ライフサイエンスコーパス: membrane potential

1 ecies or depolarization of the mitochondrial membrane potential.

2 ndrial biogenesis and restores mitochondrial membrane potential.

3 , again recapitulating two levels of resting membrane potential.

4 erve respiration capacity, and mitochondrial membrane potential.

5 ntermembrane space, sustaining mitochondrial membrane potential.

6 and even cellular properties, such as pH and membrane potential.

7 function by inducing a loss of mitochondrial membrane potential.

8 assium channels are opened by ligands and/or membrane potential.

9 simulate Ca(2+) oscillations and changes in membrane potential.

10 No differences were observed in baseline membrane potential.

11 ns are strongly modulated by the prestimulus membrane potential.

12 enetically distant species by altering their membrane potential.

13 Q and VGSC conductances in the regulation of membrane potential.

14 e cell membrane balance, determining resting membrane potential.

15 er analytes, and physical parameters such as membrane potential.

16 ethyl ester (TMRE) reports on mitochondrial membrane potential.

17 nger duration changes in synovial fibroblast membrane potential.

18 t pH accompanying light-evoked changes in HC membrane potential.

19 ondria, and parasites retained mitochondrial membrane potential.

20 enced by intracellular ATP concentration and membrane potential.

21 us firing rate without affecting the resting membrane potential.

22 drial membrane that contribute to control of membrane potential.

23 fluorophore microenvironment depended on the membrane potential.

24 naptic cleft pH in response to changes in HC membrane potential.

25 ependent ion channels is gated by changes in membrane potential.

26 teins, and SIRT3 is required for recovery of membrane potential.

27 electron transfer and overcome a barrier of membrane potential.

28 NT1, despite greater losses of mitochondrial membrane potential.

29 channels recapitulate two levels of resting membrane potential.

30 t potentials match the two levels of resting membrane potential.

31 ansporter function in response to changes in membrane potential.

32 ctive cationic channels which depolarize the membrane potential.

33 1 and K2P1 channels to two levels of resting membrane potential.

34 activity may be secondary to altered resting membrane potential.

35 nsport and are critical for establishing the membrane potential.

36 ed mitochondrial DNAs and the maintenance of membrane potential.

37 -1 and disrupts mitochondrial morphology and membrane potential.

38 c ICC that might contribute to regulation of membrane potential.

39 tabolism, ultimately impacting mitochondrial membrane potential.

40 rrents, reconstituting two levels of resting membrane potential.

41 probability density distribution of neuronal membrane potentials.

42 , altering plasma membrane and mitochondrial membrane potentials.

43 t more negative and physiologically relevant membrane potentials.

44 ge dependence of TRPA1 towards more negative membrane potentials.

45 significant as it occurs at extreme positive membrane potentials.

46 a generate large hyperpolarizing currents at membrane potentials above the Nernst equilibrium potenti

47 ental work, we show that the oscillations in membrane potential accompanying the calcium oscillations

48 d 1 also prevented the loss of mitochondrial membrane potential, adenosine triphosphate production, a

49 e:glycerol-3-phosphate ratio), mitochondrial membrane potential, ADP, Ca(2+), 1-monoacylglycerol, dia

50 trongly on its onset potential, and that the membrane potential after the AP (Vafter) was close to th

51 lectrophysiology suggest that changes in the membrane potential alone, a universal yet dynamic cellul

52 larger cells experience a greater degree of membrane potential alteration.

53 illations are accompanied by oscillations in membrane potential, although the membrane potential osci

54 in MCF-7 cells, including the mitochondrial membrane potential analysis and the caspase-9 activity.

55 ate conditions and with dynamically changing membrane potential and [Ca(2+) ]i during an AP.

56 functional mitochondria characterized by low membrane potential and a high level of reactive oxygen s

57 eurons showed impaired maturation of resting membrane potential and action potential firing, decrease

58 ic synaptic inputs on thalamocortical neuron membrane potential and allow these synapses to act as sy

59 bypasses CI and supports electron transport, membrane potential and ATP production.

60 In particular, Kv1.3 channels regulate the membrane potential and Ca(2+) influx in human effector m

61 nnels regulate peptide release by modulating membrane potential and calcium levels.

62 rms like G-protein coupled receptor pathway, membrane potential and cation transport.

63 xacerbate the initial effects of chilling on membrane potential and cellular function, and these pert

64 actococcus lactis catalyses drug efflux in a membrane potential and chemical proton gradient-dependen

65 Measurement of membrane potential and contraction indicated that ANO1 a

66 cardiac macrophages have a negative resting membrane potential and depolarize in synchrony with card

67 abolites, as well as decreased mitochondrial membrane potential and deranged mitochondrial ultra-stru

68 ion of reactive oxygen species (ROS) reduces membrane potential and disrupts membrane integrity, caus

69 into the channels that regulate the resting membrane potential and electrical activity of retinal ce

70 Activation of neurons not only changes their membrane potential and firing rate but as a secondary ac

71 gs new thinking about regulation of lysosome membrane potential and function.

72 Arg2-deficient mice had lower mitochondrial membrane potential and greater HIF-2alpha than WT animal

73 I inhibition resulted in lower mitochondrial membrane potential and higher cytosolic ROS production.

74 evoked large depolarizations of the resting membrane potential and impaired action potential generat

75 assium currents that act to regulate resting membrane potential and levels of cellular excitability.

76 rome bd oxidase) is capable of maintaining a membrane potential and menaquinol oxidation in the prese

77 ing that ROS, and their subsequent impact on membrane potential and metabolism, may play a broad role

78 mitochondrial dysfunction, including reduced membrane potential and mitochondrial content.

79 al content increases linearly, mitochondrial membrane potential and oxidative phosphorylation are hig

80 rast, SbSUT5 Suc affinity was independent of membrane potential and pH but supported high transport r

81 hannel that is important for maintaining the membrane potential and pH stability in lysosomes.

82 The Suc affinity of SbSUT1 was dependent on membrane potential and pH.

83 optimal, reciprocal indirect regulation via membrane potential and PIP2, especially within the speci

84 ondrial fragmentation, loss of mitochondrial membrane potential and production of reactive oxygen spe

85 Transient changes of mitochondrial membrane potential and reactive oxygen species ROS produ

86 ion (chill coma) that is caused by decreased membrane potential and reduced excitability of the neuro

87 ne was associated with loss of mitochondrial membrane potential and reduced protein expression of Mfn

88 rally play a key role in setting the resting membrane potential and regulate the response of excitabl

89 ealed by electron microscopy, and had higher membrane potential and respiratory activity.

90 lded protein response, loss of mitochondrial membrane potential and sensitivity to mitochondrial remo

91 miting depolarization of the horizontal cell membrane potential and suggest actions of these channels

92 lay of the plasma membrane ion transporters, membrane potential and the consumption of energy for mai

93 tophagy failure reflected in the recovery of membrane potential and the decrease of PINK1 and mitocho

94 mechanism prevents collapse of mitochondrial membrane potential and the subsequent release of mitocho

95 PITX2 mRNA modulates atrial resting membrane potential and thereby alters the effectiveness

96 h is likely to hyperpolarize the myocellular membrane potential and thus reduces their spontaneous ac

97 DCA treatment restored cardiac mitochondrial membrane potential and tissue ATP in the rats following

98 ed with cell excitability through changes in membrane potential and with water secretion.

99 Oscillators had lower mitochondrial membrane potentials and budded more slowly than non-osci

100 Whereas not affecting cardiomyocyte membrane potentials and cardiomyocyte-cardiomyocyte gap

101 accumulating in the synaptic cleft modulated membrane potentials and extended the range of informatio

102 to generate an ultrasensitive indicator for membrane potentials and foreshadow targeted drug synthes

103 bolic responsiveness (NAD(P)H, mitochondrial membrane potential), and signal transduction (H2O2 and c

104 al fragmentation, reduction in mitochondrial membrane potential, and a significant loss of mitochondr

105 aldehyde levels, disruption of mitochondrial membrane potential, and ATP decline.

106 sed excitability by depolarizing the resting membrane potential, and decreasing the latency of action

107 itochondrial motility, reduced mitochondrial membrane potential, and diminished mitochondrial respira

108 lts in decreased respiratory growth, reduced membrane potential, and hampered respiration, as well as

109 in mitochondrial trafficking, mitochondrial membrane potential, and mitochondrial bioenergetics.

110 ted mitochondria and increased mitochondrial membrane potential, and RNA-sequencing analysis indicate

111 function, restoring dissipated mitochondrial membrane potential, and thus cell energy and metabolism,

112 ge dependence of TRPA1 towards more negative membrane potentials, and is therefore intrinsic to the T

113 s small neurons had more depolarized resting membrane potentials, and required smaller current inject

114 of O2(*-), O2 consumption, and mitochondrial membrane potential as well as significantly decreased (4

115 ing a combination of (14)C-citrate uptake, a membrane potential assay and electrophysiology.

116 cardiomyocytes exhibit two levels of resting membrane potential at subphysiological extracellular K(+

117 s independent of the effect of mitochondrial membrane potential but dependent on acidification of the

118 annel gating is not directly mediated by the membrane potential but rather by the direction and ampli

119 a-cell peak outward K(+) current at positive membrane potentials, but also left-shifted its voltage d

120 s couple intracellular signaling pathways to membrane potential by providing Ca(2+) ions as second me

121 because of hyperpolarization of the baseline membrane potential by the Na(+)/K(+) pump, balanced by a

122 At low concentrations, the difference in membrane potentials can be too small for reliable potent

123 SLO3 K(+) channels are responsible for these membrane potential changes critical for fertilization in

124 dependently of potassium channel regulation, membrane potential changes or changes in cell-cycle dist

125 erse-axial tubular system (TATS), propagates membrane potential changes to the cell core, ensuring sy

126 red in the conformational changes induced by membrane potential changes.

127 nts synaptic drive by depolarizing the basal membrane potential close to the action potential thresho

128 MP-Red-Dye exhibited depolarized equilibrium membrane potentials compared with GABAAR-null cells.

129 ns, the Nalcn current influences the resting membrane potential, contributes to maintenance of stable

130 Because mitochondrial membrane potential controls calcium homeostasis, and AMP

131 lectrical coupling ensures slow subthreshold membrane potential correlations by equalizing membrane p

132 by monitoring the changes in mitrochondrial membrane potential, cytochrome c leakage, activation of

133 s physiological impacts on neurons including membrane potential, cytosolic Ca(2+) and synaptic vesicl

134 CXCL12 depolarized the resting membrane potential, decreased the rheobase, and increase

135 a direct link between loss of mitochondrial membrane potential (DeltaPsi) and mitophagy has not been

136 Although the membrane potential (Deltapsi) is considered to drive tra

137 The mitochondrial membrane potential (DeltaPsi), a component of Deltap, dr

138 Mitochondrial membrane potential (DeltaPsi), cell viability, reactive

139 The generation of a membrane potential (Deltapsi), the major constituent of

140 Heterogeneity of the mitochondrial membrane potential (Deltapsi), which is central to organ

141 light-dependent control of the mitochondrial membrane potential (Deltapsim) and coupled mitochondrial

142 in the absence of glycolysis, mitochondrial membrane potential (DeltaPsim) of EM cells declined and

143 duces rapid dissipation of the mitochondrial membrane potential (DeltaPsim) that is accompanied by th

144 dria into autophagy without collapsing their membrane potential (DeltaPsim).

145 onic mechanisms of the two levels of resting membrane potential, demonstrating a previously unknown m

146 Transport by the uniporter is membrane potential dependent and sensitive to ruthenium

147 Cell Metabolism, Logan et al. (2016) exploit membrane potential-dependent mitochondrial accumulation

148 Succinate-induced, membrane potential-dependent reverse electron transfer s

149 changes in mossy fibre input rate that drive membrane potential depolarisation and high-frequency bur

150 ppears to attenuate ERG currents, leading to membrane potential depolarization and increased input re

151 eocortical sub- and suprathreshold dendritic membrane potential (DMP) from putative distal-most dendr

152 induced apoptosis via loss in mitochondrial membrane potential, down-regulated autophagy, and inhibi

153 ffects of abrupt increases in calcium ion on membrane potential during reperfusion.

154 Fluorometric imaging plate reader membrane potential dye (FMP-Red-Dye) is a proprietary to

155 , (2) that more complex models with detailed membrane potential dynamics are necessary for simulation

156 s that allow us to simultaneously record the membrane potential dynamics of a large population of neu

157 extracellular recordings to characterize the membrane potential dynamics of identified CA1 pyramidal

158 d PYRs were depolarizing and entrained their membrane potential dynamics regardless of the presence o

159 had spatially uniform effects on place cell membrane potential dynamics, substantially reducing spat

160 hypoxia at different levels of resting cell membrane potential (Em ).

161 e range of hypoxia at different resting cell membrane potential (Em ).

162 SD imaging enabled simultaneous recording of membrane potential events from almost all of the identif

163 block of BKCa current increased depolarizing membrane potential excursions, raising the average resti

164 tal cells, BKCa channels subdue depolarizing membrane potential excursions, reduce the average restin

165 ular events, such as a loss in mitochondrial membrane potential, externalization of phosphatidylserin

166 Kv1.3, regulating the membrane potential, facilitates downstream Ca(2+) -depen

167 gating of CaV1.3 channels at quite negative membrane potentials, facilitating the regulation of neur

168 axons in an all-or-none manner, subthreshold membrane potential fluctuations at the soma affect neuro

169 neurons within clusters, in which increased membrane potential fluctuations facilitated the initiati

170 embrane potential correlations by equalizing membrane potential fluctuations, such that coupled neuro

171 nger synaptic inputs and displayed increased membrane potential fluctuations.

172 ccelerates the recovery of the mitochondrial membrane potential following mitochondrial uncoupling.

173 At the membrane potential for maximal SNR, the amplitude of eac

174 and can simultaneously record intracellular membrane potentials from hundreds of connected in vitro

175 rized by a relatively hyperpolarized resting membrane potential, higher spontaneous and induced actio

176 l-driven eCB release leads to a long-lasting membrane potential hyperpolarization in hippocampal prin

177 l role in osmoregulation, pH homeostasis and membrane potential in all domains of life.

178 ompanied by increased synaptic mitochondrial membrane potential in both wt and Tg2576 mice.

179 rrents, reconstituting two levels of resting membrane potential in cardiomyocytes.

180 where they bind to ankyrin-G and coregulate membrane potential in central nervous system neurons.

181 optical perturbation and optical readout of membrane potential in diverse cell types.

182 rrents, accounting for two levels of resting membrane potential in human cardiomyocytes and demonstra

183 2) identifying regions of high mitochondrial membrane potential in live animals, (3) monitoring regio

184 tive stress level and impaired mitochondrial membrane potential in motor neurons affected by SMA.

185 unction revealed a decrease in mitochondrial membrane potential in mutant Hsp27 expressing motor axon

186 drial NADH levels and restored mitochondrial membrane potential in p62-deficient cells.

187 t PA stimulation decreased the mitochondrial membrane potential in podocytes and induced podocyte apo

188 l azoles, which was attributed to an altered membrane potential in the mutant strain.

189 neuronal Ca(2+) responses and mitochondrial membrane potential in these nerve tissues.

190 ) leak current that affects the steady state membrane potential in VP neurons.

191 and superoxide levels, as well as increased membrane potential, increased respiratory dehydrogenase

192 tes, we generated mutant proteins catalysing membrane potential-independent dye efflux by removing on

193 1 (K2P1) recapitulate two levels of resting membrane potential, indicating the contributions of Kir2

194 successfully predicting the dynamics of the membrane potential induced by 20-50 different current pr

195 xidative stress and decline in mitochondrial membrane potential induced by T-2 toxin and/or DON.

196 -dependent, dissipation of the mitochondrial membrane potential, inhibition of the mitochondrial tran

197 ecies, emerges through the transformation of membrane potential into intracellular calcium concentrat

198 Loss of mitochondrial membrane potential is accompanied by reduced juxtapositi

199 Regulation of membrane potential is complicated because SMC are electr

200 The JC-1 staining shows the mitochondrial membrane potential is decreased after the treatment.

201 however, unlike pathological fragmentation, membrane potential is maintained and regulators of mitop

202 ss of KCNQ2 channel activity at subthreshold membrane potentials is sufficient to drive large changes

203 ic reactivation, visualized by presence of a membrane potential, is immediate upon rehydration.

204 cells, such as dynamics of ion channels and membrane potentials, is useful and essential in the stud

205 mPTP opening decreases the mitochondrial membrane potential leading to the activation of Ca(2+)-i

206 ablation or loss-of-function at subthreshold membrane potentials leads to increased neuronal excitabi

207 poptotic population elevation, mitochondrial membrane potential loss, increase of cytosolic cytochrom

208 Resting membrane potential measured using intracellular microele

209 The membrane potential method used for pore size measurement

210 S13C was associated with lower mitochondrial membrane potential, mitochondrial fragmentation, increas

211 in, histone H3, alpha tubulin, mitochondrial membrane potential, mitochondrial mass, cell cycle arres

212 Blue/green reduced mitochondrial membrane potential (MMP) and lowered intracellular pH, w

213 ulation depth increases and slow down as the membrane potential modulation depth decreases.

214 es such that their responses speed up as the membrane potential modulation depth increases and slow d

215 pproach used, and the cell and mitochondrial membrane potentials, more than 1000-fold higher mitochon

216 n balances synaptic excitation and maintains membrane potential near spike threshold.

217 y currents was voltage sensitive, peaking at membrane potentials near resting potential.

218 nt contributed to the more depolarized basal membrane potential observed in VP neurons in the high sa

219 the inward tail current (Cl(-) efflux) at a membrane potential of -100 mV due to the lowered outward

220 xternal calcium concentration of 1 mM, and a membrane potential of -20 mV, we found that the average

221 red outward current (gluconate(-) influx) at membrane potential of 100 mV.

222 Intracellular recording revealed a resting membrane potential of approximately -70 mV.

223 e bacterial channel MscS, leads to increased membrane potential of Arabidopsis mitochondria under spe

224 hCSF did not affect the resting membrane potential of CA1 interneurons but caused depola

225 Conversely, macrophages render the resting membrane potential of cardiomyocytes more positive and,

226 annels primarily maintain the normal resting membrane potential of cardiomyocytes.

227 ir2) channels primarily maintain the resting membrane potential of cardiomyocytes.

228 In this study, the membrane potential of CV was manipulated while crawling

229 otassium emitted from the biofilm alters the membrane potential of distant cells, thereby directing t

230 psins are widely used to modulate the plasma membrane potential of excitable cells, mitochondria have

231 Interestingly, NCX1/3 regulated membrane potential of HCT116 cells only when alpha1D was

232 rrents, accounting for two levels of resting membrane potential of human cardiomyocytes.

233 provide a method to study changes of axonal membrane potential of human sympathetic nerve fibres in

234 voltage input is substantial and boosts the membrane potential of intraretinal blood vessels to a su

235 increased oxidative stress and decreased the membrane potential of mitochondria in SNc dopaminergic n

236 mps maintain ionic gradients and the resting membrane potential of neurons, but increasing evidence s

237 their biophysical properties and the resting membrane potential of smooth muscle.

238 MnSOD rescued mitochondrial redox status and membrane potential of SNc dopaminergic neurons from Sirt

239 in a fluorescently detectable change in the membrane potential of the acceptor vesicles.

240 normal culture conditions, the mitochondrial membrane potential of the probands' fibroblasts was inta

241 otassium currents, and increased the resting membrane potential of these neurons.

242 ve and speed-sensitive graded changes in the membrane potential of these non-spiking cells.

243 ABSTRACT: Membrane potentials of gastrointestinal muscles are impo

244 cently were bacteria shown to modulate their membrane potential on the timescale of seconds, and litt

245 ning and then recovers during hyperpolarized membrane potentials or channel closure.

246 m ([Ca(2+)]i) and recovered with depolarized membrane potentials or elevated [Ca(2+)]i Constitutively

247 inactivation occurred during hyperpolarized membrane potentials or with decreased intracellular calc

248 llations in membrane potential, although the membrane potential oscillations are too small to generat

249 dulates TPC2 activity to control melanosomal membrane potential, pH, and regulate pigmentation.

250 rents were maximal at +50 mV and declined at membrane potentials positive to this value.

251 ese mice neuronal mitochondria have abnormal membrane potentials, produce elevated levels of reactive

252 leads to a hyperpolarization of the neuron's membrane potential, providing an important component of

253 eas blocking P2Y12 receptors does not affect membrane potential, ramification, or surveillance.

254 Subthreshold changes in membrane potential recorded from single neurons discrimi

255 Whole-cell membrane potential recordings and silicon probe recordin

256 licylate-induced ROS cause a decrease in the membrane potential, reduce metabolism and lead to an inc

257 channels with apamin depolarized the resting membrane potential, reduced resting conductance, and aff

258 Previously, we reported that mitochondrial membrane potential regulates STING-dependent IFN-beta in

259 maintaining the ionic gradients and resting membrane potential required for generating action potent

260 Neuronal membrane potential resonance (MPR) is associated with su

261 input resistance and hyperpolarized resting membrane potential, respectively.

262 This in turn led to abnormal mitochondrial membrane potential, respiratory chain activity and morph

263 asurements of mitochondrial Ca(2+) handling, membrane potential, respiratory rate and production of r

264 undown of inhibitory SK responses at resting membrane potentials (RMPs) reflects depletion of intrace

265 ation of VMH GI neurons in low glucose using membrane potential sensitive dye in vitro was measured b

266 on in vitro, while in vivo recordings reveal membrane potential signatures consistent with recruitmen

267 ction with concomitant loss of mitochondrial membrane potential, SIRT3 dissociates.

268 stolic potential, and rates of change of the membrane potential such as the diastolic depolarization

269 ding time intervals such as the AP duration, membrane potentials such as the maximum diastolic potent

270 hances the channel activity at physiological membrane potentials, suggesting that PIP2 exerts a tonic

271 tor coordination and exhibit oscillations in membrane potential that are subthreshold for spiking.

272 ast recovery from depression and an inter-AP membrane potential that minimizes changes on the next AP

273 homa cells exhibited a reduced mitochondrial membrane potential that resulted in an irreversible disi

274 tivity of ANO1 is rather low and at negative membrane potentials the channel requires several micromo

275 nsducing sound energy into graded changes in membrane potentials, the so called "receptor potentials.

276 both hyperpolarized and depolarized resting membrane potentials; these depolarized potentials cause

277 , by targeting damaged mitochondria with low membrane potential to mitophagy.

278 t-voltage relationships, causing the resting membrane potential to spontaneously jump from hyperpolar

279 fective since they did not modulate the cone membrane potential to the same extent.

280 ation promotes calcium entry at subthreshold membrane potentials to rapidly refill calcium stores, th

281 tant fibroblasts exhibit lower mitochondrial membrane potential, uncoupled respiration, and reduced A

282 the establishment and maintenance of resting membrane potentials upon which action potentials are gen

283 e the ability to bidirectionally control the membrane potential using depolarizing and hyperpolarizin

284 dria or by increasing maternal mitochondrial membrane potential using oligomycin.

285 e activates inward current which depolarizes membrane potential (Vm) and can trigger action potential

286 Low-frequency membrane potential (Vm) oscillations were once thought t

287 ion making.SIGNIFICANCE STATEMENT A neuron's membrane potential (Vm) strongly shapes how information

288 [K(+)]e is independent of changes in plasma membrane potential (Vm), it requires an increase in intr

289 nt Ca(2+) imaging and measurement of resting membrane potential (Vm).

290 ) agonist, was used to modulate cell resting membrane potential (Vmem) according to methods described

291 However, upon H2O2 exposure, the membrane potential was significantly elevated in cells h

292 put conductance and synaptic fluctuations in membrane potential was suggested to originate from inten

293 Intracellular calcium and membrane potential were evaluated in endothelial cell tu

294 Furthermore, genes involved in regulating membrane potentials were constitutively expressed only i

295 y MSL1 leads to dissipation of mitochondrial membrane potential when it becomes too high.

296 cium stores, and run down rapidly at resting membrane potentials when calcium stores become depleted.

297 y transmitter glutamate depends primarily on membrane potential, which would drive non-vesicular effl

298 chemistry, and their use as tools to control membrane potential with light is fundamental to optogene

299 ormed Ca(2+) clamp tests in which we clamped membrane potential with the KATP channel-opener diazoxid

300 valinomycin (10 nM) to prevent buildup of a membrane potential without artificially increasing the m