ライフサイエンスコーパス: depolarisation

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

2 calcium influx occurring upon nerve-terminal depolarisation.

3 aky perineurium allowing K+ entry and axonal depolarisation.

4 ived fibroblasts stimulated by mitochondrial depolarisation.

5 by flow cytometry analysis of mitochondrial depolarisation.

6 idney) 293 cells stimulated by mitochondrial depolarisation.

7 thematical simulations of cardiac electrical depolarisation.

8 ivated by intracellular calcium and membrane depolarisation.

9 low at negative voltages, but increased with depolarisation.

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

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

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

13 (2+) from the cytosol after its elevation by depolarisation.

14 y eliminates trajectories with noise-induced depolarisation.

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

16 duce suprathreshold or subthreshold endplate depolarisations.

17 generated in response to long duration, step depolarisations.

18 ase is the key factor underlying spontaneous depolarisations.

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

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

21 5-HT evoked a direct membrane depolarisation (8.45 +/- 3.8 mV, P < 0.001) and increase

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 Endplate depolarisation and quantal content per unit area varied

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

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

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

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

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

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

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

44 /208; 32 %) exhibited neither Ih nor rebound depolarisations and only a fast monophasic AHP.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 Blockade of neuronal depolarisation by tetrodotoxin during preconditioning at

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

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

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

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

64 Addition of depolarisation category to the regression model increase

65 Adiabatic depolarisation cooling, based on the electrocaloric effe

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

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

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

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

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

71 No depolarisation events were observed throughout the recor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 ontractile but exhibited regular spontaneous depolarisations in current clamp.

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

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

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

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

94 A depolarisation index was developed.

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

96 Depolarisation-induced constriction was depressed by rot

97 Depolarisation-induced constriction was unaffected by hy

98 45 mM) caused a short-term, greatly enhanced depolarisation-induced release of [125I]BDNF during supe

99 The depolarisation-induced release of brain-derived neurotro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 +/- 9.9% in 4 out of 7 neurones tested) and depolarisations of membrane potential (9.8 +/- 3.4 mV in

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

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

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

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

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

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

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

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

126 Indeed, the depolarisation parallels the expression of neurological

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 mPTP-induced depolarisation under succinate subsequently inhibited re

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

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

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

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

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

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

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

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

152 Spreading depolarisations were associated with unfavourable outcom

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

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

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

156 Spreading depolarisations were monitored by electrocorticography d

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

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

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

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

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

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