ライフサイエンスコーパス: resting potential

1 olarizing current to establish the hair cell resting potential.

2 nhibited oscillations and hyperpolarized the resting potential.

3 the response in bipolar cells near and below resting potential.

4 s leads to pronounced, slow undershoots near resting potential.

5 nal repolarization to a stable and polarized resting potential.

6 making it more difficult to reestablish the resting potential.

7 s an important role in the regulation of the resting potential.

8 east a 0.35-pA unitary Ca(2+) current at the resting potential.

9 erties consistent with a role in maintaining resting potential.

10 t resistance (50-fold), and a hyperpolarized resting potential.

11 change, but not when it was clamped near the resting potential.

12 sisted after current-mediated restoration of resting potential.

13 linear current-voltage curve with a high (H) resting potential.

14 imately 50% inhibition at a typical neuronal resting potential.

15 myocardial membrane potential at or near the resting potential.

16 dent components on patch depolarization from resting potential.

17 e conditions reflected changes in the axonal resting potential.

18 is poised to respond maximally to changes in resting potential.

19 e firing, with a reversal potential close to resting potential.

20 elayed rectifier, gK,L, that is activated at resting potential.

21 -dependent ion channels, active close to the resting potential.

22 all, yet significant depolarization from the resting potential.

23 elated mechanisms did not contribute to cell resting potential.

24 on potential inhibition at the physiological resting potential.

25 zing) near -70 mV so that cells had a stable resting potential.

26 ecular defects that cause instability of the resting potential.

27 ransient outward potassium window current at resting potential.

28 ) abbreviated the APD and hyperpolarized the resting potential.

29 ing in axons and contributing to setting the resting potential.

30 ic channels began to activate just below the resting potential.

31 ET)) provide a depolarizing influence to the resting potential.

32 nsitive, peaking at membrane potentials near resting potential.

33 d release probability through alterations in resting potential.

34 mal planaria via global patterns of cellular resting potential.

35 k sodium conductance also contributes to the resting potential.

36 eceptors is required for induction of LTD at resting potentials.

37 depends on light-induced currents active at resting potentials.

38 associated with a hyperpolarization of their resting potentials.

39 oltage responses occurred from more negative resting potentials.

40 slope within the physiological range of OHC resting potentials.

41 tead an intermediate state to predominate at resting potentials.

42 ased short-pass selectivity without changing resting potentials.

43 -aspartate (NMDA) receptors and is silent at resting potentials.

44 ed by reduced excitability and more negative resting potentials.

45 se in inward current on activation at normal resting potentials.

46 rent-voltage relation in the vicinity of the resting potential (-50 mV).

47 At resting potential (-63.7 +/- 0.6 mV), approximately 90%

48 At resting potential (-70 mV), bumps averaged 10 pA in peak

49 NaP) was found to be active at cell membrane resting potentials, a finding that may explain why I(KNa

50 yocardium, potassium (K(+)) channels control resting potentials, action potential waveforms, automati

51 The depolarized resting potential activates a voltage-dependent K+ condu

52 cess by which cardiomyocytes return to their resting potential after each beat, is a highly regulated

53 lation of I(h) produced hyperpolarization of resting potential, along with increased input resistance

54 hus, ion channel determinants of presynaptic resting potential also control synaptic strength.

55 icate endogenous spatio-temporal patterns of resting potentials among non-excitable cells as instruct

56 At -60 mV, a physiological resting potential, AMPH did not induce DA efflux in hDAT

57 application produced a depolarization of the resting potential, an increase in input resistance, and

58 delayed rectifier that activated positive to resting potential and a fast inward rectifier, gK1.

59 oximately 7 pS showing sustained activity at resting potential and above was identified.

60 The results demonstrate that the myocyte resting potential and action potential waveform are modu

61 ackground K(+) channel (I(AC)) that sets the resting potential and acts pivotally in ACTH-stimulated

62 ke neuronal M currents, activate negative to resting potential and are modulatable.

63 nt downregulation of IK(IR) destabilizes the resting potential and causes spontaneous action potentia

64 ecreasing the tonically active I(A) near the resting potential and causing the cell to depolarize.

65 ane segment bTREK-1 K+ channel that sets the resting potential and couples hormonal signals to depola

66 ane potential excursions, reduce the average resting potential and decrease oscillations.

67 Whether the depolarizing shift in resting potential and enhanced spontaneous firing are du

68 h exists as the Re(I)/Fe(III) cluster at the resting potential and exhibits six clear one-electron re

69 To study the relationship between resting potential and exocytosis, we combined pre- and p

70 reversal potential was shifted close to the resting potential and GGABA produced a shunting inhibiti

71 deinactivated by hyperpolarization from the resting potential and give rise to rebound excited Ca(2+

72 These channels contribute to the resting potential and help regulate the degree of excita

73 K(V)) channels play key roles in setting the resting potential and in the activation cascade of human

74 ncrease excitability via a depolarisation of resting potential and increased evoked firing.

75 ggests that these channels contribute to the resting potential and input resistance in several neuron

76 The membrane resting potential and input resistance of the GEPR-9 CA1

77 rent activated by hyperpolarization from the resting potential and is an important modulator of actio

78 tance appears to contribute significantly to resting potential and may regulate excitability of GI mu

79 tant channel, D623N, associated with SFN, on resting potential and membrane potential during interspi

80 In contrast, the resting potential and membrane resistance of the recorde

81 shold M-currents that stabilize the neuronal resting potential and prevent repetitive firing of actio

82 that depends in a complicated manner on the resting potential and previous history of action potenti

83 ega current that most likely depolarizes the resting potential and produces the hypokalaemia-induced

84 ne potential excursions, raising the average resting potential and producing oscillations.

85 re allowed the current to determine both the resting potential and resting conductance of the nerve t

86 resistance, which in turn hyperpolarized the resting potential and significantly attenuated the ampli

87 i) in a voltage range near the smooth-muscle resting potential and slows activation and deactivation.

88 reversal potential (E(GABA)) was positive to resting potential and spike threshold in VP neurons, but

89 layer, which is impeded by a hyperpolarized resting potential and strong GABA(A)-mediated tonic inhi

90 ippocampal subfield are the more depolarized resting potential and the higher input resistance; addit

91 ide in neurons, a partial determinant of the resting potential and the inhibitory reversal potentials

92 ted that a U-shaped relationship between the resting potential and the neuronal action potential thre

93 olarization to values more positive than the resting potential and then by slow repolarization.

94 -state inactivation, and appears to modulate resting potential and to amplify small depolarizations.

95 rom scrapie-infected mice showed depolarized resting potentials and an increased membrane resistance

96 conductance contributes to the regulation of resting potentials and excitability of colonic muscles.

97 required for correct regionalization of the resting potentials and for establishment of endogenous e

98 Voltage-gated channels maintain cellular resting potentials and generate neuronal action potentia

99 nt should be most important at physiological resting potentials and in response to brief stimuli.

100 Hyperpolarized resting potentials and larger command potentials acceler

101 II (LII) pyramidal cells, with more positive resting potentials and lower spike thresholds.

102 and muscle fibers become inexcitable despite resting potentials and membrane resistances similar to t

103 ed non-functional connections to transmit at resting potentials and required NMDA receptors (NMDA-Rs)

104 of Kir2 gene products, with this regulating resting potentials and the excitability of colonic muscl

105 capacitance, nonlinear active sources of the resting potential, and a hysteretic model of electropora

106 ctifying K+ current (IK(IR)), which sets the resting potential, and Ca2+ and outward K+ currents, whi

107 to metabolic efficiency and the stability of resting potential, and channel noise might be exploited

108 throughout the return of the membrane to the resting potential, and deactivation of HERG current coul

109 t in I(h) activation, along with depolarized resting potential, and decreased input resistance and te

110 nhancement of fast inactivation close to the resting potential, and enhanced use-dependent inactivati

111 g action potential characteristics, cellular resting potential, and gross cellular morphology during

112 r current-voltage (I-V) curve with a low (L) resting potential, and the second model neuron has a lin

113 nal progenitors had depolarized zero-current resting potentials, and lacked action potentials.

114 neurones exhibit lower input resistances and resting potentials, and require more current to be injec

115 oth muscle hyperpolarization, increasing the resting potential (approx. -53 mV) by around 20 mV at 3

116 pproximately 92% of VGSCs inactivated at the resting potential (approximately -58 mV).

117 Given the relatively hyperpolarized resting potentials (approximately -70 mV) reported for n

118 These channels are available at the resting potential, are activated by the action potential

119 s, typically multipolar, were GABAergic, had resting potentials around -50 mV, and exhibited spontane

120 al excitability when depolarized to the same resting potentials as affected SD fibres.

121 quent simulations using n(6) and setting the resting potential at the in vivo value simplifies the HH

122 N can account for the observed difference in resting potentials between the two cell groups.

123 (BKCa) and KV channels do not determine the resting potential but have separate functions to underli

124 Iberiotoxin did not affect the resting potential but inhibited spontaneous transient hy

125 eurons, APs do not immediately return to the resting potential, but instead exhibit a period of depol

126 elicit firing from cartwheel cells at their resting potentials, but could also reduce rapid firing d

127 Exposure to TTX hyperpolarized resting potential by 7mV, increased current-threshold, d

128 dy-state current that positively shifted the resting potential by almost 30 mV.

129 Rods were depolarized to near the dark resting potential by bath application of high K(+) solut

130 Resting potentials can be restored by nifedipine, sugges

131 els, this further delays the recovery of the resting potential, causing a prolonged effect.

132 , dominated by the chloride conductance; the resting potential changed to -82 mV when the K+ conducta

133 eurotransmitter release when the presynaptic resting potential changes.

134 so stabilizes responses when the presynaptic resting potential changes.

135 tial only increased just beyond the original resting potential (circa -58 mV).

136 Instructive signals mediated by changes in resting potential control proliferation, differentiation

137 Using this method, the resting potentials could accurately be measured showing

138 depolarizing current steps, depolarized the resting potential, decreased the threshold current requi

139 2+, which inhibits 86% of IK(IR) at the cell resting potential, depolarized cells by 6.1 +/- 0.7 mV f

140 hair cell drives afferent firing rates, the resting potential dictates spontaneous transmitter relea

141 or enhance LGN activity, hyperpolarizes the resting potential due to increased basal GIRK activity a

142 a(J)/Va(J) mice additionally had depolarized resting potentials due to an inwardly rectifying leak co

143 the roles of spatial differences in cellular resting potentials during large-scale brain morphogenesi

144 and inhibitory inputs that promote a stable resting potential (E/I balance).

145 microelectrode measurements of steady-state resting potentials (E(m)).

146 not take into account the effect of nonzero resting potentials (E(rest)) and junctional reversal pot

147 Under physiological resting potentials, EGF activates TRPP2 by releasing the

148 When B21 is peripherally activated at its resting potential, electrotonic potentials in the latera

149 control two fundamental cellular parameters, resting potential (Em) and cell volume (Vc), thereby cla

150 racellular sodium concentration ([Na+]i) and resting potential (Em) of cultured mouse glomus cells (c

151 potentials, it was depolarizing at the cell resting potentials estimated from the reversal potential

152 At more negative resting potentials, GnRH-EGFP neurons exhibited oscillat

153 nal dysfunction: patients with normal axonal resting potentials had normal serum potassium, although

154 rent (IPO), activated by depolarization from resting potential, has been identified and characterized

155 ials near a filament exhibiting i), elevated resting potential, ii), reduced amplitude relative to pa

156 Resting potential in DRG neurons expressing D623N was de

157 s play a key role in maintaining the correct resting potential in eukaryotic cells.

158 ility from paradoxical depolarization of the resting potential in low potassium.

159 sponsible for the re-establishment of Ca(2+) resting potential in muscle cells, neuronal signalling a

160 Functional data have implicated gradients of resting potential in processes such as limb regeneration

161 ASK-1 channels are major contributors to the resting potential in pulmonary artery smooth muscle.

162 regenerative membrane current, active at the resting potential in sensory and at least some motor ner

163 There was no depolarization of axon resting potential in septic rats, which ruled out a cont

164 expression of GKIR:GKD led to more negative resting potentials in nonproliferating (-60 mV) versus p

165 rectifying currents and 13 mV more negative resting potentials (in 3 mM [K+]o) than non-transfected

166 hod from a family of impulse responses below resting potential, indicates a channel that is permeable

167 EGABAA is positive to the resting potential, indicating that GABA serves to depola

168 high membrane conductance and a depolarized resting potential, indicating the presence of a large, c

169 n combination with the depolarization of the resting potential induced by denervation results in inex

170 s not detected electrophysiologically at the resting potential, infrequent or brief opening could acc

171 y measured physiological properties included resting potential, input resistance (R(N)), threshold (r

172 Resting potential, input resistance, time constant, elec

173 neuronal pacemaker activity, the setting of resting potentials, input conductance and length constan

174 ether, these studies suggest that control of resting potential is a powerful means for regulating syn

175 The auditory hair cell resting potential is critical for proper translation of

176 The data suggest that resting potential is determined by background K+ channel

177 The resting potential is determined largely by the activity

178 e the response reverses 10-20 mV positive to resting potential, is dependent on chloride concentratio

179 y, associated with determination of cellular resting potential, is not markedly apparent until late s

180 GABA was hyperpolarizing at the zero-current resting potentials, it was depolarizing at the cell rest

181 Simulations show that this difference in resting potential leads to longer first spike latencies

182 n was prominent only in cells that had a low resting potential (less negative than -60 mV).

183 an AP, a stronger stimulus is needed if the resting potential lies further away from the INa thresho

184 produced a paradoxical depolarization of the resting potential, loss of muscle excitability, and weak

185 ium-mediated triggered activity, despite the resting potential lying further away from the INa thresh

186 so evoked an inward current that shifted the resting potentials more positive compared with the sham-

187 eous activity and usually resulted in stable resting potentials near -60 mV to -55 mV, 10-15 mV below

188 Light-evoked changes in membrane resting potential occur in about 100 milliseconds.

189 ady-state current was -21.2 mV, close to the resting potential of -21.4 mV.

190 Single cells had a mean resting potential of -38 mV and were depolarized by 130

191 ls hyperpolarized the plasma membrane from a resting potential of -40 mV to -90 mV, as monitored in p

192 olarized cells by 6.1 +/- 0.7 mV from a mean resting potential of -59.6 +/- 0.8 mV.

193 dent hyperpolarization of the oocyte, from a resting potential of -63 mV under control conditions to

194 hed the rectification and hyperpolarized the resting potential of A-type neurons from -55 +/- 3 mV to

195 eased inactivation of sodium channels at the resting potential of affected fibers.

196 er control recording conditions, cells had a resting potential of approximately -40 mV when bathed in

197 of approximately -30 mV compared with a cone resting potential of approximately -50 mV; thus, crossta

198 polarize spiny projection neurons from their resting potential of approximately -85 mV, which is the

199 activity of K(ATP) channels to regulate the resting potential of beta-cells.

200 e anaesthetics cause changes in the membrane resting potential of central neurons.

201 A863P depolarized resting potential of DRG neurons by +6 mV compared with

202 channels (K2P channels) control the negative resting potential of eukaryotic cells and regulate cell

203 ical imaging and recording the transmembrane resting potential of HL-1 cells.

204 results indicate that Ih contributes to the resting potential of layer I interneurons and is subject

205 The K(+) channels that generate the resting potential of mammalian neurons have been difficu

206 ive membrane holding potentials to mimic the resting potential of neurons and symmetrical chloride to

207 cally relevant conditions is near the normal resting potential of neurons and that reversal can occur

208 hese cells, thereby influencing the membrane resting potential of neurons.

209 oximately 10-fold greater than HERG near the resting potential of smooth muscle.

210 can move up to its maximal limit even at the resting potential of the cell.

211 ls have an important role in determining the resting potential of the cell.

212 K+ channels may be important to control the resting potential of the endothelium and may contribute

213 ique can be extended for measurements of the resting potential of the first (voltage-clamped) membran

214 % of the current was available at the normal resting potential of these cells (-60 mV).

215 tracellular stimulation although the average resting potential of these fibers was no different from

216 We also show that the true resting potential of these neurons is more hyperpolarize

217 he "leak" conductance thought to mediate the resting potential of vertebrate myelinated neurons but w

218 The resting potential of VNO neurons was approximately -60 m

219 Whole DDT1 MF-2 cells had resting potentials of -10 mV, dominated by the chloride

220 tic transmission by dynamically shifting the resting potentials of both presynaptic and postsynaptic

221 annel gene family that may contribute to the resting potentials of cells and control their basal leve

222 oth areas, approximately 15 mV more negative resting potentials of DG compared with CA1 PCs underlie

223 ermeability that contributes to the negative resting potentials of GI muscles.

224 mV and thus would be active under the normal resting potentials of lactotrophs (-35 to -45 mV).

225 s are not sufficient to explain the negative resting potentials of these cells.

226 2.7 +/- 0.2 spikes per second, n = 69) with 'resting' potential of -54 +/- 0.4 mV (n = 77) and input

227 epolarization but 3,4-DAP did not affect the resting potential or induce constriction in the intact a

228 0 microM) alone had no significant effect on resting potential or input resistance and did not consis

229 els at voltages near the normal cardiac cell resting potential or with drug washout.

230 With resting potential preset to -80 mV, -20 pA current injec

231 Spontaneous release at hair-cell resting potentials presumably results from Ca(V)1.3 L-ty

232 reduction of IPSCs and increase in membrane resting potential produced GABA dose-dependent increases

233 Resting potentials ranged from -49 to -40 mV (mean +/- S

234 56D mutant channels demonstrated depolarized resting potential, reduced current threshold, increased

235 h these channel variants display depolarized resting potential, reduced current-threshold, increased

236 xcitability at voltages just positive to the resting potential, reduced delay to action potential fir

237 nt Kcnj2 changes the normal pattern of Vmem (resting potential) regionalization found in the ectoderm

238 uration of the action potential and made the resting potential (RP) more positive (mean 9.0 +/- 7 mV)

239 n rat telencephalic slices, we have followed resting potential (RP) properties and the functional exp

240 The initial resting potentials (RPs) displayed a bimodal distributio

241 currents on step depolarizations from normal resting potentials, showing that all slow TTX-resistant

242 had a small anomalous inward current at the resting potential, similar to our observations in the Na

243 s of aqueous electrolytes and membranes; 2), resting potential source; and 3), asymptotic membrane el

244 When cells were held at their resting potentials, taste stimulation resulted in conduc

245 of and K(+) into the cytosol, maintaining a resting potential that is essential for the function of

246 w a broad band of low power frequencies near resting potential that transition to more narrowband osc

247 endent neurotransmitter release at hair-cell resting potentials that are maintained within the activa

248 In simulations at the physiological resting potential, the persistent component of the sodiu

249 es for the voltage sensitivity at the cell's resting potential, the voltage where the SHG is minimal,

250 ltage clamp mode at a holding potential near resting potential, there were small and inconsistent cha

251 ked by tetrodotoxin, clamp the response near resting potential thus preventing saturation.

252 re, but endplate potentials depolarizing the resting potential to -40 mV failed to excite action pote

253 t a third conductance is required to set the resting potential to a point on the I(Ca) and I(BK) acti

254 f Held, a giant mammalian terminal, we found resting potential to be controlled by KCNQ (Kv7) K(+) ch

255 To assess the contribution of depolarized resting potential to DRG neuron excitability, we mimicke

256 valuate membrane potential correlations near resting potential to study how excitation and inhibition

257 ptic rats, which ruled out a contribution of resting potential to the increased inactivation of sodiu

258 tions induced with voltage steps from normal resting potentials to -40 mV are thought to represent VD

259 so that they overlapped and also caused the resting potentials to be comparable.

260 mp, depolarizing current injections from the resting potential triggered action potentials in OHCs du

261 By altering cells' resting potentials using other ion translocators, we sho

262 etic cost of maintaining the oligodendrocyte resting potential usually outweighs the saving on action

263 ents using K methylsulphate electrodes, cell resting potential (V(m)) and spike firing properties wer

264 rrent, and their loss results in depolarized resting potentials (V(rest)), spike broadening, and rema

265 Their resting potential (Vm) and input resistance (Ro) were th

266 revealed that specific alteration of cells' resting potential (Vmem) is a powerful tool to direct pr

267 e cytoplasmic Ca2+ concentration at the dark resting potential was 2-4 microM.

268 y our observations in parkin larvae that the resting potential was depolarized, oxygen consumption an

269 lamide-sensitive currents were large and the resting potential was hyperpolarized by approximately 20

270 on current, I(h) participates in setting the resting potential, we applied I(h) antagonists.

271 Ca2+ and Na+ currents that activate near the resting potential, we examined whether these two conduct

272 Moreover, IKN and the resting potential were enhanced by halothane (1 mmol/L),

273 Both IKN and the resting potential were found to be exquisitely sensitive

274 These effects of MET current on resting potential were independently confirmed using a t

275 Threshold variations in the model at resting potential were not primarily due to fluctuations

276 ure suggest that this current is active near resting potential, where it may play an important role i

277 ype conductance transients (reversing at the resting potential), which simulated independent activity

278 cation leak current that contributed to the resting potential, which explains the neuronal depolariz

279 -inactivating K+ current (IAC) that sets the resting potential while it is activated by intracellular

280 out of ten cells, 1 mM Ba2+ depolarized the resting potential, while in the other cells the potentia

281 nductance; cells have relatively depolarized resting potentials (with firing stopped by TTX and nimod

282 itional depolarizing influence maintains the resting potential within the activation range of Ca(V)1.