ライフサイエンスコーパス: resting potential

1 nsitive, peaking at membrane potentials near resting potential.

2 mal planaria via global patterns of cellular resting potential.

3 olarizing current to establish the hair cell resting potential.

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

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

6 nhibited oscillations and hyperpolarized the resting potential.

7 nal repolarization to a stable and polarized resting potential.

8 making it more difficult to reestablish the resting potential.

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

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

11 erties consistent with a role in maintaining resting potential.

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

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

14 sisted after current-mediated restoration of resting potential.

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

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

17 myocardial membrane potential at or near the resting potential.

18 dent components on patch depolarization from resting potential.

19 e conditions reflected changes in the axonal resting potential.

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

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

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

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

24 elated mechanisms did not contribute to cell resting potential.

25 all, yet significant depolarization from the resting potential.

26 age-dependent manner, favoring inhibition at resting potential.

27 crease in input resistance and a depolarized resting potential.

28 gh K(+) conductance, returning a cell to its resting potential.

29 nsequence of sustained depolarization of the resting potential.

30 lure of ECC induced by depolarization of the resting potential.

31 on potential inhibition at the physiological resting potential.

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

33 ecular defects that cause instability of the resting potential.

34 ransient outward potassium window current at resting potential.

35 ) abbreviated the APD and hyperpolarized the resting potential.

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

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

38 d release probability through alterations in resting potential.

39 k sodium conductance also contributes to the resting potential.

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

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

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

43 associated with a hyperpolarization of their resting potentials.

44 oltage responses occurred from more negative resting potentials.

45 slope within the physiological range of OHC resting potentials.

46 tead an intermediate state to predominate at resting potentials.

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

48 ased short-pass selectivity without changing resting potentials.

49 ed by reduced excitability and more negative resting potentials.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 ents, which cause aberrant depolarization of resting potential and induce spontaneous action potentia

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

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

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

84 A similar depolarized resting potential and left-shift in rheobase was observe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 nnel currents that contribute to setting the resting potential and to subthreshold fluctuations in me

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

104 R-deficient (Casr-/-) mice had more negative resting potentials and did not fire spontaneously in red

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

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

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

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

109 Hyperpolarized resting potentials and larger command potentials acceler

110 to resting potential, confers very negative resting potentials and low input resistances, and enhanc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 tantly, no changes were observed in membrane resting potential, AP amplitude, or the inward K(+) curr

126 antitative relationships established between resting potential, AP properties, AP conduction and Ca(2

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 Resting potentials can be restored by nifedipine, sugges

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

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

145 eurotransmitter release when the presynaptic resting potential changes.

146 so stabilizes responses when the presynaptic resting potential changes.

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

148 uctance, g(K,L), which activates negative to resting potential, confers very negative resting potenti

149 Depolarization of skeletal muscle resting potential contributes to failure of ECC in disea

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

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

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

153 2+, which inhibits 86% of IK(IR) at the cell resting potential, depolarized cells by 6.1 +/- 0.7 mV f

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

169 Resting potentials hyperpolarized and resting conductanc

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

171 Resting potential in DRG neurons expressing D623N was de

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 Resting potential, input resistance, time constant, elec

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

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

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

191 ation, is strongly enhanced when the somatic resting potential is depolarized, likely as a result of

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

193 The resting potential is determined largely by the activity

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

230 % of the current was available at the normal resting potential of these cells (-60 mV).

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

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

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

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

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

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

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

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

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

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

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

242 2.7 +/- 0.2 spikes per second, n = 69) with 'resting' potential of -54 +/- 0.4 mV (n = 77) and input

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

244 0 microM) alone had no significant effect on resting potential or input resistance and did not consis

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

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

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

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

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

250 56D mutant channels demonstrated depolarized resting potential, reduced current threshold, increased

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

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

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

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

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

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

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

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

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

260 ion potentials, but, during subthreshold and resting potentials, spines often experienced different v

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 /2)) and sped up the rate of activation near resting potential twofold.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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