ライフサイエンスコーパス: resting membrane potential

1 ge, IHCs retained a normal KCNQ4 current and resting membrane potential.

2 ns and in neurons with an extremely negative resting membrane potential.

3 n by influencing the membrane resistance and resting membrane potential.

4 Na(+) current, nor did it influence neuronal resting membrane potential.

5 reduce the firing rate or hyperpolarize the resting membrane potential.

6 n and hyperpolarization of the cardiomyocyte resting membrane potential.

7 riation in their spontaneous firing rate and resting membrane potential.

8 ction potential amplitude by stabilizing the resting membrane potential.

9 ons including the control of cell volume and resting membrane potential.

10 important mediators of Ca(2+) entry near the resting membrane potential.

11 sent a key pathway for Ca(2+) entry near the resting membrane potential.

12 etigabine or flupirtine to hyperpolarize the resting membrane potential.

13 sively in the nervous system and control the resting membrane potential.

14 d for spike generation but did not alter the resting membrane potential.

15 rough which this lipid can regulate a cell's resting membrane potential.

16 nt synaptic waveforms by hyperpolarizing the resting membrane potential.

17 inergic pulses had negligible effects on the resting membrane potential.

18 te response dynamics are due to the shift in resting membrane potential.

19 creased AP height by 16 mV without affecting resting membrane potential.

20 ring; SLO-2 is also important in setting the resting membrane potential.

21 nfluenced by sustained depolarization of the resting membrane potential.

22 ble taste cells to maintain a hyperpolarized resting membrane potential.

23 following an action potential initiated from resting membrane potential.

24 sed polarity near the OHC's presumed in vivo resting membrane potential.

25 ificantly higher in neurons with depolarized resting membrane potential.

26 nship and also led to a hyperpolarization of resting membrane potential.

27 + channels were constitutively active at the resting membrane potential.

28 by background K+ conductances that determine resting membrane potential.

29 ity to intracellular Ca(2+), and an elevated resting membrane potential.

30 in the myometrial smooth muscle cell (MSMC) resting membrane potential.

31 teps to varying voltages 0-80 mV positive to resting membrane potential.

32 of K2P1 channels recapitulate two levels of resting membrane potential.

33 o-current potentials match the two levels of resting membrane potential.

34 of Kir2.1 and K2P1 channels to two levels of resting membrane potential.

35 ynaptic activity may be secondary to altered resting membrane potential.

36 ation currents, reconstituting two levels of resting membrane potential.

37 otential, again recapitulating two levels of resting membrane potential.

38 cross the cell membrane balance, determining resting membrane potential.

39 pontaneous firing rate without affecting the resting membrane potential.

40 rpolarized voltages and increased I (NaP) at resting membrane potential.

41 patterns, and in setting and stabilizing the resting membrane potential.

42 ar Cl(-) levels in RGCs, hyperpolarizing the resting membrane potential.

43 ubstrate, all constructs displayed identical resting membrane potentials.

44 ive membrane properties and AMPA currents at resting membrane potentials.

45 ents and displayed substantially depolarised resting membrane potentials.

46 ese low voltage-activated channels closed at resting membrane potentials.

47 electrogram amplitude, and depolarization of resting membrane potentials.

48 Manipulating resting membrane potential, +/-15-20 mV, did not alter t

49 (+) channels are partially active at the IHC resting membrane potential (-60 mV).

50 gs to be -65.3 +/- 5.0 mV, lying between the resting membrane potential (-75.3 +/- 1.1 mV) and the ac

51 otassium (K2P) channels act to maintain cell resting membrane potential--a prerequisite for many biol

52 ontaneous network activity without affecting resting membrane potential, action potential threshold,

53 pening of voltage-gated Ca(2+) channels near resting membrane potentials, activation of NMDA receptor

54 l potential of GABA-induced currents and the resting membrane potential after GABA(A) receptor blocka

55 can vary in time, and small fluctuations in resting membrane potential alter spike frequency and eve

56 ing in increased Ca(2+) influx closer to the resting membrane potential, an effect recapitulated by A

57 SNHL neurons displayed a depolarized resting membrane potential, an increased input resistanc

58 , we observe a slow hyperpolarization of the resting membrane potential and a decrease in input resis

59 tion potential associated with a depolarized resting membrane potential and a unique, incomplete "pha

60 reased plasma membrane permeability, reduced resting membrane potential and accelerated protein catab

61 In contrast, resting membrane potential and action potential amplitud

62 tle, but not significant, differences in the resting membrane potential and action potential characte

63 or leak) channels that collectively regulate resting membrane potential and action potential firing p

64 erived neurons showed impaired maturation of resting membrane potential and action potential firing,

65 onduction velocity primarily by altering the resting membrane potential and are associated with signi

66 ly in the nervous system to control cellular resting membrane potential and are regulated by mechanic

67 voltage-gated K(+) conductance that controls resting membrane potential and cell excitability.

68 This 'gating pore current' is active at the resting membrane potential and closed by depolarizations

69 anglia, whereas tutor exposure increased the resting membrane potential and decreased the spike ampli

70 nctions, cardiac macrophages have a negative resting membrane potential and depolarize in synchrony w

71 s would cause increased sodium influx at the resting membrane potential and during trains of action p

72 insight into the channels that regulate the resting membrane potential and electrical activity of re

73 rrent in atrial myocytes, and regulating the resting membrane potential and excitability of smooth mu

74 nnels in many cell types which regulate cell resting membrane potential and excitability.

75 ssium background currents that stabilize the resting membrane potential and facilitate action potenti

76 t that acute inhibition of pERK1/2 regulates resting membrane potential and firing properties of DRG

77 These channels were open at the resting membrane potential and had an apparent half-acti

78 nd L811P evoked large depolarizations of the resting membrane potential and impaired action potential

79 ish a role for these channels in setting the resting membrane potential and in regulating the respons

80 sively decreases due to hyperpolarization of resting membrane potential and increased resting conduct

81 in mHb ChNs, which likely led to depolarized resting membrane potential and increased spontaneous fir

82 ng pressure from 30 to 90 mmHg decreased the resting membrane potential and increased the amplitude o

83 ane excitability by hyperpolarization of the resting membrane potential and increasing resting conduc

84 Changes in astrocyte resting membrane potential and input conductance correla

85 neuronal background currents that establish resting membrane potential and input resistance; their m

86 jority of this current and contribute to the resting membrane potential and intrinsic properties of d

87 eak channel, KCNK3, is vital for setting the resting membrane potential and is the primary target for

88 type potassium currents that act to regulate resting membrane potential and levels of cellular excita

89 singly, scavengers of ROS did not rescue the resting membrane potential and locomotory phenotypes.

90 also prevented glutamate-mediated changes in resting membrane potential and membrane capacitance.

91 annels play an important role in setting the resting membrane potential and modulating membrane excit

92 annels play an important role in setting the resting membrane potential and modulating membrane excit

93 sociated with painful neuropathy depolarizes resting membrane potential and produces an enhanced inwa

94 annels play an important role in maintaining resting membrane potential and promoting depolarization

95 7.2/7.3 heterotetramers, 4% activated at the resting membrane potential and rapidly activated with si

96 ardly rectifying K(+) (Kir) channels set the resting membrane potential and regulate cellular excitab

97 fibers with a focus on channels that set the resting membrane potential and regulate discharge patter

98 hey generally play a key role in setting the resting membrane potential and regulate the response of

99 They play a crucial role in setting the resting membrane potential and regulating cellular excit

100 stent voltage-gated sodium current affecting resting membrane potential and seizure threshold at the

101 r electrophysiological properties, including resting membrane potential and somal action potentials,

102 GABA reversal potential positive to both the resting membrane potential and spike threshold.

103 sufficient to mediate the galanin effect on resting membrane potential and spontaneous firing; co-ac

104 n perfusion significantly hyperpolarized the resting membrane potential and suppressed the spontaneou

105 s present in nodose neurons, is activated at resting membrane potential and that it is physiologicall

106 these thalamic properties by controlling the resting membrane potential and the availability of the t

107 ential role in the determination of the cell resting membrane potential and the inorganic ion distrib

108 he entire developmental age range tested, as resting membrane potential and the IPSC reversal potenti

109 the ion channels controlling the myometrial resting membrane potential and the mechanism of transiti

110 Regulation of the resting membrane potential and the repolarization of neu

111 Pase') contributes to the maintenance of the resting membrane potential and the transmembrane gradien

112 PITX2 mRNA modulates atrial resting membrane potential and thereby alters the effect

113 Enhanced summation depolarizes the resting membrane potential and thus lowers the response

114 eurons in the tish neocortex exhibited lower resting membrane potentials and a tendency toward higher

115 appeared physiologically normal with typical resting membrane potentials and action potentials.

116 PC6-deficient VSMCs exhibited more polarized resting membrane potentials and higher protein kinase B

117 MI-Fb had more hyperpolarized resting membrane potentials and increased outward curren

118 lowered firing thresholds, more depolarized resting membrane potentials and reduced input resistance

119 n beta3 expression leads to more depolarized resting membrane potentials and results in later reducti

120 s are required for both the establishment of resting membrane potentials and the generation of action

121 (+) channels functions to stabilize negative resting membrane potentials and thereby opposes electric

122 ent potassium channels that are activated at resting membrane potentials and therefore provide a powe

123 a increased excitability by depolarizing the resting membrane potential, and decreasing the latency o

124 icantly higher input resistance, depolarized resting membrane potential, and higher action potential

125 owed increased I(K1) density, hyperpolarized resting membrane potential, and increased action potenti

126 stead influences axonal conduction velocity, resting membrane potential, and nociceptive threshold.

127 tionship between inorganic ion distribution, resting membrane potential, and the DeltaG' of ATP hydro

128 ich is important for maintenance of the cell resting membrane potential, and the sodium current (I(Na

129 CaV3.1 mediated a substantial current at resting membrane potentials, and its deficiency had no e

130 75% and approximately 95%, respectively, at resting membrane potentials, and only activate appreciab

131 periments small neurons had more depolarized resting membrane potentials, and required smaller curren

132 e lower I(K1), resulting in more depolarized resting membrane potential ( approximately 7 mV).

133 ltaSynCaK was characterized by a depolarized resting membrane potential, as determined by a potential

134 Human cardiomyocytes exhibit two levels of resting membrane potential at subphysiological extracell

135 se drugs also led to a depolarization of the resting membrane potential at values as negative as -60

136 Except for resting membrane potential, basic properties were unalte

137 nd static-a negative spatial gradient of the resting membrane potential between the normal and ischae

138 Around resting membrane potentials, between -65 and -50 mV, Cav

139 The calcium deficit was related to resting membrane potential changes that led to abnormal

140 nificantly faster and had a more depolarized resting membrane potential compared with GFP-expressing

141 TN neurons, the Nalcn current influences the resting membrane potential, contributes to maintenance o

142 Near resting membrane potentials, DA suppressed integration o

143 onsequence of SCI (chronic depolarization of resting membrane potential) decrease sensitivity to opio

144 e displayed a significantly more depolarized resting membrane potential, decreased rheobase, and grea

145 receiving Delta9-THC showed a hyperpolarized resting membrane potential, decreased spontaneous firing

146 CXCL12 depolarized the resting membrane potential, decreased the rheobase, and

147 clamp studies reveal that R1279P depolarizes resting membrane potential, decreases current threshold,

148 reveal ionic mechanisms of the two levels of resting membrane potential, demonstrating a previously u

149 Resting membrane potential did not differ significantly

150 ion potential firing rates and more positive resting membrane potentials during the day.

151 relationship between cell volume (V(c)) and resting membrane potential (E(m)) was investigated in Ra

152 opathic pain models with more hyperpolarized resting membrane potentials (Ems) have lower SF rates.

153 rization-activated current (Ih), depolarized resting membrane potential, faster action potentials, in

154 0.3 kHz) have significantly more depolarized resting membrane potentials, faster kinetics, and shorte

155 in electrophysiological properties including resting membrane potential, firing pattern, input resist

156 a fixed, +100 mV depolarisation relative to resting membrane potential following 40 mV hyperpolarisi

157 re the onset of hearing in most rodents, the resting membrane potential for IHCs is apparently more h

158 y I(H) in nodose neurons, hyperpolarized the resting membrane potential from -63 +/- 1 to -73 +/- 2 m

159 PS neurons had a more hyperpolarized resting membrane potential from infancy to adulthood and

160 neuronal cells progressively decrease their resting membrane potential, gain characteristic Na+ and

161 During this period, Vm remains at the resting membrane potential >80% of the time, regardless

162 of 3 different tissues with widely different resting membrane potentials has been shown to be equal t

163 cells held at more depolarized in vivo-like resting membrane potentials have a tonic influx of Ca2+;

164 characterized by a relatively hyperpolarized resting membrane potential, higher spontaneous and induc

165 hannels are implicated in the control of the resting membrane potential, hormonal secretion, and the

166 t 2 weeks, membrane resistance decreased and resting membrane potential hyperpolarized due in part to

167 The mean delay increased, whereas the resting membrane potential hyperpolarized with a time co

168 By controlling the resting membrane potential, I(K1) modifies sodium channe

169 At the resting membrane potential if most NCX is localized to t

170 Although this mutation depolarizes resting membrane potential in both types of neurons, it

171 ation currents, reconstituting two levels of resting membrane potential in cardiomyocytes.

172 type potassium channel is thought to set the resting membrane potential in cochlear HCs.

173 The cell resting membrane potential in each of 3 different tissue

174 potassium channels enforce tight control of resting membrane potential in excitable cells.

175 m channels contributes to the maintenance of resting membrane potential in excitable cells.

176 K2P1 currents, accounting for two levels of resting membrane potential in human cardiomyocytes and d

177 and regularity, as well as depolarizing the resting membrane potential in mHb ChNs in control-sleep

178 tability, but was accompanied by depolarized resting membrane potential in mHb ChNs.

179 nnel, SLO2.1, is expressed and active at the resting membrane potential in MSMCs.

180 Channels contributing to resting membrane potential, including HCN2 responsible i

181 gnificantly decreased amplitude, depolarized resting membrane potential, increased duration and reduc

182 ncreased excitability was due to depolarized resting membrane potential, increased resistance, increa

183 itability of bladder neurons by depolarizing resting membrane potential, increasing action potential

184 isoform 1 (K2P1) recapitulate two levels of resting membrane potential, indicating the contributions

185 ual stimuli that evoked sustained changes in resting membrane potential, input resistance, and membra

186 ons did not differ from normal in their mean resting membrane potentials, input resistances, or thres

187 s action-potential firing patterns and their resting membrane potential is modulated by a background

188 The resting membrane potential is viewed as a diffusion pote

189 PITX2 and ion channels regulating the resting membrane potential may provide novel targets for

190 Resting membrane potential measured using intracellular

191 knock-out mice (BDNF(Pax2) KO) we found that resting membrane potentials, membrane capacitance and re

192 ard-rectifying K+ channel, which lowered the resting membrane potential, mimicked the effect of prema

193 nnels play a significant role in setting the resting membrane potential, modulating action potential

194 Rods maintained tonic release at resting membrane potentials near those in darkness, caus

195 e to many basic neuronal functions including resting membrane potential, neurotransmitter release and

196 The resting membrane potential of aging type I neurons in th

197 Intracellular recording revealed a resting membrane potential of approximately -70 mV.

198 The current produces a major impact on the resting membrane potential of basal neurons.

199 bTREK-1 K(+) channels set the resting membrane potential of bovine adrenal zona fascic

200 hCSF did not affect the resting membrane potential of CA1 interneurons but cause

201 Conversely, macrophages render the resting membrane potential of cardiomyocytes more positi

202 ily 2 (Kir2) channels primarily maintain the resting membrane potential of cardiomyocytes.

203 Kir2) channels primarily maintain the normal resting membrane potential of cardiomyocytes.

204 ICC Ca(2+) transient firing regulated the resting membrane potential of colonic tissues as a speci

205 ential (-60.6+/-0.5 versus -70.6+/-0.6 mV of resting membrane potential of control cells; P<0.01) and

206 nction attributes to the channel, depolarize resting membrane potential of dorsal root ganglion neuro

207 ial (AP) threshold without any change in the resting membrane potential of hippocampal CA3 pyramidal

208 ation currents, accounting for two levels of resting membrane potential of human cardiomyocytes.

209 potassium (GIRK) channels contribute to the resting membrane potential of many neurons, including do

210 M-type (Kv7, KCNQ) K(+) channels control the resting membrane potential of many neurons, including pe

211 18beta-GA had no detectable effect on the resting membrane potential of motoneurons, but led to a

212 Mutated channels diminish the resting membrane potential of mouse primary sensory neur

213 strating steady state window currents at the resting membrane potential of myometrium at term.

214 The pumps maintain ionic gradients and the resting membrane potential of neurons, but increasing ev

215 The resting membrane potential of phospholamban-knockout ant

216 netic loss of GIRK2 depolarized the day-time resting membrane potential of SCN neurons compared to co

217 nnels play a central role in maintaining the resting membrane potential of skeletal muscle fibres.

218 ds upon their biophysical properties and the resting membrane potential of smooth muscle.

219 , Na(+), and Ca(2)(+) ions all influence the resting membrane potential of the neuron.

220 Histamine hyperpolarized the resting membrane potential of the ON bipolar cells by 5

221 tifier potassium currents, and increased the resting membrane potential of these neurons.

222 effect on voltage-dependent K(+) currents or resting membrane potential of UBSM cells, suggesting tha

223 SNP hyperpolarized the resting membrane potential of wild-type antrum smooth mu

224 reshold sodium conductance that controls the resting membrane potentials of neurons.

225 The resting membrane potentials of the mutant neurons are re

226 s activity in ORNs tonically depolarizes the resting membrane potentials of their target PNs and loca

227 s application of PACAP did not affect either resting membrane potential or membrane excitability of C

228 coupled to its ability to modulate neuronal resting membrane potential, perhaps through effects on l

229 as high degree of automaticity, depolarized resting membrane potential, Phase 4- depolarization, and

230 lum via IP3Rs contributes to the decrease in resting membrane potential, prolongation of the action p

231 function in the SCN contributes to day-time resting membrane potential, providing a mechanism for th

232 K(2P) channels regulate the resting membrane potential, providing background K(+) cu

233 king SK channels with apamin depolarized the resting membrane potential, reduced resting conductance,

234 el agonist, significantly hyperpolarized the resting membrane potential, reduced the number of action

235 e platelet and megakaryocyte, which sets the resting membrane potential, regulates agonist-evoked Ca(

236 this study, we show that by depolarizing the resting membrane potential relative to the reversal pote

237 nown for maintaining the ionic gradients and resting membrane potential required for generating actio

238 ncreased input resistance and hyperpolarized resting membrane potential, respectively.

239 s predominantly influence input conductance, resting membrane potential, resting spike rate, phasing

240 ads to increased Ca(2+) influx closer to the resting membrane potential, resulting in intracellular C

241 e that ion channels controlling the neuronal resting membrane potential (RMP) also control anesthetic

242 ntials (APs) and an unstable and depolarized resting membrane potential (RMP) because of lack of I(K1

243 s are considered to simply hyperpolarize the resting membrane potential (RMP) by increasing the potas

244 A transwall gradient in resting membrane potential (RMP) exists across the circu

245 rcular smooth muscle layers have a transwall resting membrane potential (RMP) gradient that is depend

246 Intracellular measurements of resting membrane potential (RMP) in uninjured and injure

247 on, the inhibition of IK and the decrease of resting membrane potential (RMP) induced by hypoxia were

248 /PeN) of males and females exhibit a bimodal resting membrane potential (RMP) influenced by K(ATP) ch

249 hology, while for the NM rate changes affect resting membrane potential (RMP) more than APD.

250 TREK-1 and TREK-2 channels in regulating the resting membrane potential (RMP) of isolated chicken emb

251 modation response mode induced by changes in resting membrane potential (RMP) or added neurotrophin-3

252 ective K(ATP) channel inhibitor, depolarized resting membrane potential (RMP) recorded in perforated

253 hyperactivity and chronic depolarization of resting membrane potential (RMP) that is maintained by c

254 Low Ko also hyperpolarized the resting membrane potential (RMP) without significant alt

255 modulation of action potential threshold and resting membrane potential (RMP), amplified by control o

256 lLN(v) resting membrane potential (RMP), spontaneous AP firing

257 s difference stems from the more depolarized resting membrane potential (RMP; 7 mV) and higher input

258 ' that rundown of inhibitory SK responses at resting membrane potentials (RMPs) reflects depletion of

259 ore negative in the distal dendrite than the resting membrane potential, so that GABA depolarizes and

260 se data reveal a primary functional role for resting membrane potential taking place within the first

261 have larger leak currents and more negative resting membrane potentials than CA1 neurons, and conseq

262 er input resistances and more hyperpolarized resting membrane potentials than OML interneurons.

263 milarly, rods lacking CNG channels exhibit a resting membrane potential that was ~10 mV hyperpolarize

264 We propose that at the IHC resting membrane potential, the ribbon synapse operates

265 ded IA channels do contribute to controlling resting membrane potentials, the regulation of current t

266 erve fiber conduction by hyperpolarizing the resting membrane potential, thereby increasing Na(+) cha

267 ductance when AIIs were hyperpolarized below resting membrane potential, thereby increasing the avail

268 receptors on amacrine cells with depolarized resting membrane potentials therefore can mediate the la

269 tes show both hyperpolarized and depolarized resting membrane potentials; these depolarized potential

270 om AS model mice and observed alterations in resting membrane potential, threshold potential, and act

271 Our results show how PIP(2) can control the resting membrane potential through a specific ion-channe

272 hin injured cortex are healthy with a normal resting membrane potential, time constant (tau), and inp

273 d current-voltage relationships, causing the resting membrane potential to spontaneously jump from hy

274 king in several conditions, ranging from the resting membrane potential to stimuli designed to approx

275 ential is hyperpolarized with respect to the resting membrane potential, type-1 metabotropic glutamat

276 ant for the establishment and maintenance of resting membrane potentials upon which action potentials

277 On the other hand, at the resting membrane potential (V(m) ~-80 mV), NCX removes C

278 lls express bTREK-1 K+ channels that set the resting membrane potential (V(m)) and couple angiotensin

279 which was also linked to pFUS increasing the resting membrane potential (V(m)) of islets.

280 ansmitter acetylcholine fine-tunes the IHC's resting membrane potential (V(m)), and as such is crucia

281 Hair cell resting membrane potential (V(rest)) remained surprising

282 luorescent Ca(2+) imaging and measurement of resting membrane potential (Vm).

283 tor (GLR) agonist, was used to modulate cell resting membrane potential (Vmem) according to methods d

284 Rheobase decreased, resting membrane potential was depolarized, and electrog

285 The fibroblast resting membrane potential was hyperpolarized (?53 +/- 2

286 Resting membrane potential was more depolarized in Pitx2

287 r proper dendritic tip location, and the DBC resting membrane potential was restored.

288 anced effectiveness of Na-channel block when resting membrane potential was slightly depolarized.

289 In addition, the "resting" membrane potential was dependent on ongoing spi

290 Resting membrane potentials were equivalent in TNs (-48

291 ular calcium stores, and run down rapidly at resting membrane potentials when calcium stores become d

292 However, near resting membrane potentials where I(h) is engaged, IPSPs

293 ms), thalamic neurons reached a depolarized resting membrane potential which affected key features o

294 cts upon degeneration through changes in the resting membrane potential, which in turn regulates the

295 pes of cells, the NKA generates the negative resting membrane potential, which is the basis for almos

296 balances in sarcolemmic ion permeability and resting membrane potential, which modifies excitation-co

297 on produced a small hyperpolarization of the resting membrane potential, which was accompanied by an

298 5.0%) increased LA diastolic tension and the resting membrane potential with decreased action potenti

299 All preparations exhibited elevated resting membrane potential within and near the PZ and ac

300 The hyperpolarization of the resting membrane potential would also reduce neurotransm