ライフサイエンスコーパス: calcium spike

1 ns of cytoplasmic calcium ion concentration (calcium spiking).

2 oad-range PLC mutant produced only the first calcium spike.

3 d little effect on the depolarization-evoked calcium spike.

4 period of 30-60 s following an InsP3-induced calcium spike.

5 that developed during the downstroke of the calcium spike.

6 hat each burst was terminated by a dendritic calcium spike.

7 chanosensory cilia, activating an asymmetric calcium spike.

8 large, broad sodium spike; and a large broad calcium spike.

9 potentials and suppressed the generation of calcium spikes.

10 es combined with high- but not low-frequency calcium spikes.

11 rmination of each spike and the frequency of calcium spikes.

12 he dendrites and prevented the occurrence of calcium spikes.

13 ocess that defines the time interval between calcium spikes.

14 us to quantitatively describe the timing of calcium spikes.

15 allidal inputs via post-inhibitory 'rebound' calcium spikes.

16 ials and prevent the generation of dendritic calcium spikes.

17 arked increase in amplitude and frequency of calcium spikes.

18 a cells as indicated by sporadic short-lived calcium spikes.

19 els prevent generation of random spontaneous calcium spikes.

20 ge-gated calcium channels and fire dendritic calcium spikes.

21 tive juxtamembrane Ca2+ wave during temporal calcium spikes.

22 modulation, induced antioxidant activity and calcium spiking.

23 ncreases in cytosolic calcium levels, termed calcium spiking.

24 none, and U-73122 inhibit Nod factor-induced calcium spiking.

25 esponses tested, including the initiation of calcium spiking.

26 branching in response to NF, are normal for calcium spiking.

27 to dmi1 and dmi2 mutants but displays normal calcium spiking.

28 ly steps of infection and nodulation and for calcium spiking.

29 n alfalfa are also essential for stimulating calcium spiking.

30 nduction of calcium influx without affecting calcium spiking.

31 rs differentially induced calcium influx and calcium spiking.

32 ed skewed root growth, and rapid cytoplasmic calcium spiking.

33 tion pathway, at or above Nod factor-induced calcium spiking.

34 a, with direct effects on Nod factor-induced calcium spiking.

35 roximity to the origin of Nod-factor-induced calcium spiking.

36 fails to transduce the signal downstream of calcium spiking.

37 ment for these enzymes in Nod factor-induced calcium spiking.

38 ansduction for effects on Nod factor-induced calcium spiking.

39 vivo resting MET current, evoked all-or-none calcium spikes (39-75 mV amplitude) in 37% of hair cells

40 Because alterations in neuronal calcium spike activity alter transmitter specification i

41 This interaction between calcium spike activity and BMP signaling regulates the s

42 a(+), K(+)-ATPase plays a role in initiating calcium spike activity and regulating calcium homeostasi

43 th muscle cells suppresses early spontaneous calcium spike activity in neurons and the presence of mu

44 t that coincides with the onset of prominent calcium spike activity in spinal neurons.

45 Here we show that spontaneous calcium spike activity in the hindbrain of developing Xe

46 identified a mechanism that links endogenous calcium spike activity with an intrinsic genetic pathway

47 act on plasma membrane receptors to trigger calcium spike activity, other mechanisms for spontaneous

48 s correlated with characteristic spontaneous calcium spike activity.

49 The calcium spike among aged rats correlated with task acqui

50 The molecular mechanisms that terminate each calcium spike and define the spike frequency are not yet

51 In addition, the low-threshold calcium spike and the sustained endogenous oscillation f

52 P3 increases that resulted in a near maximal calcium spike and was expressed as an 80-100% reduction

53 m channels concurrently eliminated dendritic calcium spikes and caused a switch from regular bursting

54 retinas spontaneously generated semiperiodic calcium spikes and long-lasting after-hyperpolarizations

55 Fc gamma RIIA that affects the amplitude of calcium spikes and the spatiotemporal dynamics of calciu

56 2 functions downstream of Nod-factor-induced calcium spiking and a calcium/calmodulin-dependent prote

57 and that both Nod factor-induced perinuclear calcium spiking and calcium influx at the root hair tip

58 h Medicago truncatula mutant, dmi3, exhibits calcium spiking and root hair swelling in response to No

59 -stringency receptor that is responsible for calcium spiking and transcriptional responses.

60 ations in cytoplasmic calcium levels (termed calcium spiking) and alterations in root hair growth.

61 Here, we challenge the view that these calcium spikes are all-or-none and only signal whether t

62 Repetitive calcium spikes are initiated by phospholipase C-mediated

63 matic patch-pipette recordings, we show that calcium spikes are initiated in the apical dendrites of

64 At higher concentrations trains of calcium spikes are seen.

65 We find that calcium spikes are triggered by metabotropic GABA and gl

66 We further show that dendritic calcium spikes arising during REM sleep are important fo

67 ity in the resting state, the importance of "calcium spike" artifacts from flash photolysis, or both.

68 y to use genetics to study ligand-stimulated calcium spiking as a signal transduction event.

69 Initiation of calcium spikes at the soma was suppressed in part by pot

70 glutamate/GABA selector gene, accounting for calcium-spike BDNF-dependent transmitter switching.

71 depends upon a specific temporal pattern of calcium spikes before sound-driven neuronal activity.

72 ual platelets, which display an asynchronous calcium spiking behavior in response to ADP.

73 These action potentials were calcium spikes, blocked by cadmium and L-type calcium ch

74 ttern of Mthal neurons, called low-threshold calcium spike bursts (LTS bursts), is observed in reduce

75 x, is due to the generation of low-threshold calcium spike bursts by thalamic cells.

76 rization and the initiation of low-threshold calcium spike bursts.

77 he sufficiency of the nod genes for inducing calcium spiking by using Escherichia coli BL21 (DE3) eng

78 sing Cav 2.1 and Cav 2.2 displayed increased calcium spiking compared with cells not expressing this

79 nonnodulating alfalfa mutant is defective in calcium spiking, consistent with the possibility that th

80 Our findings indicate that the calcium spikes decreased rapidly with osteodifferentiati

81 ntaining newly formed synapses via dendritic calcium spike-dependent mechanisms.

82 With Kv1 channels blocked, dendritic calcium spikes drive bursts of somatic sodium spikes and

83 action potentials mediated by low-threshold calcium spikes due to T-type Ca(2+) channel activation.

84 polarization and calcium influx generated by calcium spikes during strong, synchronous network excita

85 e of the voltage-clamped current following a calcium spike elicited in the presence of tetraethylammo

86 Calcium spikes established by IP(3) receptor-mediated Ca

87 dent, explaining its ability to operate as a calcium spike frequency detector.

88 s the percentage of active cells (15.7%) and calcium spiking frequency (2.8 to 1.5 spikes/30 min).

89 (26.2 and 40.5%, respectively) and decreases calcium spiking frequency (4.5 to 1.0 and 2.5 to 1.0 spi

90 eases the percentage of active cells and the calcium spiking frequency, while larger increases in [Ca

91 duces the percentage of active cells and the calcium spiking frequency.

92 centage of active NC-derived cells and their calcium spiking frequency.

93 ded the fluorescence changes associated with calcium spikes from mice performing a lever-pressing ope

94 rded T-currents and underlying low-threshold calcium spikes from neurons of nucleus reticularis thala

95 nematode Caenorhabditis elegans, a periodic calcium spike in a pacemaker cell initiates a calcium wa

96 H3 domains block receptor-induced repetitive calcium spikes in a concentration dependent manner.

97 ynaptic activity and NMDA-receptor-dependent calcium spikes in apical tuft dendrites.

98 f synaptic vesicles triggered by spontaneous calcium spikes in bipolar cell axon terminals.

99 amic clamp), triggered rebound low-threshold calcium spikes in both cell types when peak inhibitory p

100 synaptic potentials can elicit low-threshold calcium spikes in both relay and nRt neurons, but the re

101 /= 2.4 x 10(8) photons/cm(2)/s) light-evoked calcium spikes in Mb axon terminals in an NEM-sensitive

102 l signals in single trials: the synchrony of calcium spikes in the Purkinje cell population, and the

103 Studies of calcium spiking in M. truncatula and alfalfa (Medicago s

104 cate enzymes required for Nod factor-induced calcium spiking in Medicago sp., and to identify inhibit

105 of these modifications for the induction of calcium spiking in Medicago truncatula.

106 onses to begin to understand the function of calcium spiking in Nod factor signal transduction.

107 Calcium spiking in root hairs in response to supplied No

108 at ethylene acts upstream or at the point of calcium spiking in the Nod factor signal transduction pa

109 To assess the possible role of calcium spiking in the nodulation response, we analyzed

110 s required for the generation or decoding of calcium-spiking in both symbioses.

111 illatory behavior of cytoplasmic calcium, or calcium spiking, in root hair cells, initially observed

112 Receptor stimuli that triggered repetitive calcium spikes induced a parallel repetitive translocati

113 However, the mechanisms that control calcium spike initiation and repolarization are poorly u

114 nals significantly lowered the threshold for calcium spike initiation, which originated from a shift

115 receptors and that the rising phase of each calcium spike is coincident with a brief burst of action

116 We determine that calcium spiking is a nod gene-dependent host response.

117 CPA and U-73122 suitable for testing whether calcium spiking is causal to subsequent Nod factor respo

118 tentials because of a putative low-threshold calcium spike (LTS).

119 lcium channels that eliminated low-threshold calcium spikes (LTS) in ET cells.

120 nvolved in pacemaker activity, low-threshold calcium spikes, neuronal oscillations and resonance, and

121 mporally earlier and spatially distinct from calcium spikes occurring later in the same cell.

122 s to directly assess the impact of dendritic calcium spikes on axonal AP output of Purkinje cells.

123 e indispensable for the induction of nuclear calcium spiking, one of the earliest plant responses to

124 Nod factor-induced calcium spiking, one of the earliest responses tested, i

125 ncreases in cytosolic calcium concentration (calcium spikes or calcium oscillations) are a common mod

126 arge typically did not produce low threshold calcium spikes or produced a significantly reduced trans

127 that the DMI3 gene acts either downstream of calcium spiking or downstream of a common branch point f

128 iability and the concomitant small number of calcium spikes per cell pose a significant modelling cha

129 Dendritic calcium spikes persisted in the presence of tetrodotoxin

130 Strikingly, short receptor-induced calcium spikes produced transient increases in free Ca(2

131 Gaussian processes can successfully describe calcium spike rates in these circumstances.

132 roach, we show that Gaussian processes model calcium spike rates with high fidelity and perform bette

133 e activity, other mechanisms for spontaneous calcium spike regulation may exist as well.

134 ory rebound bursts mediated by low-threshold calcium spikes renders the circuit vulnerable to both in

135 nts previously shown to be deficient for the calcium spiking response (dmi1 and dmi2) exhibited an im

136 rmine whether live Rhizobium trigger a rapid calcium spiking response and whether this response is NF

137 ells exhibited only the previously described calcium spiking response initiating 10 min after applica

138 go truncatula interaction, bacteria elicit a calcium spiking response that is indistinguishable from

139 sduction pathway that lies downstream of the calcium-spiking response.

140 CPA and U-73122 inhibit Nod factor-induced calcium spiking robustly at concentrations with no appar

141 o reliably predict the temporal evolution of calcium spike sequences for a given stimulus.

142 We employ our modelling concept to analyse calcium spike sequences from dynamically-stimulated HEK2

143 or signal transduction pathway downstream of calcium spiking, shows increased sensitivity to Nod fact

144 diminished the magnitude and duration of the calcium spike, suggesting that extracellular calcium inf

145 thylene appears to regulate the frequency of calcium spiking, suggesting that it can modulate both th

146 Medicago sp., and to identify inhibitors of calcium spiking suitable for correlating calcium spiking

147 oughout interneuron axons and dendrites, and calcium spikes that invade dendrites but not axons.

148 tential greater than -80 mV elicited rebound calcium spikes that were blocked reversibly by 100 micro

149 role in setting a high threshold for somatic calcium spikes, thus restricting initiation to the dendr

150 of calcium spiking suitable for correlating calcium spiking to other Nod factor responses to begin t

151 y albumin is to potentiate the production of calcium spike trains by promoting refilling of calcium s

152 Once initiated, repetitive firing of calcium spikes was limited by activation of putative BK-

153 Calcium spikes were of similar amplitude in all three gr

154 combined with a C18:1 N-acyl group all show calcium spiking when applied at high concentrations.

155 eus remain low during brief or low-frequency calcium spikes, whereas high-frequency spikes or persist

156 that had a propensity to fire low-threshold calcium spikes, whereas X94 GFP+ cells were stuttering i

157 n the developing Xenopus spinal cord exhibit calcium spikes, which regulate gene transcription and ne

158 je cell population, and the amplitude of the calcium spikes, which was modulated by a non-climbing fi

159 synaptic inputs and triggered low threshold calcium spikes, while in tonic mode, sodium-based APs ev

160 annel, a depolarizing input will "trigger" a calcium spike with a burst of action potentials.

161 ation, probably the result of a regenerative calcium spike within HVC neurons that could facilitate t