ライフサイエンスコーパス: Vm

1 Vm dynamics and Ca i2+ dynamics are coupled via Ca(2+) -

2 Vm dynamics during spontaneous or light-evoked activity

3 Vm factors include electrical restitution of action pote

4 Vm of the mutant protein is diminished by 56-fold, sugge

5 itudinal electric field stronger than 10(13) Vm(-1) within a plasma, accelerating particles potential

6 C) and an extremely large g33 (115 x 10(-3) Vm N(-1)) in comparison with other known single-phase ox

7 electric voltage coefficient of 252 x 10(-3) Vm N(-1).

8 nts (d(33) = 367 pm/V, g(33) = 3595 x 10(-3) Vm/N), energy harvesting property (power density is 11 W

9 and magnetic fields of approximately 10(-4) Vm(-1) and approximately 10(-13) T, respectively.

10 equivalent intra-cavity field as low as 1.9 Vm(-1) for an integration time of 100 ms, corresponding

11 is a dimer of 42-kDa subunits and exhibits a Vm = 37 units/mg, Km(ATP) = 74 microM, and Km(DL-MVA) =

12 d 2 cameras to map membrane potential alone (Vm, n=3) or Vm and intracellular calcium simultaneously

13 s of voltage gated K(+) channel activity and Vm depolarization, a loss of shoot-induced root-Vm depol

14 Apparent kinetic constants (Km(app) and Vm(app)) for 11-cis REH activity in P2 were 18 microM an

15 In ventricular myocytes, Ca and Vm are bidirectionally coupled, which can affect each ot

16 urrent-clamp recordings showed that Ca2+ and Vm oscillate in synchrony, with an average fluctuation o

17 The present U, h and Vm/Ve are in general concordance with earlier results.

18 ysis of the relationship between [Ca2+]i and Vm showed a threshold for activation of hyperpolarisatio

19 ransporter, ICAM-1 ligation increases Km and Vm of the amino acid transporter LAT-2.

20 Whereas CD98 ligation decreases the Km and Vm of the LAT-2 transporter, ICAM-1 ligation increases K

21 on, allowing simultaneous optical pacing and Vm mapping.

22 On average, U, h, s and Vm/Ve (indicates an estimate) are 0.84 [corrected], 0.30

23 ues, the U and h are lower bounds, and s and Vm/Ve upper bounds.

24 The temperature- and Vm-dependent properties of transient charge movements we

25 At 80 degrees C (pH 8.0), the apparent Vm value for pyruvate decarboxylation was about 40% of t

26 ecarboxylation was about 40% of the apparent Vm value for pyruvate oxidation rate (using P. furiosus

27 However, the k- of IEM-1754 and IEM-1460 at Vm values more hyperpolarized than -90 mV were much more

28 ignificantly altered by 3 microM IEM-1857 at Vm values from -90 to -150 mV, as expected of a drug tha

29 n, while all naive NCX recovered to baseline Vm and Rm when re-oxygenated, exposed NCX exhibited a mu

30 ular activity revealed a correlation between Vm depolarization and spike discharges in adjacent cells

31 We define the coupling between Vm and Ca i2+ cycling dynamics ( Ca i2+-->Vm coupling) a

32 of this threshold in the interaction between Vm and Ca2+ release during oscillations are discussed.

33 Gj was not affected by Vm in 50% of the cases.

34 ium-calcium exchanger (NCX) is determined by Vm as well as Na and Ca concentrations.

35 s are identified, which are either driven by Vm oscillations or Ca oscillations alone, or oscillation

36 an initial hyperpolarization is followed by Vm shift to a more positive level.

37 gest that glial cell Na/K pump regulation by Vm may be an important factor in determining the partici

38 intracellular Ca(2+) equilibrium, and caused Vm depolarization.

39 developed a technique to perform whole-cell Vm measurements from the cortex of behaving monkeys, foc

40 s, we performed two-photon guided whole-cell Vm recordings from primary visual cortex layer 2/3 excit

41 ally dissociated from muscle O2 consumption (Vm,O2) due to the influence of the intervening venous bl

42 ssue and their relationship to corresponding Vm changes (DeltaVm) are lacking.

43 Correspondingly, Vm is strongly regulated by Ca(2+) and less so by pHi.

44 both increased Km (634 microM) and decreased Vm [855 nmol of Ins(1,4,5)P3 hydrolyzed min-1 (mg of pro

45 ased Vm values and L35 mutants had decreased Vm values.

46 Amiloride (1 mM) decreased Vm and increased Rm in the resting condition but changed

47 ted electrode current distribution and delta Vm produced by unipolar line stimulation in isolated rab

48 of transmembrane voltage (Vm) change (delta Vm) in the heart during unipolar point stimulation is no

49 aive NCX showed anoxic depolarization (delta Vm > 20 mV/min) much sooner (mean latency of 4.8 +/- 0.4

50 uated both the rate of depolarization (delta Vm/dt) and the rate of decline of Rm (delta Rm/dt) by ab

51 Exposed NCX depolarized 5 x more (delta Vm = 53.2 +/- 7.0 mV; n = 13; mean +/- S.E.M.) than naiv

52 = 13; mean +/- S.E.M.) than naive NCX (delta Vm = 10.6 +/- 2.0; n = 8) in response to 20% O2.

53 beyond the ends exhibited a nonuniform delta Vm sign, whereas epicardium between the ends exhibited a

54 Spatial distributions of delta Vm during line stimulation were qualitatively predictabl

55 imited ability of summation to predict delta Vm.

56 4-ANEPPS, and a laser scanner provided delta Vm measurements at 63 spots in an 8 x 8-mm epicardial re

57 For biphasic line stimulation, delta Vm during the second phase was weakly correlated with th

58 The delta Vm sign between the ends became less uniform when the st

59 At 90 degrees, the delta Vm sign between the ends was nonuniform and was frequent

60 Thus, uniformity of the delta Vm sign during stimulation is enhanced in the region bet

61 s increases regional uniformity of the delta Vm sign.

62 m between the ends exhibited a uniform delta Vm sign that was essentially negative (hyperpolarized) d

63 ted oxidative response and a K(+) -dependent Vm-activated jasmonate response associated with the rele

64 ercome a weakened current sink to depolarize Vm and trigger action potentials.

65 Depolarized Vm reduces NCX-mediated efflux, elevating [Ca]i, and thu

66 catecholamines and flecainide at depolarized Vm and the shortened APD95 could facilitate arrhythmogen

67 At depolarized Vm, isoproterenol amplified the flecainide-induced reduc

68 Moreover, depolarized Vm promotes spontaneous Ca releases that can cause initi

69 Local Ca waves depolarized Vm in HF but not CTL hearts, suggesting weaker gap junct

70 eled with after-shock elevation of diastolic Vm.

71 measured the membrane potential difference (Vm) of villus-attached enterocytes by direct microelectr

72 Two distinct Vm -dependent gating modes were uncovered: a fast-mode o

73 Hypoxia increased duodenal Vm (-57.7 vs. -49.3 mV, P < 0.001).

74 The increase was consistent at each Vm with the predictions of the sequential scheme of bloc

75 pha-adiol) metabolism 60-70% as efficiently (Vm/Km) as RDH1.

76 show, for the first time, that low-frequency Vm oscillations can significantly modulate sensory signa

77 Recently, low-frequency Vm oscillations have been described in inactive awake an

78 very little is known about how low-frequency Vm oscillations influence sensory processing and whether

79 Therefore, low-frequency Vm oscillations play a role in shaping sensory processin

80 ular Ca(2+) to membrane voltage (CAi(2+) --> Vm ) coupling.

81 easing IKs and ISK promote negative Ca i2+-->Vm coupling at the cellular level.

82 en Vm and Ca i2+ cycling dynamics ( Ca i2+-->Vm coupling) as positive (negative) when a larger Ca(2+)

83 In this study, we investigate how Vm affects Ca sparks and waves.

84 ed PepT2-mediated currents at hyperpolarized Vm, our data are consistent with the concept that hyperp

85 Adenosine still hyperpolarized Vm from -48+/-2 to -65+/-1 mV (P<0.001).

86 When 3-5 Hz Vm oscillations coincided with visual cues, excitatory n

87 we found visually evoked stereotyped 3-5 Hz Vm oscillations that disrupt excitatory responsiveness t

88 visual cues were critical for evoking 3-5 Hz Vm oscillations when animals performed discrimination ta

89 We recorded stereotyped 3-5 Hz Vm oscillations where the Vm baseline hyperpolarized as

90 response magnitude, expressed as a change in Vm relative to baseline, was linearly correlated with th

91 xhibits only approximately 2-fold changes in Vm and Km values.

92 via fast ( approximately 0.1 ms) changes in Vm mediated by the voltage and Ca-sensitive NCX.

93 Following step-changes in Vm, in the absence of Gly-Sar, hPEPT1 exhibited H+-depen

94 apsigargin induced a small depolarization in Vm.

95 n capillaries, showed drastic differences in Vm foot as predicted.

96 is stable, exhibiting >50-fold diminution in Vm and elevated Km values for ATP (approximately 20-fold

97 Furthermore, spontaneous fluctuations in Vm were correlated with the surrounding network activity

98 put events that elicit large fluctuations in Vm.

99 oupling unless there are large variations in Vm.

100 m values, but two (L36A, R58A) had increased Vm values and L35 mutants had decreased Vm values.

101 tential model that is capable of independent Vm and Ca oscillations to investigate the roles of Vm an

102 ular excitability as a result of BPA-induced Vm hyperpolarization.

103 We conclude that TMEM16 CaCCs have intrinsic Vm - and Cl(-) -sensitive dual gating that elicits compl

104 mulated Ip with no change in the shape of Ip-Vm curves.

105 Under conditions that cause the Ip-Vm (membrane potential) relationship to express a positi

106 hell structure was estimated to be - 1.92 kA/Vm (- 24 Oe/V).

107 n adjacent frames removes artifacts, leaving Vm (excitation ratiometry).

108 , using confocal microscopy to measure local Vm and intracellular [Ca] simultaneously.

109 nd show that EADs in these models are mainly Vm-driven.

110 e, we present a method to simultaneously map Vm and epicardial contraction in the beating heart.

111 show that the method can simultaneously map Vm and strain in a left-sided working heart preparation

112 e predictions of an asynchronous state, mean Vm during fixation was far from threshold (14 mV) and sp

113 consistent with an asynchronous state: mean Vm approached threshold, fluctuations became more Gaussi

114 tive dye di-4-ANEPPS was utilized to measure Vm directly from quasi two-dimensional preparations of c

115 n compared to native enzyme [Km = 75 microM, Vm = 8300 nmol of Ins(1,4,5)P3 hydrolyzed min-1 (mg of p

116 CA1 neurons in hippocampal slices, monitored Vm and measured input resistance (Rm) with periodic inje

117 t became more rapid at increasingly negative Vm values in an ion concentration-dependent fashion.

118 No Vm isotope effect is observed when 2-2H-IMP is the subst

119 No Vm isotope effect is observed when [2-2H]IMP is the subs

120 y to prevent motion artifacts from obscuring Vm signals.

121 antioxidants in conjunction with an observed Vm recovery after termination of laser scanning further

122 During moderate exercise, an association of Vm,O2 and [phosphocreatine] ([PCr]) kinetics is a necess

123 Spike-triggered averaging of Vm revealed that visually evoked action potentials arise

124 M) induced a rapid overall depolarization of Vm that was accompanied by first a decrease and then an

125 e the required second spatial derivatives of Vm.

126 This may lessen arrhythmogenic dispersion of Vm-dependent ion channel states in the region.

127 Distributions of Vm values were skewed beyond that expected for a range o

128 This study is the first examination of Vm and the stimulation mechanisms throughout the cardiac

129 ar the myenteric edge, rapid fluctuations of Vm with a mean frequency of 18 contractions min-1 were r

130 f the transient currents were independent of Vm and Tl+o at positive potentials, but became more rapi

131 sumably L-type Ca2+ channels) independent of Vm.

132 be linearly correlated with the magnitude of Vm fluctuations in the gamma (20-70 Hz) frequency band.

133 annel types can contribute to maintenance of Vm, Ca2+ signals, and gene expression.

134 Simultaneous optical mapping of Vm (with RH237) and [Ca(2+)]SR (with Fluo-5N AM) was per

135 rate apparent Michaelis-Menten parameters of Vm = 0.34 fmol/s and kcat/Km on the order of 104 s-1 M-1

136 Ca oscillations to investigate the roles of Vm and Ca coupling in EAD genesis.

137 acid load, but without the negative shift of Vm that is characteristic of electrogenic Na+-HCO3- cotr

138 ble propagation from fluorescence signals of Vm at thousands of sites (3 kHz), thereby introducing tr

139 nal propagation there was initial slowing of Vm foot that resulted in deviations from a simple expone

140 rm, which introduces dispersion of states of Vm-dependent ion channels that depends on fiber orientat

141 stimate of tauPCr and by implication that of Vm,O2 (tauVm,O2).

142 with a time constant within 10 % of that of Vm,O2.

143 predicts that the phase-plane trajectory of Vm foot will deviate from linearity in the presence of a

144 t Ca(2+) sensitivity such that at a value of Vm of -30 mV, a mean value of [Ca(2+)]i of 39 mum was re

145 aliotoxin (KTX) and charybdotoxin (CHTX), on Vm, calcium influx, and cell proliferation.

146 We hypothesized that the effect on Vm foot observed in the experimental data was created by

147 Simultaneous optical Vm mapping showed that conduction velocity, action poten

148 to map membrane potential alone (Vm, n=3) or Vm and intracellular calcium simultaneously (Ca(i), n=4)

149 ignificantly affect membrane current, Rm, or Vm in AV nodal myocytes.

150 Application of a physiological oscillating Vm waveform to non-oscillating cells under voltage clamp

151 During this period, Vm remains at the resting membrane potential >80% of the

152 ke complexes separated by quiescent periods (Vm approximately -60 mV).

153 lecainide-superfused fibers at physiological Vm increased theta2 by 8% to 1.84+/-0.6 (m/s)2 (P<.01) w

154 At physiological Vm, the action potential duration (APD95) was reduced fr

155 rating [Na+]i, [ATP]i, [K+]o and at positive Vm).

156 156.3 mV (compared with a membrane potential Vm of -43.1 mV in a HCO3(-)-free solution) and a slope c

157 of the foot of the cardiac action potential (Vm foot) during propagation in different directions in a

158 eously mapped epicardial membrane potential (Vm) and Ca(i) during 6-ms MW and 3-ms/3-ms BW shocks in

159 (PCP) was studied on the membrane potential (Vm) and Ca2+ uptake in isolated single skeletal muscle c

160 urrent which depolarizes membrane potential (Vm) and can trigger action potentials in isolated myocyt

161 We measured membrane potential (Vm) and input resistance (Rm) at rest and in response to

162 mbrane conductance (Gm), membrane potential (Vm) and junctional conductance in the intact lens.

163 ear relationship between membrane potential (Vm) and resting [Ca2+]cyt was observed, indicating the i

164 5.0 were dependent upon membrane potential (Vm) between -150 mV and +50 mV.

165 The diastolic membrane potential (Vm) can be hyperpolarized or depolarized by various fact

166 probability (NPo) versus membrane potential (Vm) curves were more left-shifted in cerebral versus cre

167 and stable subthreshold membrane potential (Vm) depolarization associated with wakefulness/alertness

168 l basis by measuring the membrane potential (Vm) fluctuations and spike activity during brief epochs

169 ATPase but decreased the membrane potential (Vm) generated by this proton pump, suggesting that tamox

170 tate are that a neuron's membrane potential (Vm) hovers just below spike threshold, and its aggregate

171 channel, which sets the membrane potential (Vm) in a strongly pHi-dependent manner.

172 ion optical recording of membrane potential (Vm) in intact specimens.

173 Membrane potential (Vm) is tightly controlled in T cells through the regulat

174 electrodes to record the membrane potential (Vm) of intact murine colonic smooth muscle.

175 hat shifting the resting membrane potential (Vm) of lymphatic muscle to a more negative voltage might

176 The effect of membrane potential (Vm) on ADP-evoked [Ca2+]i oscillations was investigated

177 Low-frequency membrane potential (Vm) oscillations were once thought to only occur in slee

178 tamuH) or increasing the membrane potential (Vm) shifts this binding site from an outwardly to an inw

179 NCE STATEMENT A neuron's membrane potential (Vm) strongly shapes how information is processed in sens

180 o countercurrent, the SR membrane potential (Vm) would quickly (<1 ms) reach the Ca(2+) equilibrium p

181 duced changes in resting membrane potential (Vm), IK,ADO, and membrane resistance (Rm) in rabbit isol

182 ent of changes in plasma membrane potential (Vm), it requires an increase in intracellular potassium

183 Resting membrane potential (Vm), recorded at various positions through the thickness

184 ('off') step changes in membrane potential (Vm).

185 d measurement of resting membrane potential (Vm).

186 pump cycle regulation by membrane potential (Vm).

187 luorescent dyes to image membrane potential (Vm).

188 Their resting potential (Vm) and input resistance (Ro) were thus measured.

189 erval (CI) or the optical takeoff potential (Vm).

190 responses of plasma transmembrane potential (Vm) depolarization, voltage gated K(+) channel activity,

191 responses of plasma transmembrane potential (Vm) depolarization, voltage gated K(+) channel activity,

192 The lack of transmembrane potential (Vm) distribution data makes it impossible to analyse the

193 -fidelity (200 kHz) transmembrane potential (Vm) signals with glass microelectrodes at one site using

194 At physiological membrane potentials (Vm) ([K+]o=5.4 micromol), 1 micromol flecainide decrease

195 th overshooting APs and membrane potentials (Vm) more negative than -40 mV were analysed: 40 C-, 45 A

196 The rise of Ca(i) preceded Vm activation at the sites of focal discharge in 6 episo

197 The QON-Vm data were fit by a sum of two Boltzmann expressions a

198 d was superimposed upon slow waves and rapid Vm fluctuations.

199 maximum specific substrate utilization rate (Vm) and the half saturation coefficient (KS) for P4B1 (3

200 Reconstructed Vm signals were validated by comparison to monophasic ac

201 ost 20% of the exposed NCX failed to recover Vm and Rm following in vitro hypoxia.

202 Resting Vm and Rm were not different between exposed and naive n

203 (v)1.2 channel activity and when the resting Vm is more hyperpolarized than normal.

204 electrode recordings monitoring the resting Vm variations induced by laser-scanning illumination.

205 depolarization, a loss of shoot-induced root-Vm depolarization, a loss of activation and regulation o

206 by P=ae(kV)+b and logarithmically by P=-Sln[(Vm-V)/(Vm-V0)], where V0 indicates volume at P=0, and th

207 th fluctuations in the preceding spontaneous Vm.

208 ly correlated with the preceding spontaneous Vm.

209 R K(+) balance after RyRs close, assuring SR Vm stays near 0 mV.

210 tigaptide) increased coupling and suppressed Vm depolarization during Ca waves.

211 We find that Vm depolarization promotes Ca wave propagation and hyper

212 Our data suggest that Vm changes are active components of the feedback/feedfor

213 The Vm-sensitive fluorescent dye, di-4-ANEPPS, and a laser s

214 where the Vm baseline hyperpolarized as the Vm underwent high amplitude rhythmic fluctuations lastin

215 pproximately -70 mV, which is just below the Vm for sodium channel activation.

216 Furthermore, disrupting the Vm gradient blocked the emergence of patterned prolifera

217 f extra-cellular ion binding can explain the Vm dependence of ion transport by the Na+,K(+)-ATPase.

218 changes had to be large (>+/-40 mV from the Vm).

219 echanisms were observed that depended on the Vm magnitude during S2 cathodal stimulation.

220 The k- of IEM-1857 and IEM-1592 over the Vm range studied, and of IEM-1754 and IEM-1460 from -30

221 r exponential dependence on voltage over the Vm range studied.

222 stereotyped 3-5 Hz Vm oscillations where the Vm baseline hyperpolarized as the Vm underwent high ampl

223 voltage dependent, suggesting that at these Vm values the two drugs can occupy a deeper binding site

224 y slowing of Vp,O2 kinetics in comparison to Vm, O2.

225 With K+ depolarization to Vm=-70 mV, flecainide further reduced Vmax from 306+/-10

226 fluorescence have different sensitivities to Vm, but other signal features, primarily motion artifact

227 K0.5 for Gly-Sar (K0.5GS) was dependent upon Vm and pH; at -50 mV, K0.5H was minimal (approximately 0

228 voltage-clamp technique or pHi changes using Vm/pH-sensitive microelectrodes.

229 (kV)+b and logarithmically by P=-Sln[(Vm-V)/(Vm-V0)], where V0 indicates volume at P=0, and the const

230 (s), and scaled genomic mutational variance (Vm/Ve).

231 used by instability of the membrane voltage (Vm ), instability of the intracellular Ca(2+) ( Ca i2+)

232 heir gating is dictated by membrane voltage (Vm ), intracellular calcium concentrations ([Ca(2+) ]i )

233 mic factors are related to membrane voltage (Vm) and Ca(i).

234 as well as by gradients in membrane voltage (Vm), which is defined as the electric potential differen

235 xperimental observations, i.e., the voltage (Vm)-driven and intracellular calcium (Ca)-driven mechani

236 The sign of transmembrane voltage (Vm) change (delta Vm) in the heart during unipolar point

237 nduced sensitivity to transmembrane voltage (Vm).

238 d channel were studied at membrane voltages (Vm) from -170 to +30 mV.

239 However, there was Vm-dependence in the others, but voltage changes had to

240 he roles of Ca cycling and its coupling with Vm in the genesis of EADs have not been well understood.

241 ands (width=0.8 mm) were double-stained with Vm-sensitive dye RH-237 and a low-affinity Ca(i)2+-sensi

242 the two hexoses, Km(Glc) x Vm(FDG)/Km(FDG) x Vm(Glc) x MRGlc equals the FDG metabolic rate (MRFDG) di

243 ylation ratio for the two hexoses, Km(Glc) x Vm(FDG)/Km(FDG) x Vm(Glc) x MRGlc equals the FDG metabol