ライフサイエンスコーパス: holding potential

1 ize and intruder pressure (relative resource-holding potential).

2 ceived chances of winning contests (resource holding potential).

3 g skeletal and cardiac RyRs recorded at 0 mV holding potential.

4 ubconductance at a positive but not negative holding potential.

5 slow kinetics that were not affected by the holding potential.

6 by 20 to 30% in the presence of Iso at each holding potential.

7 ffeine-induced release did not depend on the holding potential.

8 hasic with time constants that depend on the holding potential.

9 1 s voltage steps of +60 to +90 mV from the holding potential.

10 egative potentials and was very sensitive to holding potential.

11 ChR than for alpha4beta4-nAChR at a positive holding potential.

12 threshold, and was relatively insensitive to holding potential.

13 This effect was independent of membrane holding potential.

14 n characteristics brought about by shifts in holding potential.

15 duce a response with outward currents at all holding potentials.

16 effect of Waglerin-1 was greater at negative holding potentials.

17 spikes when depolarized from hyperpolarized holding potentials.

18 channel activities at positive and negative holding potentials.

19 e tonic block in IZs than NZs at depolarized holding potentials.

20 IZ channels at depolarized (> or = -100-mV) holding potentials.

21 he fast component decreased with depolarized holding potentials.

22 plain why I(KNa) can be evoked from negative holding potentials.

23 tive firing (< or = 1 spike/stimulus) at all holding potentials.

24 Channel activity remained low at positive holding potentials.

25 ng open time constants were seen at negative holding potentials.

26 picosiemens (pS) in the +/- 100 mV range of holding potentials.

27 This block was evident only at positive holding potentials.

28 entials and increased activities at positive holding potentials.

29 dulation of the open probability at negative holding potentials.

30 uncharged molecules at negative and positive holding potentials.

31 of current flow was reversed by changing the holding potentials.

32 itions to 29% at either positive or negative holding potentials.

33 modulated by small changes in difference of holding potentials.

34 has the opposite direction at physiological holding potentials.

35 ased taurine-induced inward currents at both holding potentials.

36 rease in channel availability at depolarized holding potentials.

37 transport across cell membranes at positive holding potential, (3) alters the pH inside liposomes ex

38 elicited an inward current (9.7 +/- 0.9 pA; holding potential, -40 to -55 mV; n = 25 neurons) that r

39 1/2 values for activation from -70 or -90 mV holding potentials (-44 mV vs. -24 mV; p<0.01).

40 ed to 184 % of baseline) in voltage-clamped (holding potential = -60 mV) preBotC inspiratory neurons

41 pendent inward currents in all cells tested (holding potential, -62 mV), with EC50 values of 437, 15

42 alternated our mapping protocol between two holding potentials (-70 and +40 mV) allowing us to detec

43 rd current activated between -50 and -40 mV (holding potential, -80 mV) and was maximal near -10 mV.

44 Whole-cell Na+ currents (holding potential, -80 mV; test potential, -30 mV) in ra

45 The effects of BDM were compared at two holding potentials, -80 and -30 mV, using the halpha1C-D

46 s of whether the imposed transition from the holding potential (-90 mV) to the test potential took pl

47 ed hamster SCN neurons from a hyperpolarized holding potential activated both I(A) and I(DR).

48 the currents obtained from more depolarized holding potentials activating more slowly and deviating

49 Metaflumizone perfusion at a hyperpolarized holding potential also shifted the conductance-voltage c

50 rd current that was sensitive to the initial holding potential and had properties similar to the A-ty

51 activated by small depolarizations above the holding potential and reversed near 0 mV.

52 The peak current was dependent on the holding potential and showed little rectification; howev

53 Length reduction at the holding potential and voltage shifts of the motile activ

54 a decrease in channel activities at negative holding potentials and increased activities at positive

55 fast-mode gating was favored by depolarized holding potentials and rapid depolarizations.

56 in cardiac RyR at negative but not positive holding potentials and several subconductances in skelet

57 ow-mode gating was favored by hyperpolarized holding potentials and slow depolarizing rates, whereas

58 [Ca2+] was similar at negative and positive holding potentials and was not influenced by high cytoso

59 ms with similar affinity and a dependence on holding potential, and drug off-rate was slowed at depol

60 efradil was increased at less hyperpolarized holding potentials, and the apparent affinity was correl

61 and required hyperpolarization and prolonged holding potentials at -130 mV.

62 ere reduced compared with controls, even for holding potentials at which all NaV1.4 are fully recover

63 + and exhibited steady-state inactivation at holding potentials below -60 mV.

64 Currents recorded at 40 mV from holding potentials between -60 and -120 mV showed an unu

65 dione-sensitive glutamate EPSCs, recorded at holding potentials between -80 and -90 mV, was reversibl

66 der which small changes in the difference of holding potentials between cells forming heterotypic jun

67 sible to MTSET in choline buffer at negative holding potentials, but there was no effect of voltage i

68 mewhat surprisingly, we find that effects of holding potential can be relatively modest when presynap

69 At resting or holding potentials close to threshold either single or b

70 ed at progressively more depolarized preopen holding potentials, cross-linking of F57Bpa with KCNQ1 w

71 2b), or beta(3a) produced currents that were holding potential dependent.

72 us, the present study measures the effect of holding potential, duration, and intensity on the light-

73 Defined holding potentials eliminated differences in flecainide'

74 eurons, when depolarized from hyperpolarized holding potentials, exhibited a high-frequency burst of

75 he degree of EPSC inhibition by the prepulse holding potential followed the current-voltage relations

76 -ferromagnetic transition can be gate tuned, holding potential for applications in magnetic storage a

77 demonstrated, with the use of -100 mV as the holding potential for fully reprimed channels and -65 mV

78 In both cases shifts in holding potential from -90 to -50 mV produced a partial

79 ion of an outwardly rectifying K+ current at holding potentials from -50 to +50 mV.

80 ane potential in cells clamped at a range of holding potentials from -90 to -45 mV.

81 20 and +40 mV prepulse states with long-term holding potentials (> 2 min) at -80 mV was 14.67 +/- 0.9

82 In contrast, the holding potential had little effect on mEPSC kinetics.

83 ous research in this area is that effects of holding potential have been studied in relative isolatio

84 Under patch clamping, at holding potential (HP) = -120 mV, the peak I(Na) was sim

85 Changes in holding potential (HP) markedly altered the severity of

86 elective cation channel, ICa elicited from a holding potential (HP) of -100 mV showed significant pot

87 , at various subthreshold and near-threshold holding potentials in the presence of synaptic blockers.

88 olarizing current pulses from hyperpolarized holding potentials in whole-cell recordings in vitro.

89 n of bovine alpha(1B) with beta(2a) produced holding potential-independent calcium currents that clos

90 lamp studies, carried out at the appropriate holding potential, indicate that NBQX enhances glutamate

91 Furthermore, at a holding potential intermediate for the reversal potentia

92 ent synapses: they do not respond unless the holding potential is moved from -70 mV to +40 mV.

93 Using steady holding potentials, lacosamide block was very weak at -1

94 In voltage clamp mode at a holding potential near resting potential, there were sma

95 This current peaked at holding potentials near -25 mV and was blocked by the NM

96 inward current (6-68 pA) in most neurons at holding potentials near rest.

97 inward and outward currents in SON cells at holding potentials near resting membrane potential follo

98 At holding potentials negative to -50 mV, 5-HT increased st

99 ed a region of negative slope conductance at holding potentials negative to around -70 mV.

100 At a holding potential of +40 mV, spermine at the intracellul

101 ccording to the polarity of the current at a holding potential of +40 to +60 mV (with Ringer's in the

102 The rate of desensitization was faster at a holding potential of +50 mV than at -70 mV.

103 From a holding potential of -100 mV, step depolarizations elici

104 e amplitude and current density of I(h) at a holding potential of -130 mV was significantly larger in

105 , but these differences were diminished at a holding potential of -150 mV, suggesting that the differ

106 was a large reduction of IPSC amplitude at a holding potential of -20 mV in neurons from bilaterally

107 HVA current was inactivated completely at a holding potential of -35 mV and fully deinactivated at a

108 more depolarized potentials from a prolonged holding potential of -40 mV and was sensitive to all thr

109 The predominant K+ current evoked from a holding potential of -40 mV was slowly activating, long-

110 evoked by depolarizing voltage steps from a holding potential of -40 mV were recorded using the whol

111 From a holding potential of -40 mV, depolarizing voltage steps

112 nsensitive outward current was evoked from a holding potential of -40 mV.

113 y 300-ms depolarizing pulses to 0 mV, from a holding potential of -50 mV at 0.5 Hz.

114 kaloid (-)-indolactam (20-100 microM) from a holding potential of -50 mV elicited an inward current,

115 s (e.g. -34.0+/-1.5 to -38.4+/-1.7 mV from a holding potential of -50 mV in phasic PGN, P<0.005).

116 slowed by hyperpolarization to -90 mV from a holding potential of -50 mV, consistent with a 1 Ca2+ :

117 ited by hyperpolarizing voltage steps from a holding potential of -50 mV.

118 ses, activated a "noisy" inward current at a holding potential of -50 mV.

119 It occurred at a constant holding potential of -60 mV and was not inhibited by the

120 At a constant holding potential of -60 mV ET-1 induced a transient fol

121 K(ATP) currents were measured at a holding potential of -60 mV in high K(+) external soluti

122 d external solutions, voltage steps from the holding potential of -60 mV to levels positive to +20 mV

123 logical temperature of 35 degrees C and at a holding potential of -60 mV we recorded three kineticall

124 Sodium currents elicited from a holding potential of -60 mV were blocked with an IC(50)

125 This current was reduced at a holding potential of -60 mV, activated on depolarization

126 At a holding potential of -60 mV, in NaCl external saline and

127 At a holding potential of -60 mV, rapid application of extrac

128 vated an inward current in DRG neurones at a holding potential of -60 mV.

129 ntial of -35 mV and fully deinactivated at a holding potential of -65 mV (V50, -52.26 mV +/- 0.27; n

130 LVA current was inactivated completely at a holding potential of -65 mV and deinactivated fully at a

131 little or no current in 0.3 microM TTX at a holding potential of -67 mV.

132 trazepam (1 microM) slowed deactivation at a holding potential of -70 mV but not at +50 mV.

133 Depolarization to 0 mV from a holding potential of -70 mV increased [Ca2+]i.

134 y of INa from inactivation was slower from a holding potential of -70 mV than from -90 mV; isoflurane

135 In the whole-cell recording configuration (holding potential of -70 mV) while buffering internal ca

136 In the whole-cell recording configuration (holding potential of -70 mV) while buffering internal ca

137 At a holding potential of -70 mV, a maximally effective conce

138 At a holding potential of -70 mV, application of capsaicin (0

139 At a holding potential of -70 mV, quisqualate (2 microM) indu

140 At a holding potential of -70 mV, the Kapp for mibefradil inh

141 ith a range in hundreds of milliseconds at a holding potential of -70 mV.

142 s (sIPSCs) were seen as inward currents at a holding potential of -70 mV.

143 S in turn 4 to 40 nS in turn 2 measured at a holding potential of -70 mV.

144 at both chemicals reduced cell length at the holding potential of -75 mV and induced positive shifts

145 At a holding potential of -75 mV, spontaneous sparks were inf

146 Stepping back to the holding potential of -80 mV evoked large inward tail cur

147 smooth muscle cells by depolarization from a holding potential of -80 mV using the whole-cell patch-c

148 ep depolarizations positive to -50 mV from a holding potential of -80 mV were decreased by up to 70%

149 At a holding potential of -80 mV, 10(-5)M ACh decreased L-typ

150 At a holding potential of -80 mV, the Ca2+ current (ICa) reac

151 between -42 and +49 mV (44% at 0 mV) from a holding potential of -80 mV.

152 nditions, the mean NP(o) value was 1.06 at a holding potential of -80 mV.

153 s with 2 ms long test depolarizations from a holding potential of -89 mV.

154 +) currents in vitro with IC(50) values at a holding potential of -90 mV ranging from 2.8 to 40 micro

155 oked along with the sustained current from a holding potential of -90 mV.

156 a sixfold acceleration of recovery rate at a holding potential of -90 mV.

157 tial induction (by 15-16 mV) assessed from a holding potential of -90 mV.

158 ntial of -65 mV and deinactivated fully at a holding potential of -95 mV (mean, V50 = -82.40 mV +/- 0

159 For a prepulse to -150 mV, from a holding potential of 0 mV, V(pkcm) shifted 6.4 mV, and w

160 evoked Ca2+-activated potassium current at a holding potential of 0 mV.

161 e was 20 pA in both NRT and relay cells at a holding potential of 0 mV.

162 The inhibitory effect of 5-HT was evident at holding potentials of +60 and -60 mV; with the calcium c

163 ll conductances were 18 microM and 960 nM at holding potentials of -120 mV and -50 mV, respectively.

164 With holding potentials of -120 to -150 mV, which completely

165 At holding potentials of -70 or -90 mV, isoflurane inhibite

166 membrane conductance or holding current (at holding potentials of -80 to -90 mV), suggesting that th

167 l by small changes in the difference between holding potentials of the coupled cells.

168 monstrate that small differences in resting (holding) potentials of communicating cells can fully blo

169 We also explored the effects of varying the holding potential on current threshold, and the effect o

170 described as a graded potentiating effect of holding potential on spike-mediated synaptic transmissio

171 earch suggests a novel view of the effect of holding potential on synaptic transmission.

172 investigated the influence of transmembrane holding potential on the kinetics of interaction of a ca

173 rder to investigate the effects of different holding potentials on the rate of development and amplit

174 At holding potentials positive to approximately -50 mV, a s

175 Voltage steps from the holding potential preceding the measurement of capacitan

176 Firstly, negative holding potentials reduced inward currents (i.e. at nega

177 Ca2+ concentrations or positive postsynaptic holding potentials reduced paired-pulse depression of NM

178 More positive holding potentials replicated the increased effectivenes

179 efly depolarizing from a relatively negative holding potential resulted in a low-affinity inhibition

180 tatory and inhibitory inputs using different holding potentials revealed that inhibition could be evo

181 Recordings under different holding potentials revealed that the enhanced response w

182 are considered to have the highest resource holding potential (RHP) in MMA.

183 assesses its own fighting ability (Resource Holding Potential, RHP) and compares it to that of its o

184 Channel amplitudes at different holding potentials showed that single-channel conductanc

185 At hyperpolarized holding potentials, small numbers of unitary currents (a

186 FSCV parameters (holding potential, switching potential, and scan rate) w

187 e, current passed linearly over the range of holding potentials tested.

188 sinusoidal voltage signals was a function of holding potential, tether diameter, and tether length.

189 ted an inward whole-cell current at negative holding potentials that was inwardly rectifying and show

190 At -100 mV holding potential, the reduction in LA affinity was maxi

191 At -80 mV holding potentials, the current was also suppressed by a

192 similar current amplitudes across a range of holding potentials; the T721A channel is not functional.

193 Current amplitude increased on changing the holding potential to -107 mV.

194 cal characteristics to use negative membrane holding potentials to mimic the resting potential of neu

195 ng depolarizations and that require negative holding potentials to remove inactivation, many chromaff

196 0 mV, with flickering increasing at negative holding potentials to the point where single-channel cur

197 )) in 51 of 58 voltage clamped DRG neurones (holding potential (V(h)) = -80 mV) that were in contact

198 At a holding potential (V(H)) of -30 mV, the enzyme decreased

199 Voltage ramps (-110 to -30 mV) from a holding potential (V(h)) of -60 mV in the absence and pr

200 f INa from inactivation was dependent on the holding potential (VH) in both cell types but was signif

201 At a pHo of 7.0 and a holding potential (Vh) of -50 mV, the charge movements w

202 potentiated the peak amplitude of Icat at a holding potential (Vh) of -50 mV.

203 ge ramps required much smaller currents at a holding potential (Vh) of -60 mV than at -80 mV and were

204 Changing the membrane holding potential (Vh) to +40 mV for brief period before

205 (0.5 microM) was significantly less when the holding potential (Vh) was +40 mV rather than -60 mV.

206 This relationship was obtained when holding potential (Vh) was either -40 or -70 mV; however

207 are held at more physiological, in vivo-like holding potentials (Vh = -60 mV) that facilitate multive

208 current, activated by hyperpolarizing steps (holding potential, Vh = -40 mV), with a reversal potenti

209 ular Ca(2+) concentration was 0.5 mm and the holding potential was -80 mV.

210 s exhibited virtually no inactivation as the holding potential was altered whereas others exhibited s

211 ICa,L at -40 mV inactivated when the holding potential was decreased (VL = -57.8 +/- 0.49 mV)

212 itude of inward current was decreased as the holding potential was depolarized.

213 nt potentiation (above 38%) at more positive holding potentials was precisely equal to a K(+)-depende

214 At more positive holding potentials, which produced steady-state inactiva

215 ) displayed inward rectification at positive holding potentials, which were not altered by lowering b

216 onship between LTS amplitude and the initial holding potential without affecting the maximum LTS ampl