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

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

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

3 etigabine or flupirtine to hyperpolarize the resting membrane potential.

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

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

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

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

8 nt synaptic waveforms by hyperpolarizing the resting membrane potential.

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

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

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

12 nfluenced by sustained depolarization of the resting membrane potential.

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

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

15 following an action potential initiated from resting membrane potential.

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

17 ificantly higher in neurons with depolarized resting membrane potential.

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

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

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

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

22 ata (AZF) cells, bTREK-1 K+ channels set the resting membrane potential.

23 artate receptor and thus are "silent" at the resting membrane potential.

24 otor neuron B8 does not occur when B21 is at resting membrane potential.

25 e of an outward current around and above the resting membrane potential.

26 ove +10 mV and was without effect around the resting membrane potential.

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

28 pontaneous firing rate without affecting the resting membrane potential.

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

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

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

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

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

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

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

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

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

38 n and hyperpolarization of the cardiomyocyte resting membrane potential.

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

40 ction potential amplitude by stabilizing the resting membrane potential.

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

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

43 ents and displayed substantially depolarised resting membrane potentials.

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

45 electrogram amplitude, and depolarization of resting membrane potentials.

46 nward currents were occasionally observed at resting membrane potentials.

47 ubstrate, all constructs displayed identical resting membrane potentials.

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

49 ted in glomus cells of HF rabbits, and their resting membrane potentials (-34.7 +/- 1.0 mV) were depo

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

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

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

53 d electrophysiological properties, including resting membrane potential, action potential (AP) proper

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

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

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

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 In contrast, resting membrane potential and action potential amplitud

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

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

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

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

65 in K+ channels are important determinants of resting membrane potential and cellular excitability.

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

67 st that IK(V) plays a role in regulating the resting membrane potential and contributes to the repola

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

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

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

71 Potassium channels control the resting membrane potential and excitability of biologica

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

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

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

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

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

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

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

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

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

81 Changes in astrocyte resting membrane potential and input conductance correla

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

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

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

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

86 itatory inputs when PFC neurons are near the resting membrane potential and may provide a mechanism b

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

88 These effects on resting membrane potential and membrane resistance persi

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

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

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

92 Because of their ability to stabilize the resting membrane potential and oppose electrical activit

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

100 mbryonic based on the relatively depolarized resting membrane potential and slow AP upstroke.

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 rties of K(+) channels that may regulate the resting membrane potential and the excitability of MNCs

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

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

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

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

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

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

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

115 regulators of neuronal excitability, setting resting membrane potentials and firing thresholds, repol

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

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

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

119 T but not 11(R),12(S)-EET hyperpolarized the resting membrane potentials and shortened the duration o

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

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

129 75% and approximately 95%, respectively, at resting membrane potentials, and only activate appreciab

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

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

132 oltage-gated K+ channels activating close to resting membrane potentials are widely expressed and dif

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 only evident from just after birth, when the resting membrane potential became sufficiently negative

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

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

140 hus, these channels do not contribute to the resting membrane potential but are activated by a rise i

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

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

143 Near resting membrane potentials, DA suppressed integration o

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

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

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

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

148 Resting membrane potential did not differ significantly

149 cing relative changes in cell volume (V) and resting membrane potential (E(m)) following osmotic chal

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

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

152 uscle studies revealed no abnormality of the resting membrane potential, evoked quantal release, syna

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 ium (Kir) channels are prime determinants of resting membrane potential in neurons.

175 background K+ current (IKN), which sets the resting membrane potential in rabbit pulmonary artery sm

176 current (Ih) is important in the control of resting membrane potential, in the regulation of network

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

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

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

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

181 eveloping rats, without a change in the mean resting membrane potential, indicating that lasting alte

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

183 Although the resting membrane potential, input resistance and action

184 Passive membrane properties included a mean resting membrane potential, input resistance and time co

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

186 r intrinsic electrophysiological properties (resting membrane potential, input resistance, single spi

187 ent effect on cellular physiology, including resting membrane potential, input resistance, spike thre

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

189 input, but three recent studies show how the resting membrane potential interacts with integrative pr

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

191 or distortion by the shunt suggests that the resting membrane potential is no more negative than -75

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

193 Resting membrane potential measured using intracellular

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

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

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

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

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

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

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

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

202 The resting membrane potential of bovine pulmonary artery en

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

204 l recordings showed that the variance in the resting membrane potential of CA1 stratum oriens interne

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

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

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

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

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

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

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

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

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

214 18beta-GA had no detectable effect on the resting membrane potential of motoneurons, but led to a

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

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

217 Background potassium channels control the resting membrane potential of neurones and regulate thei

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

219 The resting membrane potential of phospholamban-knockout ant

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

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

222 vascular tone is strongly influenced by the resting membrane potential of smooth muscle cells, depol

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

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

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

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

227 by promoting a depolarizing influence on the resting membrane potential of vascular smooth muscle cel

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

229 Resting membrane potentials of LC neurons in brain slice

230 The resting membrane potentials of the mutant neurons are re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 icantly lower threshold but exhibited normal resting membrane potential (RMP) and action potential am

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

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

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

249 ardiac repolarization and maintenance of the resting membrane potential (RMP) in guinea pig ventricul

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

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

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

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

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

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

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

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

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

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

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

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

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

263 of CO lead to hyperpolarization of a cell's resting membrane potential, suggesting that CO may funct

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

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

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

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

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

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

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

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

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

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

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

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

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

280 K)) results in a small depolarization in the resting membrane potential (V(rest)).

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

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

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

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

285 Resting membrane potential was more depolarized in Pitx2

286 In large terminals (10-16 microm diameter), resting membrane potential was more negative than in sma

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 Baseline myogenic tone and resting membrane potential were not affected by DM.

291 Resting membrane potentials were equivalent in TNs (-48

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

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

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

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

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