (TRP) melastatin 4 (TRPM4) channels to cause membrane depolarization and vasoconstriction.

112 d or so between ON periods, characterized by membrane depolarization and wake-like tonic firing, and

113 that are considered responsible for the host membrane depolarization and, as a consequence, the efflu

114 s between the source of electric activation (membrane depolarization) and the load that cardiac tissu

115 y in the root apex, (2) greater salt-induced membrane depolarization, and (3) a higher reactive oxyge

116 plex I oxidative damage, mitochondrial inner membrane depolarization, and apoptotic neuronal death.

117 through decreased ENaC activity and enhanced membrane depolarization, and by elevating ROS production

118 Acyl-CoA levels, ATP/ADP increases, membrane depolarization, and Ca(2+) fluxes were all mark

119 ne increases their input resistance, induces membrane depolarization, and consequently augments their

120 hondrial respiration, elicited mitochondrial membrane depolarization, and disrupted mitochondrial mor

121 und to be defective in lysis, insensitive to membrane depolarization, and dominant to the wild-type a

122 isceral distension, induces channel opening, membrane depolarization, and initiation of pain signalin

123 chondrial membrane hyperpolarization, plasma membrane depolarization, and insulin secretion, when sti

124 nished glucose-induced actin reorganization, membrane depolarization, and insulin secretion.

125 lta346-347 did not cause cell vacuolation or membrane depolarization, and it was impaired in the abil

126 Nav channels are essential for metazoan membrane depolarization, and Nav channel dysfunction is

127 ochondria can compensate for damage, reverse membrane depolarization, and obviate mitophagy.

128 el of reactive oxygen species, mitochondrial membrane depolarization, and premature senescence in a p

129 ivating types of Ca2+ currents, take part in membrane depolarization, and strongly activate Ca2+-acti

130 t translates into transient calcium flux and membrane depolarization ( approximately 20 mV).

131 The elevation of intracellular Ca(2+) and membrane depolarization are both believed to be involved

132 on of RyR2, SR Ca(2+) leak and mitochondrial membrane depolarization are critically involved in the a

133 Retraction can be acutely reversed by membrane depolarization at E15.5, and the induced events

134 ical signal of neurotransmitter release into membrane depolarization at excitatory synapses in the br

135 g adaptation, parallel with modifications to membrane depolarization, ATP generation, and production

136 he plasma membrane potential and that plasma membrane depolarization blocks cellular uptake of N-acyl

137 Membrane depolarization, brain-derived neurotrophic fact

138 sarcomere contraction in response to plasma membrane depolarization, but whether there is a similar

139 d serine trigger transient Ca(2+) influx and membrane depolarization by a mechanism that depends on t

140 It is triggered upon membrane depolarization by entry of Ca(2+) via L-type Ca

141 KCNK3 antagonizes norepinephrine-induced membrane depolarization by promoting potassium efflux in

142 glycine-induced Cl(-) currents that promote membrane depolarization, Ca(2+) entry, and insulin secre

143 After membrane depolarization, Ca2+ channels first open but th

144 allow abnormal Na+ conductance, resulting in membrane depolarization, calcium influx, aldosterone pro

145 itor cell regulator neurogenin3 but requires membrane depolarization, calcium influx, and calcineurin

146 Thus, through Ser-513, membrane depolarization/calcium signaling controls a cri

147 Here we report that membrane depolarization can induce RyR-mediated local Ca

148 Plasma membrane depolarization can trigger cell proliferation,

149 NaV1.9 mutations that evoke small degrees of membrane depolarization cause hyperexcitability and fami

150 l neuropathy, while mutations evoking larger membrane depolarizations cause hypoexcitability and inse

151 Thus, membrane depolarization caused by early GABA excitation

152 The membrane depolarization caused by these pores activates

153 Membrane depolarization causes voltage-gated ion channel

154 This activation results in membrane depolarization, cessation of intracellular pept

155 at hyperpolarizing potentials, but not upon membrane depolarization compared with wild-type channels

156 euromuscular synapses are less responsive to membrane depolarization, compared to the wildtypes.

157 ntrations (</=2.5 ng/mL), causes substantial membrane depolarization concomitant with a several-fold

158 c input or simply a minimum level of overall membrane depolarization critical for integration.

159 cation of TRH caused concentration-dependent membrane depolarization, decreased input resistance, and

160 AT-101 also induced potent mitochondrial membrane depolarization (Delta Psi m) and apoptosis when

161 This synergy caused membrane depolarization, destruction of the cell wall, a

162 However, membrane depolarization did not induce an increase in in

163 in the S105 dimer, support a model in which membrane depolarization drives the transition of S105 fr

164 ant mode for neuronal excitation by inducing membrane depolarization due to Cl(-) efflux through GABA

165 While the increase in the peak membrane depolarization during coincident pre- and post-

166 However, the pattern of the membrane depolarization during singing, the fine dendrit

167 Stable membrane depolarization during wakefulness finally emerg

168 ent (I(Cat)) caused by Na(+) influx, induced membrane depolarization, elevated [Ca(2+)](i), and stimu

169 Additionally, we found DAT-induced membrane depolarization enhances plasma membrane localiz

170 Additionally, we found DAT-induced membrane depolarization enhances plasma membrane localiz

171 n mutant exhibits a high rate of spontaneous membrane depolarization events in dark conditions but re

172 At room temperature (20-25 degrees C) membrane depolarization evokes responses that saturate a

173 a transient inward current associated with a membrane depolarization followed by a prolonged outward

174 ergo a series of conformational changes upon membrane depolarization, from a down state when the chan

175 Membrane depolarization has been suggested, but never sh

176 ivation of NF-kappaB prevented mitochondrial membrane depolarization; however, when NF-kappaB activit

177 thode electrode is nominally associated with membrane depolarization/hyperpolarization, which cellula

178 Reversing the initial membrane depolarization improved motor function and Purk

179 extensive investigation of ion transport and membrane depolarization in a bacterial system.

180 ing revealed that hypoxia caused endothelial membrane depolarization in alveolar capillaries that pro

181 ting mechanisms that involve aggregation and membrane depolarization in bacteria and pore formation i

182 ore-operated Ca(2+) entry in fibroblasts and membrane depolarization in beta-cells.

183 NT-3 release instead of mature NT-3, whereas membrane depolarization in cerebellar granule neurons st

184 ts showed decreased hypoxia-induced cellular membrane depolarization in Cox4i2(-/-) PASMCs compared w

185 PsChR mediated sufficient light-induced membrane depolarization in cultured hippocampal neurons

186 ouabain or dihydro-ouabain) induced either a membrane depolarization in current clamp, or inward curr

187 e we show that Ca(2+) transients elicited by membrane depolarization in fiber segments with defective

188 FRD produced mitochondrial swelling and membrane depolarization in FRD-WT mice but not in FRD-S2

189 in intracellular mobilization of Ca(2+), and membrane depolarization in gliomas.

190 We show that whisker-evoked membrane depolarization in L2 PNs arises from highly spe

191 es was inhibited by CCCP and sucrose induced membrane depolarization in LjSUT4-expressing oocytes.

192 Furthermore, we found that membrane depolarization in murine heart mitochondria was

193 ever, at postnatal days 13-15, leptin causes membrane depolarization in NAG neurons, rather than the

194 CaCC with a single Ca(2+) occupancy requires membrane depolarization in order to open (C.J.P. et al.,

195 n II, endothelin-1, U46619, and K(+)-induced membrane depolarization in the presence of Ca(2+), which

196 y used as a biotechnological tool to control membrane depolarization in various cell types and tissue

197 that call duration is encoded by a sustained membrane depolarization in vocal prepacemaker neurons th

198 FRD produced mitochondrial membrane depolarization in WT mice but not in S2814A mic

199 ent-(+)-verticilide prevented arrhythmogenic membrane depolarizations in cardiomyocytes without signi

200 Mechanically induced membrane depolarizations in the ischemic region are the

201 n embryonic hearts leads to ventricular cell membrane depolarization, inability to generate action po

202 In response to a prolonged membrane depolarization, inactivation autoregulates the

203 Blockade of I(tonic) induced membrane depolarization, increased firing activity, and

204 Light activation of CRY is transduced to membrane depolarization, increased firing rate, and acut

205 atanoprost free acid and fluprostenol caused membrane depolarization; increased [cAMP](i), [cGMP](i),

206 is study, we defined the mechanisms by which membrane depolarization increases Ca(2+) sparks and subs

207 Membrane depolarization increases ciliary [Ca(2+)], but

208 Instead, we found that these agents cause membrane depolarization, indicating that the bacterial m

209 Estradiol increases membrane depolarization induced by GABA(A) receptor acti

210 Membrane depolarization-induced changes in [Ca2+]i were

211 nly knockdown of MEF2C significantly impairs membrane depolarization-induced expression of Bdnf exon

212 Here, we show that plasma membrane depolarization induces nanoscale reorganization

213 on for these antibiotics include cell lysis, membrane depolarization, inhibition of cell wall biosynt

214 Membrane depolarization initiates asynchronous movements

215 hemical coupling that reliably convert brief membrane depolarization into precisely timed intracellul

216 e in cellular excitability, amplifying small membrane depolarizations into action potentials.

217 nctions conduct ions between CMs, triggering membrane depolarization, intracellular calcium release,

218 ortant because the natural stimulus, surface membrane depolarization, is rapidly pulsatile.

219 support a model in which surfactin-mediated membrane depolarization maintains viability through slow

220 indicators that change color in response to membrane depolarization may offer a key advantage over t

221 inhibited C. difficile growth in vitro via a membrane depolarization mechanism.

222 During a membrane depolarization movement, the S4s in the voltage

223 We observed immediate cytoplasmic membrane depolarization, not seen with enterococci or me

224 e proton leakage and may explain the gradual membrane depolarization observed with daptomycin.

225 and Ca(2+) channel activation indicates that membrane depolarization occurs.

226 of an inhibitory FMRP antibody into BCs, or membrane depolarization of BCs, enhances GABA release in

227 tylation of histone H3 Lys27 (H3K27ac) after membrane depolarization of cortical neurons functions to

228 factor, Osteocrin (OSTN), that is induced by membrane depolarization of human but not mouse neurons.

229 The method may be used to detect membrane depolarization of sympathetic nerve fibres in h

230 Its function is essential to maintain membrane depolarization of the photoreceptors upon repet

231 efold increase in spike frequency and direct membrane depolarization of up to 22 mV (mean, 17.9+/-7.2

232 epolarize receptor cells and (2) Ca(2+) plus membrane depolarization opens ATP-permeable gap junction

233 leukemia cells did not undergo mitochondrial membrane depolarization or apoptosis despite a similar a

234 acellular Ca(2+) release in response to K(+)-membrane depolarization or caffeine stimulation, suggest

235 in most K(+) channels occurs upon sustained membrane depolarization or channel opening and then reco

236 enal cells and had reduced capacity to cause membrane depolarization or death of AZ-521 cells.

237 y calcium entry channels activated by plasma membrane depolarization or depletion of internal calcium

238 control cell volume by gating in response to membrane depolarization or hyperpolarization.

239 romol g(-1) h(-1), was not commensurate with membrane depolarization or increases in root respiration

240 olyamine antagonists had no effect on either membrane depolarization or modulation of NMDA receptors.

241 Changes in membrane depolarization, particularly action potentials,

242 shared early events, including mitochondrial membrane depolarization, permeability transition pore op

243 hosphatidylserine exposure and mitochondrial membrane depolarization, PMN-SA had sustained levels of

244 The Ca(2+) signal was elicited by membrane depolarization produced by a high K(+) (40 mM)

245 extensive and persistent changes, including membrane depolarization, prolonged elevation of intracel

246 are particularly sensitive to activation by membrane depolarization, raising the possibility that th

247 ly correlates with the preceding 20-25 ms of membrane depolarization rather than the depolarization a

248 ion channel inhibitor chromanol 293B caused membrane depolarization, redistribution of beta-catenin

249 Linked with plasma membrane depolarization, reduced endothelial-NOS express

250 This paradox arises because membrane depolarization reduces the amplitude of the act

251 on of c-Jun-N-terminal kinase, mitochondrial membrane depolarization, release of cytochrome c, and ac

252 of the Slo1 potassium channel transcripts by membrane depolarization requires a highly conserved CaMK

253 transverse or sagittal slices evoked a local membrane depolarization restricted to a radial wedge, bu

254 nitially normal, but is followed by abnormal membrane depolarization resulting from a reduction in po

255 Inhibition of the current promotes membrane depolarization, resulting in activation of Ca(2

256 We propose that membrane depolarization reversibly positions R3 next to

257 Interestingly, membrane depolarization simulations predict very differe

258 KCl-induced membrane depolarization stimulated release of dendritic

259 ncluding assays in model membrane liposomes, membrane depolarization studies, and scanning electron m

260 fatty acid depletion and was not affected by membrane depolarization, suggesting that lipids flow fro

261 pregulated genes, is closely correlated with membrane depolarization, suggesting their use as markers

262 els displayed open times that decreased with membrane depolarization, suggestive of a blocking mechan

263 ells but did cause a persistent subthreshold membrane depolarization that resulted in an immediate an

264 eoplastic agents tested caused mitochondrial membrane depolarization that was inhibited by vitamin C.

265 slow wave potentials (SWPs), damage-induced membrane depolarizations that activate the jasmonate (JA

266 ells treated with 16:1Delta9 exhibited rapid membrane depolarization, the disruption of all major bra

267 r, producing increased Na(+) conductance and membrane depolarization, the signal for aldosterone prod

268 Unitary potentials, small stochastic membrane depolarizations thought to underlie slow waves,

269 F-kappaB activity was inhibited, HBx induced membrane depolarization through modulation of the mitoch

270 with positive-going fluorescence response to membrane depolarization through rational manipulation of

271 izes to T tubules, is essential for coupling membrane depolarization to Ca(2+) release from the sarco

272 ltage-gated Ca(v)1.2 calcium channels couple membrane depolarization to cAMP response-element-binding

273 , intracellular calcium signaling that links membrane depolarization to contraction occurs in the abs

274 and Ca(V)2 channels, respectively, coupling membrane depolarization to CREB phosphorylation and gene

275 s (vas deferens, uterus and bladder) rely on membrane depolarization to drive Ca2+ influx across the

276 ndent K(+) channels that open in response to membrane depolarization to regulate cell excitability.

277 n many cell types, which open in response to membrane depolarization to regulate cell excitability.

278 receptor (NMDAR)-mediated currents depend on membrane depolarization to relieve powerful voltage-depe

279 together with photorelease of caged-Ca2+ and membrane depolarization to study exocytosis.

280 hypoxic signal is propagated as endothelial membrane depolarization to upstream arterioles in a Cx40

281 when activation of GABA(A) receptors causes membrane depolarization, tonic activation of GABA(A) rec

282 Here we report that membrane depolarization triggered IKC intracellular sign

283 on which evokes Ca(2+) influx through plasma membrane depolarization, triggering insulin vesicle exoc

284 Activation of CCR2 by MCP-1 elicits membrane depolarization, triggers action potentials and

285 ance and function decreased, suggesting that membrane depolarization uncouples WNK kinases from NCC.

286 distinguished by activation only at extreme membrane depolarization (V(50) ~ +75 mV), in contrast to

287 Light-activated CRY couples to membrane depolarization via a well conserved redox senso

288 thermore, many K2P channels are activated by membrane depolarization via an SF-mediated gating mechan

289 at OPCs exhibited Ca(2+) influx after plasma membrane depolarization via L-type VOCCs.

290 NT/D entry and intoxication were enhanced by membrane depolarization via synaptic vesicle cycling, wh

291 Mitochondrial membrane depolarization was detected in flavopiridol-tre

292 d and stable nisin-like pores, however, slow membrane depolarization was observed after NAI-107 treat

293 As a result, light-evoked membrane depolarization was strongly reduced and spike i

294 d S4 helices, can drive channel opening with membrane depolarization when transplanted from an archae

295 leads to K(ATP) channel closure, triggering membrane depolarization, whereas in glucose-inhibited ne

296 arly applied LPI produces Ca(2+)-independent membrane depolarization, whereas the Ca(2+) signal induc

297 PAF26 also induced plasma membrane depolarization which, however, was independent

298 was the case for the mechanistically linked membrane depolarization, which occurs within several sec

299 What does it take for cells to respond to membrane depolarization with Ca(2+) sparks?

300 es Opa1, is regulated by short pulses of the membrane depolarization without affecting the overall me