ライフサイエンスコーパス: current amplitude

1 or the stimulating frequency (with constant current amplitude).

2 aximal peak currents by reducing the unitary current amplitude.

3 ge sensitivity and a concomitant decrease in current amplitude.

4 KF-DNA-dNTP complexes on the basis of ionic current amplitude.

5 ling because of the decrease in the synaptic current amplitude.

6 93 cells), as well as native RMCA myocyte Kv current amplitude.

7 -type current levels and kinetics, and Na(+) current amplitude.

8 lity of block varies directly with inward Na current amplitude.

9 no-activation threshold and elevated mechano-current amplitude.

10 patches, but has no effect on single-channel current amplitude.

11 the channel opening rate and the whole-cell current amplitude.

12 essed the open probability without affecting current amplitude.

13 annel-gating kinetics with no attenuation in current amplitude.

14 rate constants, increasing the steady-state current amplitude.

15 fluid flow increased endogenous native TRPM7 current amplitude.

16 d by protein kinase C (PKC), which decreases current amplitude.

17 The ASIC1a subunit was key in establishing current amplitude.

18 CNE2 may associate with ERG and suppress its current amplitude.

19 CNE2 may associate with HCN2 and enhance its current amplitude.

20 id-evoked currents, whereas Lin-7b increased current amplitude.

21 f syntaxin 1A were necessary for the reduced current amplitude.

22 e which did, however, substantially increase current amplitude.

23 limiting effects of exon 29 inclusion on the current amplitude.

24 ed synaptic release probability and synaptic current amplitude.

25 -bisphosphate depletion, and increased KCNQ2 current amplitude.

26 binding sites produced no effect on Kv7.2/3 current amplitude.

27 ces revealed only partial rescue of synaptic current amplitude.

28 mbrane properties and GABAergic postsynaptic current amplitude.

29 brane is a key determinant of the whole cell current amplitude.

30 re helix-S6 interactions, in governing KCNQ3 current amplitudes.

31 gion--have been implicated in governing KCNQ current amplitudes.

32 e kept low by PTEN and do not affect calcium current amplitudes.

33 nd reduced miniature inhibitory postsynaptic current amplitudes.

34 rally stimulated with submaximal and maximal current amplitudes.

35 on spontaneous release of GABA than on VACC current amplitudes.

36 Two of the TRPC6 mutants had increased current amplitudes.

37 s current amplitudes, including supramaximal current amplitudes.

38 d increased whole-cell Kv7.2, but not Kv7.3, current amplitudes.

39 ionally activated c-Src resulted in enhanced current amplitudes.

40 ion in the selectivity filter and increasing current amplitudes.

41 loop in CaV1.1e did not significantly reduce current amplitudes.

42 eading to an even more prominent decrease in current amplitudes.

43 utamate transport rates and associated anion current amplitudes.

44 e-cell currents, with GABA exhibiting a peak current amplitude 10-fold greater than glutamate.

45 ably expressing STIM1, potentiate I(CRAC) to current amplitudes 15-20 times larger than native I(CRAC

46 KV 7.3 subunits, either by globally reducing current amplitudes (3 pore mutations) or by a depolarizi

47 verexpression had two effects: a decrease of current amplitude (4- to 15-fold for cloned channels and

48 ctroconvulsive therapy (ECT) at conventional current amplitudes (800-900 mA) is highly effective but

49 nal whole-cell recordings, CO only decreased current amplitudes above +10 mV and was without effect a

50 manifested as a progressive increase in the current amplitude, accompanied by a slower deactivation

51 onepantel alone were larger than the maximal current amplitudes achieved with betaine or choline, mak

52 ion as divalent cation channels with similar current amplitudes across a range of holding potentials;

53 anges in lens diameter for the same stimulus current amplitudes allow the relationship between refrac

54 ally, the Q177K change resulted in decreased current amplitudes, altered desensitization decay time c

55 The voltage-dependent distribution of the current amplitudes among fast-, slow- and non-deactivati

56 KChIP2e caused a reduction in current amplitude, an acceleration of inactivation and a

57 n receptor to reduce excitatory postsynaptic current amplitudes, an effect previously shown to be med

58 Comparing the early receptor current amplitude and action spectra between WT and the

59 muscle Ca(v)1.1 channel complex, modulating current amplitude and activation and inactivation proper

60 tol-4,5-bisphosphate (PIP2) depletion on MET current amplitude and adaptation, leading to the postula

61 l nervous system by increasing NMDA receptor current amplitude and Ca(2+) flux in an isoform-dependen

62 within the physiological range can reduce Kv current amplitude and can have major effects on Kv chann

63 line ND7/23 significantly increases the peak current amplitude and causes a 4 mV depolarizing shift o

64 In line with these changes, the current amplitude and decay time of NMDARs in PFC was si

65 ifference currents also demonstrated that BK current amplitude and density were greater during the ni

66 AMPA current amplitude and duration were increased significan

67 on both channels is to produce a decrease in current amplitude and electrophysiological analyses demo

68 ced sodium channel activities with increased current amplitude and facilitated recovery, which was co

69 MST (23%), demonstrating that ECT with a low current amplitude and focal electrode placement can indu

70 ase in the miniature excitatory postsynaptic current amplitude and frequency.

71 itory effects on synaptic transmission, Ca2+ current amplitude and gating and G protein modulation.

72 h presynaptic Ca2+ channels, with effects on current amplitude and gating representing likely mechani

73 of the mutant channel revealed a decrease in current amplitude and hypersensitivity to steady-state i

74 cantly altered the relationship between Ca2+ current amplitude and inactivation in ways that were une

75 ioning voltages dramatically increase CLH-3a current amplitude and induce a slow inactivation process

76 annel-open probability without modifying the current amplitude and induced slow transitions between o

77 The peak Ca(2+) current amplitude and its rate of inactivation could be

78 homoquinolinate has identical single-channel current amplitude and mean open-channel duration but tha

79 Analysis of the ionic current amplitude and noise, as the protein unfolds and

80 Transfection with GFP alone did not affect current amplitude and overexpression of the Kv2.1 WT res

81 Based upon the observed pH dependence of the current amplitude and oxidation/reduction peaks, the cat

82 ncrease in miniature excitatory postsynaptic current amplitude and partly by a mechanism involving my

83 Activators of PKC increased current amplitude and removed inactivation of Kv3.3 curr

84 -target hERG channel by reducing the maximal current amplitude and shifting the voltage dependence of

85 KChIP2f increased the current amplitude and slowed the rate of inactivation, b

86 4 to 6.8) slowed the rise time and increased current amplitude and total charge transferred.

87 also produced a pronounced reduction of both current amplitude and variance of constitutively active

88 V1 to acid activation but did not affect the current amplitude and/or the activation-inactivation pro

89 sylation decreased peak alpha1beta2 receptor current amplitudes and altered the gating properties of

90 r, partly explaining lower alpha7beta2 nAChR current amplitudes and challenges in identifying the fun

91 Moreover, BSA alone increased peak ACh current amplitudes and diminished desensitization rates

92 Precise dose-response relationships allowed current amplitudes and firing frequencies to be tuned by

93 These receptor currents had similar peak current amplitudes and GABA EC50 values.

94 d cell size commensurate with increased K(+) current amplitudes and mimics physiological hypertrophy.

95 calculated from the state sequences, and the current amplitudes and noise variances are determined fr

96 For alpha3T115Cbeta2, both current amplitudes and potentiation were reduced.

97 The reduction in current amplitudes and the accelerated inactivation of d

98 bunit transcripts and resulting in increased current amplitudes and the normalization of current dens

99 ion and magnitude of GABAA receptor-mediated current amplitudes and was observed to have a linear cor

100 14 expression, a decrease in transient Na(+) current amplitude, and a hyperpolarizing shift in the vo

101 ed the rise in cAMP levels and L-type Ca2(+) current amplitude, and abolished the inotropic effect fo

102 Estradiol decreased the persistent sodium current amplitude, and induced a significant negative sh

103 ion of a PIP2 5'-phosphatase sharply reduced current amplitudes, and also blunted the inhibition.

104 rents that displayed ASIC-like currents, the current amplitudes, and the pH dose-response relationshi

105 However, transport uncoupling, unitary current amplitudes, and the voltage dependence of the de

106 potential reveals that very small changes in current amplitude are sufficient to prevent hormone secr

107 lmost complete loss of evoked responses, and current amplitudes are reduced by 94%.

108 aradox, RGSs do not reduce steady-state GIRK current amplitudes as expected from the accelerated rate

109 ) is constant irrespective of changes in the current amplitude, as if the direction and amplitude of

110 4 mm d-glucose, 10 nm ET-1 decreased peak Kv current amplitude at +60 mV from 23.5 +/- 3.3 to 12.1 +/

111 carinic receptors with methacholine, reduced current amplitudes at all potentials with minor effects

112 ion, the significant increase in ATP-induced current amplitudes at low IVM concentrations, and the mo

113 e transporter leads to reduction of the peak current amplitude because occupancy of the transporter b

114 ccount quantitatively for the differences in current amplitude between the 2 channel types.

115 or AP180C did not abolish the differences in current amplitudes between Kv1.1 and Kv1.1(I400V), sugge

116 mes after current perturbation depend on the current amplitude but can be kept to below 1 min for the

117 r Na+ has no effect on the peak AMPH-induced current amplitude but inhibits the steady-state current.

118 C open probability (P(o)) and single-channel current amplitude but not the unit conductance.

119 Cadmium did not affect current amplitude but reduced peak latency.

120 significantly decreased the transient sodium current amplitude, but prolonged the sodium current inac

121 V2/6) not only reduced Na(v)1.7 and Na(v)1.8 current amplitudes, but also alleviated SNI-induced mech

122 hiometry or decreased GABA-evoked whole-cell current amplitudes, but with different levels of reducti

123 ndent manner, reaching a maximal increase in current amplitude by 100% and > or = 300% (1-s test puls

124 eceptor agonist SKF 81297 reduces peak Na(+) current amplitude by 20.5%, as reported previously.

125 rminus of NaV1.4 and NaV1.6 channels reduced current amplitude by 99 and 62%, respectively.

126 R420H and R423H suppress Kv3 current amplitude by a dominant negative mechanism.

127 in voltage-dependent gating and macroscopic current amplitude by constructing a series of chimeric C

128 The reduction of sodium current amplitude by estradiol suggests a negative feedb

129 PIP2 increases the macroscopic current amplitude by stabilizing the open conformation o

130 tion) produce similar effects on macroscopic current amplitude by the different ring system analogues

131 e trafficking motif reduced kainate receptor current amplitudes by >90% and resulted in retention of

132 L subunits produced intermediate macroscopic current amplitudes by increasing incorporation of wild-t

133 estibule/pore entrance of hERG and increases current amplitudes by promoting channel activation while

134 characterized by a return to a steady-state current amplitude close to the prestimulus value, after

135 1) a gain-of-function effect on the maximal current amplitude, consistent with a stabilization of th

136 GIRK current amplitude could be partially restored after bacl

137 or function, including decreased NMDA-evoked current amplitude, cytoplasmic Ca(++), and gene expressi

138 o modify the channel protein showed that the current amplitudes decrease in steps leading to complete

139 s with minimal effects on the peak transient current amplitude, demonstrating that resurgent currents

140 onal experiments revealed that inward Ca(2+) current amplitudes/densities were also increased in caPI

141 re permeant through the RyR but with reduced current amplitude depending upon the diameter of the res

142 Open-channel current amplitude distributions were indistinguishable f

143 ne Ca(2+) induces a large decrease in T-type current amplitude due to a hyperpolarizing shift in the

144 t amplitudes indicated that the reduction in current amplitude during step depolarizations was a cons

145 how that lynx1 promotes the largest of three current amplitudes elicited by ACh through alpha(4)beta(

146 in the positive direction and suppresses its current amplitudes elicited by strong depolarizing pulse

147 The net result is increased current amplitude, enhanced Ca(2+) sensitivity, and rate

148 The flow-induced increase in current amplitude exhibited an apparent shift in steady-

149 y understood, exhibiting alterations in peak current amplitude, extents and kinetics of inactivation,

150 and increasing miniature excitatory synaptic currents amplitude/frequency, respectively.

151 um channel protein abundance and peak sodium current amplitudes (H/H, 41.0+/-2.9 pA/pF at -30 mV; DN/

152 and Ca(2+)/calmodulin strongly reduced the M current amplitude; however, at voltages near the thresho

153 VDP manifests as a potentiation of current amplitude, hyperpolarizing shift in voltage sens

154 merization process; and 3), the open-channel current amplitude (i(0)), which reports whether a mutati

155 ponding in rat drug discrimination, or alter current amplitude in alpha4beta2- and alpha3beta4-contai

156 ed NMDAR-EPSC amplitude and whole-cell NMDAR current amplitude in dissociated PFC neurons.

157 Lowering and individualizing the current amplitude in electroconvulsive therapy (ECT) has

158 revealed large cell-to-cell variance in the current amplitude in neurones from both sectioned and co

159 calcium-dependent PKC, decreased baseline T-current amplitude in nRT cells and abolished the effects

160 However, the evoked AMPA current amplitude in PVN neurons was similar in WKY and

161 CA consists of an increase in current amplitude in response to repetitive depolarizing

162 ssociated VZV significantly increased sodium current amplitude in the cell line when compared with no

163 0 confers bidirectional regulation of L-type current amplitude in transfected HEK293 cells and hippoc

164 of cations by D633 may contribute to inward current amplitude in TRPC5.

165 Overexpression of GM130 suppressed HERG current amplitude in Xenopus oocytes, as if by providing

166 TSEA+) covalently modifies the RyR to reduce current amplitudes in a time-dependent and stepwise mann

167 at these two residues reduce the macroscopic current amplitudes in cells expressing CLC-K/barttin cha

168 the effects of SE on mIPSC and tonic GABA(A) current amplitudes in granule cells, consistent with the

169 rodotoxin-sensitive resurgent and persistent current amplitudes in large, but not small, diameter DRG

170 aracterized by measuring inhibitory synaptic current amplitudes in response to repetitive stimuli.

171 vivo by morpholino knock-down reduced Na(+) current amplitudes in Rohon-Beard neurons of zebrafish e

172 s in stable hERG-HEK cells showed effects on current amplitude, inactivation, and deactivation.

173 scan ultrasonography for increasing stimulus current amplitudes, including supramaximal current ampli

174 Peak current amplitude increased by as much as approximately

175 The ACh-activated current amplitude increased with age and demonstrated th

176 channels, syntaxin 1A co-expression reduced current amplitudes, increased voltage-dependent inactiva

177 We show that current amplitude increases with indentation, not force,

178 ns, estradiol reduced miniature postsynaptic current amplitude independent of time of day.

179 brane gating charge movements and ionic tail current amplitudes indicated that the reduction in curre

180 significant reduction of the single-channel current amplitude, indicating an interaction of bile aci

181 The current amplitude is amantadine sensitive.

182 load falls to the point at which single RyR current amplitude is no longer sufficient to sustain int

183 es show that voltage-gated persistent sodium current amplitude is regulated by alternative splicing o

184 We propose that in cardiac myocytes the IKs current amplitude is under dynamic control by the availa

185 umber of recordings exhibited three separate current amplitude levels, indicating the presence of sma

186 I(2) was characterized by larger current amplitude, loss of outward rectification, and al

187 fitting model suggested that L-cys increases current amplitude mainly by increasing the transition ra

188 Lowering and individualizing the current amplitude may reduce side effects by virtue of a

189 s seemingly random variability of individual current amplitudes may obscure mechanisms that globally

190 However, mean T-type current amplitude measured in the chronically drinking a

191 strogen receptor-beta agonist DPN, decreased current amplitude measured in the morning (AM), but had

192 NT and AID peptides reduced whole-cell Ca2+ current amplitude, modified voltage dependence of Ca2+ c

193 ERG channels, ICA-105574 steeply potentiated current amplitudes more than 10-fold with an EC(50) valu

194 The current amplitude necessary for each phase-shifted test

195 Spark local control follows single RyR current amplitude, not simply SR Ca(2+) load.

196 ernal solution led to an increase in maximal current amplitude of > 300 % within 5 min.

197 The major subconductance had a current amplitude of 52% of fully open, it was reversibl

198 However, the peak current amplitude of DRG neuron response induced by ASIC

199 cal data in which GAP does not alter maximal current amplitude of G protein-activated ion channels, b

200 xide (BPAM521) potentiated the recorded peak current amplitude of GluK2a 12-fold at a concentration o

201 BPAM344 (100 muM) also potentiated the peak current amplitude of KAR subunits GluK3a (59-fold), GluK

202 With the reported method, single-channel current amplitude of native voltage-gated calcium channe

203 ing rate constants as well as the whole-cell current amplitude of the homomeric GluA2Q AMPA receptor

204 The frequency and current amplitude of the modulation states are dependent

205 T-1c and EAAT5 also differ in single-channel current amplitudes of associated anion channels.

206 Unitary current amplitudes of EAAT5 anion channels turned out to

207 ession, however, did not alter the expressed current amplitudes of Kv1.4 and Kv2.1 channels, indicati

208 respectively, suggesting that the effects on current amplitudes of the TD and the carboxy-terminus ar

209 However, the effect of current amplitude on the electric field (E-field) in the

210 over-expression did not change L-type Ca(2+) current amplitude or Ca(2+) efflux rates via the Na(+)-C

211 No differences in current amplitude or kinetics were found between ASIC2 a

212 Mutations at these sites increase current amplitudes or result in channels with deficient

213 The increases in K(+) current amplitudes paralleled the observed cellular hype

214 Measured current amplitude parallels intracellular chloride conce

215 currents, which was followed by a phase when current amplitudes partially recovered, but activation g

216 However, peak current amplitude, pH sensitivity, and selectivity were

217 dings to study the properties of acid-evoked currents (amplitude, pH sensitivity, the kinetics of des

218 r formation and oxidation-induced changes in current amplitudes predictive of the A/C conformation.

219 nactivation can not explain the reduction in current amplitude produced by co-expressing syntaxin and

220 Current amplitude promptly returned to normal control le

221 synaptic strength (assessed as the AMPA/NMDA current amplitude ratio) and increased spine head diamet

222 The glutamate- to kainate-current amplitude ratios differed, with GluR3-GFP being

223 mus neurons or striatal MSNs, it reduced the current amplitudes recorded from dentate gyrus granule c

224 Individualizing the current amplitude reduced interindividual variation in t

225 f-function effects (mostly dominant-negative current amplitude reduction) in eight patients or only g

226 the KCNQ1 current, exhibiting an increase in current amplitude, reduction of inactivation, and slowin

227 ss is reduced, suggesting that the decreased current amplitude reflects a reduction in the number of

228 , although miniature excitatory postsynaptic current amplitudes remained similar.

229 Rho abolished the inhibition of Kir2.1 with current amplitudes remaining at control levels in the pr

230 APs) during current steps, and the threshold current amplitude required to generate an AP was roughly

231 ulses) as a means of determining the minimum current amplitude required to induce a seizure with ECT

232 rvating glycolytic muscle had greater inward current amplitude responses to protons and capsaicin as

233 and Na(+) produce characteristic pulse-like current amplitude signatures that allow the identificati

234 rties upon their removal, causing changes in current amplitude, single-channel conductance, and EC50

235 an agonist, even noxious cold only increases current amplitude slightly.

236 KChIP2g increased current amplitudes, slowed the rate of inactivation and

237 Their average peak inward current amplitudes started to increase within 5 min and

238 the millisecond time scale between two ionic current amplitude states when captured atop the alpha-he

239 nificant increase in GABA EC(50) and maximal current amplitude, suggesting that the ILD must be intac

240 Rho resulted in a reduction in basal Kir2.1 current amplitudes, suggesting that Rho inhibits Kir2.1.

241 In the presence of NS206, peak current amplitudes surpassed those of maximal efficaciou

242 Our measurements of write-current amplitude, switching speed, endurance and data r

243 enetics because of its combination of larger current amplitudes than those of previously reported ACR

244 rgely because load determines the single RyR current amplitude that drives inter-RyR CICR.

245 rent ranging from approximately 1-3% of peak current amplitude that was significantly greater than WT

246 ls, GABA induced dose-dependent increases in current amplitude that were inhibited by bicuculline and

247 ence of activation and a decrease in maximal current amplitude; these effects can be ascribed to HCN1

248 voked by a wide range of electrode sizes and current amplitudes, they are invariably described as sma

249 d and reversible inhibition of whole-cell K+ current amplitudes; this was PO2 dependent with a maxima

250 brain has not been previously linked to the current amplitude threshold for seizure induction.

251 application of 1 microM GABA increased tonic current amplitude to approximately 70 pA in 100% of TC n

252 The peak current amplitude to pH 6.7 is significantly attenuated

253 the oocyte cytoplasm restores mutant K(ATP) current amplitude to that measured in the cell-attached

254 The peak current amplitudes to pH 6.0 were 0.84 +/- 0.06 nA (oxid

255 An analysis of current amplitudes, transition times, and concentrations

256 eedback of proton concentration on peak H(+) current amplitude (v(max)) and ATP consumption (K(m)) of

257 etermined by the [NH3]o, not [NH4 (+)]o, and current amplitudes varied with the [H(+)] gradient.

258 Current amplitude was also initially increased.

259 The current amplitude was also up-regulated by 25 microM int

260 mV, we found that the average single-channel current amplitude was approximately 0.04 pA, increasing

261 e decrease in arcuate miniature postsynaptic current amplitude was attributed to decreased number of

262 egative effect of the mutant subunit on K(+) current amplitude was directly responsible for the reduc

263 mV) whereas at more negative potentials the current amplitude was enhanced.

264 n the fast application experiments, the peak current amplitude was reduced and the current rise time

265 l cortex, miniature excitatory post synaptic current amplitude was slightly reduced, miniature inhibi

266 rate of ASIC2 and heteromeric ASICs, whereas current amplitude was unaffected.

267 ansport strength and GABAA receptor-mediated current amplitudes was investigated by performing gramic

268 Based on the measured time traces of current amplitude, we developed a method for determining

269 neurones was reduced, whereas changes in the current amplitude were negligible in most IB4 ve neurone

270 The capsaicin-induced current amplitudes were 2.3 +/- 0.15 nA (oxidative muscl

271 In accordance with previous studies, hTREK-1 current amplitudes were enhanced by arachidonic acid.

272 Current amplitudes were higher in neurons from AIE-expos

273 p recordings revealed that repolarizing K(+) current amplitudes were higher in ventricular myocytes i

274 AMPAR current amplitudes were increased as well, but not signi

275 Uncaging-evoked NMDA-R current amplitudes were independent of the size of the s

276 howed that miniature excitatory postsynaptic current amplitudes were larger in synaptojanin 1 knockou

277 Na+ channel protein and current amplitudes were reduced in neurons that express

278 us alpha1beta2gamma2S(R43Q) GABA(A) receptor current amplitudes were reduced when receptors were asse

279 For alpha3beta2T150C, while peak current amplitudes were reduced, potentiation was enhanc

280 Current amplitudes were voltage dependent, strongly pote

281 Several currents amplitudes were applied to evaluate the upper c

282 s and mean miniature inhibitory postsynaptic current amplitudes, whereas a dominant negative TC10 var

283 uced angioII inhibition, but did not augment current amplitudes, whereas co-expression of a PIP2 5'-p

284 KCNQ3 (A315S) also yielded greatly increased current amplitudes, whereas currents from mutant A315V c

285 nt reduced miniature inhibitory postsynaptic current amplitude, which returned to control levels with

286 been postulated to underlie KCNQ3 homomeric current amplitudes, which are small compared with those

287 iated mutations was reduced GABA-evoked peak current amplitudes while the major impact of IS-associat

288 1 Ca2+ currents increased exponentially with current amplitude with low intracellular concentrations

289 ession as revealed by increases in peak K(+) current amplitudes with CaMKII phosphorylation.

290 omeric alpha1(Q177K)beta GlyRs had decreased current amplitudes with significantly faster decay times

291 se train was varied by either modulating the current amplitude (with constant frequency) or the stimu

292 ts as a fast blocker (resulting in decreased current amplitude) with an affinity in the 75 mM range e

293 molecular determinants governing macroscopic current amplitudes, with focus on the turret and pore-lo

294 Analysis of the distribution of current amplitudes within the open channel showed MS cha

295 monstrate that CO inhibits peak human Nav1.5 current amplitude without activation of the late Na(+) c

296 However, as shown by R420H, reducing current amplitude without altering gating does not resul

297 Single-channel studies show this attenuates current amplitude without altering other aspects of RyR

298 with the KCNQ1-KCNE1 complex to suppress the current amplitude without altering the slow gating kinet

299 o a significant reduction in the peak Nav1.6 current amplitude, without a detectable effect on gating

300 alter inactivation but dramatically reduced current amplitudes, without changing cell surface expres