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

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

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

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

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

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

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

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

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

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

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

16 on, allowing simultaneous optical pacing and Vm mapping.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 = 13; mean +/- S.E.M.) than naive NCX (delta Vm = 10.6 +/- 2.0; n = 8) in response to 20% O2.

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

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

49 imited ability of summation to predict delta Vm.

50 4-ANEPPS, and a laser scanner provided delta Vm measurements at 63 spots in an 8 x 8-mm epicardial re

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

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

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

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

55 s increases regional uniformity of the delta Vm sign.

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

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

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

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

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

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

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

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

64 eled with after-shock elevation of diastolic Vm.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 apsigargin induced a small depolarization in Vm.

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

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

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

92 put events that elicit large fluctuations in Vm.

93 oupling unless there are large variations in Vm.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 y to prevent motion artifacts from obscuring Vm signals.

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

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

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

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

116 e the required second spatial derivatives of Vm.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 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

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

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

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

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

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

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

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

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

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

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

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

146 156.3 mV (compared with a membrane potential Vm of -43.1 mV in a HCO3(-)-free solution) and a slope c

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

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

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

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

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

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

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

154 5.0 were dependent upon membrane potential (Vm) between -150 mV and +50 mV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 d measurement of resting membrane potential (Vm).

175 pump cycle regulation by membrane potential (Vm).

176 luorescent dyes to image membrane potential (Vm).

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

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

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

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

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

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

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

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

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

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

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

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

189 Reconstructed Vm signals were validated by comparison to monophasic ac

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

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

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

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

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

195 th fluctuations in the preceding spontaneous Vm.

196 ly correlated with the preceding spontaneous Vm.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

222 nduced sensitivity to transmembrane voltage (Vm).

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

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

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

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

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