ライフサイエンスコーパス: calcium spike

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

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

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

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

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

6 ations, whereas the latter leads to a single calcium spike.

7 that developed during the downstroke of the calcium spike.

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

9 chanosensory cilia, activating an asymmetric calcium spike.

10 tive juxtamembrane Ca2+ wave during temporal calcium spikes.

11 potentials and suppressed the generation of calcium spikes.

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

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

14 he dendrites and prevented the occurrence of calcium spikes.

15 ocess that defines the time interval between calcium spikes.

16 us to quantitatively describe the timing of calcium spikes.

17 agating action potentials and fast dendritic calcium spikes.

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

19 trans-autophosphorylation at high-frequency calcium spikes.

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

21 ials and prevent the generation of dendritic calcium spikes.

22 arked increase in amplitude and frequency of calcium spikes.

23 els prevent generation of random spontaneous calcium spikes.

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

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

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

27 ncreases in cytosolic calcium levels, termed calcium spiking.

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

29 esponses tested, including the initiation of calcium spiking.

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

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

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

33 modulation, induced antioxidant activity and calcium spiking.

34 n alfalfa are also essential for stimulating calcium spiking.

35 nduction of calcium influx without affecting calcium spiking.

36 rs differentially induced calcium influx and calcium spiking.

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

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

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

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

41 fails to transduce the signal downstream of calcium spiking.

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

43 ctivate the NTA calcium channel and initiate calcium spiking, a second messenger for pollen tube rece

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

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

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

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

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

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

50 erence in adult mice, induces alterations in calcium spike activity of midbrain neurons, and increase

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

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

53 s correlated with characteristic spontaneous calcium spike activity.

54 BA, and lactate decreased by 40% spontaneous calcium spiking activity of primary cortical neurons fro

55 The calcium spike among aged rats correlated with task acqui

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

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

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

59 oxically reduces the generation of dendritic calcium spikes and associated somatic burst firing.

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

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

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

63 2 functions downstream of Nod-factor-induced calcium spiking and a calcium/calmodulin-dependent prote

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

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

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

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

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

69 Repetitive calcium spikes are initiated by phospholipase C-mediated

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

71 At higher concentrations trains of calcium spikes are seen.

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

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

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

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

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

77 We simulated calcium spikes at various frequencies and show that neur

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

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

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

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

82 d quantitative image analysis, we discovered calcium spikes both at the start of cleavage furrow ingr

83 ls (Cav3.1 to Cav3.3) regulate low-threshold calcium spikes, burst firing and rhythmic oscillations o

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

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

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

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

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

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

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

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

92 a compared to controls, but the frequency of calcium spikes did not rise.

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

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

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

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

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

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

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

100 (26.2 and 40.5%, respectively) and decreases calcium spiking frequency (4.5 to 1.0 and 2.5 to 1.0 spi

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

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

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

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

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

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

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

108 microscopy to longitudinally track tuft-wide calcium spikes in apical dendrites of layer 5 pyramidal

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

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

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

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

113 /= 2.4 x 10(8) photons/cm(2)/s) light-evoked calcium spikes in Mb axon terminals in an NEM-sensitive

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

115 rlie the neuronal hyperactivity and aberrant calcium spiking in FMRP KO mice and contribute to FXS, p

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

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

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

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

120 Calcium spiking in root hairs in response to supplied No

121 branching in legumes and, most importantly, calcium spiking in the host plant Populus in a CASTOR/PO

122 protein and complete loss of chitin-induced calcium spiking in the Lyk5-RNAi background.

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

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

125 almodulin-gated calcium channel required for calcium spiking in the synergid.

126 t of the pollen tube with the ovule triggers calcium spiking in the synergids(2,3) that induces polle

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

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

129 Furthermore, dendritic calcium spikes increased substantially during REM sleep,

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

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

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

133 the inhibitory impact of apamin on dendritic calcium spikes involved R-type calcium channels.

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

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

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

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

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

139 und action potentials with each depolarizing calcium spike mediated by UNC-2 followed by a hyperpolar

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

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

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

143 We also study the effect of multiple calcium spikes on CaMKII holoenzyme autophosphorylation,

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

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

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

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

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

149 m of synaptic plasticity driven by dendritic calcium spikes, or plateau potentials, has been reported

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

151 Dendritic calcium spikes persisted in the presence of tetrodotoxin

152 during REM sleep, and the blockade of these calcium spikes prevented MD- and FC-induced spine elimin

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

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

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

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

157 We show that calcium spikes rely on the T-type calcium channel Ca-alp

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

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

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

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

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

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

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

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

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

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

168 Inhibition of these calcium spikes slowed the furrow ingression and led to f

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

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

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

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

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

174 By switching from firing sodium to calcium spikes, these neurons implement a ~180 degrees r

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

176 l complex employs hyperpolarization-elicited calcium spikes to invert two-dimensional mathematical ve

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

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

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

180 Calcium spikes were of similar amplitude in all three gr

181 Some neurons, however, also fire calcium spikes when hyperpolarized.

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

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

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

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

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

187 ced platelet activation results in cytosolic calcium spiking, which was confirmed by single-platelet

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

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

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