ライフサイエンスコーパス: depolarisation

1 by flow cytometry analysis of mitochondrial depolarisation.

2 ior to SD) during specific phases of each SD depolarisation.

3 thematical simulations of cardiac electrical depolarisation.

4 calcium influx occurring upon nerve-terminal depolarisation.

5 aky perineurium allowing K+ entry and axonal depolarisation.

6 ivated chloride channel Anoctamin 1, causing depolarisation.

7 t towards chemotherapy-induced mitochondrial depolarisation.

8 ia through connexin 45 to modulate diastolic depolarisation.

9 ne activation, critically accompanied by SPN depolarisation.

10 ived fibroblasts stimulated by mitochondrial depolarisation.

11 idney) 293 cells stimulated by mitochondrial depolarisation.

12 ivated by intracellular calcium and membrane depolarisation.

13 low at negative voltages, but increased with depolarisation.

14 ntial (AP) threshold and increased firing on depolarisation.

15 nnel open probability (NP(o)) increased with depolarisation.

16 lux of and the rise in [Ca(2+)](c) evoked by depolarisation.

17 (2+) from the cytosol after its elevation by depolarisation.

18 y eliminates trajectories with noise-induced depolarisation.

19 ium current (It) giving rise to anodal break depolarisations.

20 duce suprathreshold or subthreshold endplate depolarisations.

21 generated in response to long duration, step depolarisations.

22 ase is the key factor underlying spontaneous depolarisations.

23 ist (2 microM) elicited a prolonged membrane depolarisation (6.6 +/- 0.5 mV) and an increase in actio

24 creases in [Ca(2+)](c) were evoked by either depolarisation (-70 mV to 0 mV) or by release from the S

25 5-HT evoked a direct membrane depolarisation (8.45 +/- 3.8 mV, P < 0.001) and increase

26 In no cells could a depolarisation-activated current be attributed to calciu

27 ive fluorescent dye Newport Green revealed a depolarisation-activated, nimodipine-sensitive Zn2+ infl

28 Coupling of ICC-IM to SMCs drives depolarisation, activation of Ca(v) 1.2 channels, Ca(2+)

29 PC depolarisation alone (n = 7) or PF1 stimulation paired w

30 Neurons exhibiting a profound mitochondrial depolarisation also showed a large secondary increase in

31 A sudden decrease in the depolarisation amplitude resulted in three classes of be

32 from flagellum and is activated by membrane depolarisation, an alkaline extracellular environment, t

33 OXO-M; 10 microM) produced a reversible slow depolarisation, an increase in R(N) ( approximately 90%)

34 exhibiting a small monophasic mitochondrial depolarisation and [Ca2+]i recovery upon glutamate remov

35 ous mechanisms, including membrane potential depolarisation and altered pH regulation.

36 Ca(2+)-activated K(+) channels, causing cell depolarisation and an enhancement of L-type Ca(2+) chann

37 d CDKs inhibited CCCP mediated mitochondrial depolarisation and augments the mitochondrial network.

38 tion using assays of Ca(2+)-induced membrane depolarisation and Ca(2+) retention capacity also indica

39 ane permeabilisation, mitochondrial membrane depolarisation and caspase independent cell death.

40 a primary trigger of mitochondrial membrane depolarisation and cell death.

41 ntibiotic mode-of-action, involving membrane depolarisation and chromosomal decondensation of the tar

42 on conductances contribute to agonist-evoked depolarisation and contraction, and in the present study

43 tors) to prevent CCCP mediated mitochondrial depolarisation and found that AZD5438 and AT7519, were t

44 bre input rate that drive membrane potential depolarisation and high-frequency bursting activity at p

45 nnel Na(V) 1.5 opens in response to membrane depolarisation and initiates the action potential.

46 ment, overexpressing basolateral Lgl2 causes depolarisation and internalisation of superficial cells,

47 vivo hippocampal slices induced non-synaptic depolarisation and irreversible loss of membrane potenti

48 vivo hippocampal slices induced non-synaptic depolarisation and irreversible loss of membrane potenti

49 vivo hippocampal slices induced non-synaptic depolarisation and irreversible loss of membrane potenti

50 ted that PINK1 is activated by mitochondrial depolarisation and phosphorylates serine 65 (Ser(65)) of

51 Endplate depolarisation and quantal content per unit area varied

52 n activation to then oppose further membrane depolarisation and rising intracellular calcium.

53 n cell populations, chronic MI due to tissue depolarisation and slow sinus rhythm.

54 oline function re-shaped sensory-evoked fast depolarisation and subsequent slow hyperpolarisation of

55 a striking correlation between mitochondrial depolarisation and the failure of cells to restore [Ca2+

56 ll consequently be more effective in causing depolarisation and the restoration of resting activity.

57 prevent the glutamate-induced mitochondrial depolarisation and the secondary [Ca2+]c rise.

58 had only minimal impact on the mitochondrial depolarisation and the sustained increase in [Ca2+]c dur

59 rough a gradual transition between diastolic depolarisation and upstroke, consistent with the activat

60 ded in a reproducible sequence to repetitive depolarisations and displayed the highest frequencies of

61 r spasm, microthrombosis, cortical spreading depolarisations and failure of cerebral autoregulation,

62 /208; 32 %) exhibited neither Ih nor rebound depolarisations and only a fast monophasic AHP.

63 unctions produced nearly equivalent endplate depolarisations and quantal content per unit area, sugge

64 ange (NCX) current, leading to delayed after-depolarisations and triggered action potentials.

65 am signal (corresponding to left ventricular depolarisation) and a fiducial point in the photoplethys

66 red mitochondrial respiration, mitochondrial depolarisation, and ultimately proliferation arrest and

67 m inactivation, enhance the response to slow depolarisations, and enhance activation at the channel l

68 th no inflexion; type 2 with an inflexion on depolarisation; and type 3 with an inflexion on repolari

69 vel, Ca(2+) waves resulting in delayed after-depolarisations are a key trigger of arrhythmias.

70 We aimed to ascertain whether spreading depolarisations are independently associated with unfavo

71 We conclude that GABA-evoked depolarisations are mediated via GABAA receptors, arisin

72 athological waves of spreading mass neuronal depolarisation arise repeatedly in injured, but potentia

73 A total of 1328 spreading depolarisations arose in 58 (56%) patients.

74 d, the SR Ca(2+) content increased following depolarisation as assessed by the increased magnitude of

75 he electrocardiogram, reflecting ventricular depolarisation, associate with various physiologic funct

76 ice preparation, 8-Br-cGMP caused a membrane depolarisation associated with a decrease in input resis

77 g the stimulation of one input (PF1) with PC depolarisation at 1 Hz for 5 min produced varied effects

78 the onset characteristic: e.g. coincidence, depolarisation block, and low-threshold potassium curren

79 Following run-down of Ca2+ oscillations, depolarisation briefly restimulated oscillations.

80 neurones exhibiting a profound mitochondrial depolarisation but greatly improved [Ca2+]i recovery in

81 identified by the absence of Ih and rebound depolarisations, but did possess a prolonged biphasic AH

82 Blockade of neuronal depolarisation by tetrodotoxin during preconditioning at

83 s to glutamate, induction of a mitochondrial depolarisation by the addition of NO was followed by a s

84 potassium (K(ATP)) channels, plasma membrane depolarisation, Ca(2+) influx, and finally the exocytosi

85 creased the incidence of cellular arrhythmic depolarisations (CADs; afterdepolarisations and/or abnor

86 lidated by the IMPACT studies) and spreading depolarisation category (none, CSD only, or at least one

87 th prognostic score (p=0.0009) and spreading depolarisation category (p=0.0008) were significant pred

88 Addition of depolarisation category to the regression model increase

89 Adiabatic depolarisation cooling, based on the electrocaloric effe

90 ses, but some did show evidence of hair cell depolarisation despite the disorganisation of their bund

91 ial, because activation of TRPA1 by membrane depolarisation did not cause sensitisation.

92 1st to 4th order statistical moments of the depolarisation distribution are determined, which charac

93 monstrate that Mueller matrix mapping of the depolarisation distribution of prostate tumour tissues c

94 The depolarisation distributions can be directly related to

95 Layered topographic maps of the depolarisation due to diffuse biological tissues are pro

96 We compare the measured phase shift and depolarisation due to Doppler scattering from a rotating

97 GABA evoked concentration-dependent depolarisations (EC50: 0.8 mM), which were attenuated by

98 ng membrane potential but abolished the slow depolarisation elicited by dopamine, indicating this was

99 y profiles were congruent with mitochondrial depolarisation events visualised by the JC-1 probe.

100 No depolarisation events were observed throughout the recor

101 BCT depolarisation evoked short-latency, AMPA/kainate recept

102 slice, 100 microM melatonin had no effect on depolarisations evoked by N-methyl-D-aspartate (NMDA) or

103 argin each slowed the rate of decline of the depolarisation-evoked Ca(2+) transient.

104 xcitable cell type recently shown to exhibit depolarisation-evoked Ca2+ release from intracellular st

105 ADP- and depolarisation-evoked Ca2+ waves travelled approximately

106 of PGE2 in inflammatory pain: it sensitises depolarisation-evoked responses in nociceptive axons and

107 e SR did not contribute significantly to the depolarisation-evoked rise in [Ca(2+)](c).

108 ies can move under a stress-gradient-induced depolarisation field.

109 s and a biphasic effect consisting of a slow depolarisation followed by a slow hyperpolarisation or v

110 in was associated with a small mitochondrial depolarisation, followed by mitochondrial repolarisation

111 posed 10-ms V(1) steps to varying degrees of depolarisation, followed by V(2) steps to a fixed, +100

112 potential duration and promoted early-after-depolarisations following beta-adrenergic stimulation.

113 near measure of the parent's stimulus-evoked depolarisation for firing indices up to about 60 %, corr

114 a2+]i) increases, stimulated by both ADP and depolarisation, frequently originated from a peripheral

115 vated Cl(-) current, and hence odour-induced depolarisation, had little effect upon the period of osc

116 These results show that depolarisation has marked and opposing actions on the ex

117 The possibility that spreading depolarisations have adverse effects on the traumaticall

118 However, depolarisation (high potassium)-evoked 5-HT release was

119 ic preganglionic neurones, a slow monophasic depolarisation in 28% of sympathetic preganglionic neuro

120 lopment of the second phase of mitochondrial depolarisation in cells at 11-17 DIV and increased the p

121 oth the persistent activity and the membrane depolarisation in the axons are abolished by the EP4 rec

122 We map the degree of depolarisation in the different prostate tumour tissues

123 ontractile but exhibited regular spontaneous depolarisations in current clamp.

124 mp experiments,XE 991 per se caused membrane depolarisations in LTSIs and subsequent application of s

125 arge A-like potassium currents and ramp-like depolarisations in response to step current injections,

126 d the subsequent ones) displayed much faster depolarisations in the subthreshold voltage range, indic

127 larger [Ca2+]i transients evoked by high-K+ depolarisation increased [Ca2+]L.

128 activity is unregulated leading to membrane depolarisation, increased nocturnal SCN firing, inverted

129 A depolarisation index was developed.

130 ons when a discriminant based on age and the depolarisation index was used.

131 our study shows that following mitochondrial depolarisation induced by mitochondrial toxins, MG149 tr

132 of G4s at exons that were skipped following depolarisation induced by potassium chloride.

133 Depolarisation-induced constriction was depressed by rot

134 Depolarisation-induced constriction was unaffected by hy

135 45 mM) caused a short-term, greatly enhanced depolarisation-induced release of [125I]BDNF during supe

136 The depolarisation-induced release of brain-derived neurotro

137 The orexin-induced depolarisation involved activation of pertussis toxin-se

138 Since the rate of depolarisation is dictated by cardiac microstructure, an

139 ly active cortex or as isoelectric spreading depolarisation (ISD) if they took place in isoelectric c

140 The overall depolarisation map is a convolution of the effects of th

141 Parenchymal liver tissue depolarisation maps are characterised by larger mean and

142 As mitochondrial depolarisation may represent a pivotal step in the progr

143 Averaged over all SD depolarisations, mean peak SD nitric oxide levels per de

144 The dopamine induced slow depolarisation occurring in a sub-population of sympathe

145 prathreshold ePSPs induced by suprathreshold depolarisation of a single adjoining neurone.

146 that inhibition of SK channels results in a depolarisation of action potential threshold along with

147 Interestingly, the depolarisation of axons was blocked by blocking ANO1 cha

148 ed neurological function correlates with the depolarisation of both the axonal mitochondria and the a

149 s of isolated rat type I cells, CO induced a depolarisation of ca 11 mV and a decrease in the amplitu

150 , and all antagonised the G protein-mediated depolarisation of current activation.

151 ochondrial metabolism and causes a transient depolarisation of mitochondrial membrane potential.

152 g222His channels increase excitability via a depolarisation of resting potential and increased evoked

153 cAMP pathway which culminates in a sustained depolarisation of sensory axons mediated by a chloride c

154 phasic dopamine to induce plasticity, while depolarisation of SPNs constrains the synapses eligible

155 on of guanylate cyclase can cause a membrane depolarisation of thalamic neurones in vitro, and that t

156 nd Ca loading of the cardiac cell induced by depolarisation of the cell membrane.

157 to the synaptic region of the MoG mimics the depolarisation of the chemical input and can also block

158 e defibrillation mechanism was light-induced depolarisation of the excitable gap, which led to block

159 t also the time delay between the electrical depolarisation of the heart's left ventricle and the ope

160 Ssp6 inhibits bacterial growth by causing depolarisation of the inner membrane in intoxicated cell

161 +/- 9.9% in 4 out of 7 neurones tested) and depolarisations of membrane potential (9.8 +/- 3.4 mV in

162 g indices up to about 60 %, corresponding to depolarisations of three to four times the noise S.D.

163 ent elevations in the ion produced either by depolarisation or by release from the store.

164 We conclude that pairing either PC depolarisation or CF activation with stimulation of a di

165 o-operative with respect to overall endplate depolarisation or safety margin for synaptic transmissio

166 strate that [Ca2+]i increases, stimulated by depolarisation or the agonist ADP, have indistinguishabl

167 of decline in [Ca(2+)](c), following either depolarisation or the release of Ca(2+) from the SR (by

168 of store filling was enhanced by maintained depolarisation, or by transient depolarising pulses, and

169 tamine (5-HT) on population primary afferent depolarisation (PAD) has been studied using in vitro spi

170 Indeed, the depolarisation parallels the expression of neurological

171 Current activated on depolarisation positive of about -45 mV and a large frac

172 depolarising ramp was over, decreased during depolarisations positive to approximately -35 mV and was

173 These waves depend on depolarisation produced by voltage-gated sodium channels

174 wild-type, and the generation of early-after-depolarisations promoted unidirectional patterns of exci

175 vidual, and that smoother and less intricate depolarisation propagation is the mechanism likely respo

176 , followed by V(2) steps to a fixed, +100 mV depolarisation relative to resting membrane potential fo

177 The increased SR Ca(2+) content following depolarisation returned to control values in approximate

178 In response to membrane depolarisation, secretion was initiated with a variable

179 hat the components attributable to localised depolarisation sequence abnormalities were significantly

180 the degree of intricate convolutions of the depolarisation sequence.

181 rom it, the SR accumulated the ion following depolarisation since ryanodine and thapsigargin each slo

182 Triggered by focal depolarisation, spreading depression (SD) represents a s

183 slation had no effect on the potentiation of depolarisation-stimulated (15 mM KCl) dopamine release m

184 urones undergoing only a small mitochondrial depolarisation, suggesting that the release of endogenou

185 rics, earlier occurrence of spindles on slow-depolarisation SW is associated with higher medial prefr

186 wall synthesis inhibition and (ii) membrane depolarisation that does not rely on interactions with c

187 at low K+, but at high Na+ there was a rapid depolarisation that was significantly larger in control

188 h sparks efficiently generates delayed after depolarisations that trigger premature action potentials

189 increase in an outward current activated by depolarisations that was blocked by the specific M curre

190 and discovered that GLUT2 affected membrane depolarisation through the closure of K+(ATP)-sensitive

191 LFS paired with depolarisation to -10 mV induced LTD, no change or LTP a

192 neurons allowed the effects of postsynaptic depolarisation to be studied with minimal synaptic activ

193 -type ClC-6 activation and transport require depolarisation to voltages beyond 140 mV.

194 mPTP-induced depolarisation under succinate subsequently inhibited re

195 ting [Ca(2+)](i) was accompanied by membrane depolarisation; under voltage clamp reduction of [Ca(2+)

196 le cells consistently show a small transient depolarisation upon transition to a novel environment.

197 aracterise the changing distributions of the depolarisation values through the volume of biological t

198 which characterise the distributions of the depolarisation values.

199 ts: the rate of inactivation during a single depolarisation was increased, and repetitive pulsing sho

200 spiking activity showed that the PGE2 evoked depolarisation was inhibited by Nav1.8 sodium channel bl

201 s even when the duration of PF1 pairing with depolarisation was limited to 1 min.

202 adiosensitization, GNP-induced mitochondrial depolarisation was quantified by TMRE staining, and leve

203 st sensitivity although the amplitude of the depolarisation was reduced to 48% of the control value.

204 We observed that DHPG-induced depolarisation was smaller in CA1 pyramidal cells than i

205 ncludes that the detailed convolution of the depolarisation waveform is individual, and that smoother

206 ations, mean peak SD nitric oxide levels per depolarisation were 0.73+/-0.23 microM (n=29) in cats, a

207 and duration, as well as the maximum rate of depolarisation were measured for each action potential t

208 Spreading depolarisations were associated with unfavourable outcom

209 These [Sar9,Met(O2)11]SP-induced depolarisations were attenuated by the selective NK1R an

210 In 38 participants, all spreading depolarisations were classified as CSD; 20 patients had

211 Membrane depolarisations were measured in low (0.1 mm) K+ and hig

212 Spreading depolarisations were monitored by electrocorticography d

213 the vehicle-treated group a median of eight depolarisations, were observed.

214 fect alone promoted a profound mitochondrial depolarisation when combined with high [Ca2+]c, either i

215 Sumatriptan had no effect on the number of depolarisations, whereas tonabersat significantly reduce

216 nent of outward current activated by a short depolarisation, which accounted for at least 90% of the

217 d a profound mono- or biphasic mitochondrial depolarisation, which was clearly correlated with a sust

218 d result in regions of epithelial electrical depolarisation within the breast parenchyma, which can e