ライフサイエンスコーパス: membrane depolarization

1 eostasis in excitable cells following plasma membrane depolarization.

2 ch mouse muscle cells subjected to depleting membrane depolarization.

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

4 ns through cellular membranes in response to membrane depolarization.

5 (2+) and K(+) channels that are activated by membrane depolarization.

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

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

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

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

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

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

12 ed by reactive oxygen species generation and membrane depolarization.

13 leading to voltage sensor stabilization upon membrane depolarization.

14 croscopic calcium-current traces elicited by membrane depolarization.

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

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

17 um under physiological conditions leading to membrane depolarization.

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

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

20 ivation of a slowly developing and sustained membrane depolarization.

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

22 etrusor muscle to muscarinic stimulation and membrane depolarization.

23 (L) that were accompanied with mitochondrial membrane depolarization.

24 e primary effect of activating TRPC6 will be membrane depolarization.

25 riggering of the holin and is accelerated by membrane depolarization.

26 n the rat retina does not depend on VGCCs or membrane depolarization.

27 erpolarizing currents (P < 0.01), indicating membrane depolarization.

28 n of chloride channels substantially reduced membrane depolarization.

29 epolarization and an enhanced rate of plasma membrane depolarization.

30 y a small but significant amount after gross membrane depolarization.

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

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

33 then release them in response to appropriate membrane depolarization.

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

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

36 ns to phenylephrine, accompanied by enhanced membrane depolarization.

37 itical for coupling glucose stimulation with membrane depolarization.

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

39 ses and behaviours associated with prolonged membrane depolarization.

40 sure ATP efflux and fluorescence to evaluate membrane depolarization.

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

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 Trypanosome membrane depolarization abolished the toxicity of defens

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

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

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

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

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

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

60 g glucose and certain amino acids, result in membrane depolarization and Ca(2+) entry through voltage

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

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

63 Because mitochondrial membrane depolarization and calcium are known to activat

64 oxic inhibition of potassium channels causes membrane depolarization and calcium entry through L-type

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

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

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

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

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

70 -dependent and associated with mitochondrial membrane depolarization and cytochrome c release indicat

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

72 Indo-1 revealed FimH-dependent mitochondrial membrane depolarization and elevated [Ca(2+)](in), respe

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

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

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

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

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

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

79 inhibition of alpha3NKA activity results in membrane depolarization and increased action potential f

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

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

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

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

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

85 gnaling by coupling channel activity to both membrane depolarization and intracellular Ca(2+) signali

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

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

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

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

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

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

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

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

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

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

96 K+ current [IK(M)] activates in response to membrane depolarization and regulates neuronal excitabil

97 pse that operates independently of VGCCs and membrane depolarization and reveal a previously unknown

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

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

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

101 the oxidizing agents decreased acid-induced membrane depolarization and the intracellular Ca2+ accum

102 GABA-induced membrane depolarization and the resulting activation of

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

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

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

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

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

108 process that limits channel function during membrane depolarization and thus shapes the action poten

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 id-induced increase of intracellular Ca(2+), membrane depolarization, and acidosis-mediated neuronal

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

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

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

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

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 ing to a raised cGMP level which then causes membrane depolarization, apparently by directly engaging

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

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

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

134 GF165-mediated rise in cytosolic calcium and membrane depolarization are eliminated by inhibitors of

135 whereas functional transport was ranked in a membrane depolarization assay.

136 In planar lipid bilayer and membrane depolarization assays, VacA proteins containing

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

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

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

140 Glucose triggers membrane depolarization both by closing ATP-sensitive po

141 Membrane depolarization, brain-derived neurotrophic fact

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

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

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

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

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

147 ecifically, in cardiac muscle following cell membrane depolarization, Ca(v)1.2 activates cardiac RyR

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

149 um channel)-like channels, leading to plasma membrane depolarization, Ca2+ influx, and increased chem

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

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

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

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

154 Plasma membrane depolarization can trigger cell proliferation,

155 Low MOI reduced mitochondrial membrane depolarization, caspase-3 and caspase-9 activat

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

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

158 Thus, membrane depolarization caused by early GABA excitation

159 The membrane depolarization caused by these pores activates

160 Membrane depolarization causes voltage-gated ion channel

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

162 ted a 2-fold increase in resting calcium and membrane depolarization compared with nontransgenic litt

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

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

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

166 subexcitability was normal, and the signs of membrane depolarization correlated with raised serum bic

167 or Na(V)1.8 sodium channels was increased by membrane depolarization, corresponding IC(50) values for

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

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

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

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

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

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

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

175 a root plasma membrane resulted in a smaller membrane depolarization during salt exposure, thus allow

176 Stable membrane depolarization during wakefulness finally emerg

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

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

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

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

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

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

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

184 Membrane depolarization has been suggested, but never sh

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

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

187 Reversing the initial membrane depolarization improved motor function and Purk

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 Mechanically induced membrane depolarizations in the ischemic region are the

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

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

211 Membrane depolarization increased Ca2+ influx via low-ac

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

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

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

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

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

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

218 transduced with QHGAD67 was not increased by membrane depolarization induced by 60 mM extracellular K

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

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

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

222 Membrane depolarization initiates asynchronous movements

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

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

225 e of extracellular Na+ ions, suggesting that membrane depolarization is not a prerequisite for this e

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

227 The chronic membrane depolarization may contribute to the developmen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 Changes in membrane depolarization, particularly action potentials,

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

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

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

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

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

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

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

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

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

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

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

257 s led to P2Y receptor stimulation along with membrane depolarization, resulting from increases in ATP

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

259 We propose that membrane depolarization reversibly positions R3 next to

260 Interestingly, membrane depolarization simulations predict very differe

261 KCl-induced membrane depolarization stimulated release of dendritic

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

263 rneurons in CA1 stratum radiatum and induced membrane depolarization suggesting that TRH increases th

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

265 tely 100-fold when preventing TRPM4-mediated membrane depolarization, suggesting that the BTP2-mediat

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

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

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

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

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

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

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

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

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

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

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

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

278 oltage-gated calcium channels (VGCCs) couple membrane depolarization to neurotransmitter release, fee

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

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

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

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

283 The membrane depolarization triggered by Glu was greatly red

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

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

286 nal amplification via calcium permeation and membrane depolarization, TRP channels appear well adapte

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

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

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 hat their facilitation by BTP2 supports cell membrane depolarization, which reduces the driving force

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