ライフサイエンスコーパス: depolarization-induced

1 As a result, the time course of depolarization-induced 2-AG signaling was shortened, and

2 this decrease was reflected in reduction of depolarization-induced [(3)H]glutamate release.

3 triatum, sulpiride (10 microM) increased the depolarization-induced [3H]GABA overflow to 193% of cont

4 opamine receptor antagonist, to increase the depolarization-induced [3H]GABA overflow.

5 In contrast, TRPP2 knockdown did not alter depolarization-induced (60 mmol l K(+)) vasoconstriction

6 ation and vasoconstriction but did not alter depolarization-induced (60 mmol/L K(+)) vasoconstriction

7 s using fura-2 microfluorometry, we measured depolarization-induced (80 mM KCl) accumulation of myopl

8 Depolarization induced a reduction in the number of dend

9 the L596P or W733R mutation displays normal depolarization-induced activation and outward rectificat

10 Depolarization-induced activation of CaM kinase I was re

11 e results are consistent with the model that depolarization-induced activation of excitation-contract

12 on its ability to induce a cortical flash, a depolarization-induced activation of L-type Ca(2+) chann

13 vity of cAMP-PKA pathway attenuates membrane depolarization-induced activation of MEF2 activity and n

14 Depolarization-induced activation of VGCCs resulted in a

15 nversely, depletion of PI(4,5)P(2) by either depolarization-induced activation or chemically induced

16 Its ability to block peptide A-induced and depolarization-induced activation was considerably impai

17 mplitudes, and the voltage dependence of the depolarization-induced activation were not altered by lo

18 not postsynaptic receptor blockade, reversed depolarization-induced adaptation, and TTX added to norm

19 PA, indicating that this rise in pH(i) was a depolarization-induced alkalinization (DIA).

20 The latter would enhance depolarization-induced alkalinization of astrocytes, and

21 While depolarization-induced aortic contraction was unchanged

22 channels expressed in GT1 cells allowed the depolarization-induced AP broadening to facilitate Ca(2+

23 hypothesis explaining the importance of the depolarization-induced breakdown of cytosolic ACh to cen

24 s in [K+]o reduced the increase in R(in) and depolarization induced by 5-HT with 50% inhibition of th

25 d with QHGAD67 was not increased by membrane depolarization induced by 60 mM extracellular K+ nor red

26 BTP2 did not block divalent cation entry by depolarization induced by activating monovalent cation e

27 Depolarization induced by elevated extracellular K(+) re

28 The depolarization induced by exogenous acetylcholine was no

29 predominantly VDAC3 were least sensitive to depolarization induced by increased free tubulin.

30 Cell membrane depolarization induced by increased potassium concentrat

31 onist dexmedetomidine each reversed the VLPO depolarization induced by isoflurane in slices in vitro.

32 ed basal DeltaPsim and converted a transient depolarization, induced by physiologic concentrations of

33 ) receptors and for their ability to inhibit depolarizations induced by AMPA (40 microM), NMDA (40 mi

34 ) receptors and for their ability to inhibit depolarizations induced by AMPA (40 microM), NMDA (40 mi

35 euronal firing was correlated with transient depolarizations induced by GABA(A) receptors; however, G

36 pulsed nicotine did not enhance postsynaptic depolarizations induced by iontophoretically applied NMD

37 "Early after-depolarizations" induced by dofetilide were also complet

38 Ca(2+) ([Ca(2+)](i)) clearance after brief, depolarization-induced Ca(2+) entry.

39 Both types of vesicles fuse in response to depolarization-induced Ca(2+) entry.

40 ith results obtained in ileal smooth muscle, depolarization-induced Ca(2+) influx fails to induce NFA

41 naling and attenuates cocaine enhancement of depolarization-induced Ca(2+) influx in rat hippocampal

42 Depolarization-induced Ca(2+) influx triggered NS-type e

43 report that GABA can alter the properties of depolarization-induced Ca(2+) influx.

44 However, depolarization-induced Ca(2+) release and its functional

45 s Gln(489) to Trp(503) resulted in a loss of depolarization-induced Ca(2+) release, a severe reductio

46 +) release); peptide C also blocked T-tubule depolarization-induced Ca(2+) release.

47 s approach and applications to understanding depolarization-induced Ca(2+) responses in sympathetic n

48 The restitution of depolarization-induced Ca(2+) transients, assessed by a

49 doubled the peak and slowed the decay of the depolarization-induced Ca(2+) transients.

50 be, which previously allowed us to resolve a depolarization-induced Ca(2+)-dependent close-to-open tr

51 second messenger that is liberated following depolarization-induced Ca2+ activation of phospholipase

52 coupled in time and graded in intensity with depolarization-induced Ca2+ currents and well correlated

53 tore via Ca2+-induced Ca2+ release, and that depolarization-induced Ca2+ entry evoked Ca2+-induced Ca

54 weak acids, acidify the taste bud and evoke depolarization-induced Ca2+ entry into a select subset o

55 nsients recorded using FFP18 during membrane depolarization-induced Ca2+ influx show that near-membra

56 , whereas high K+ (50 mM) exposures (causing depolarization-induced Ca2+ influx through voltage-sensi

57 annels and using indo-1 photometry following depolarization-induced Ca2+ loading.

58 no acids 1-1,680 of RyR1 were able to render depolarization-induced Ca2+ release to RyR3.

59 Depolarization-induced Ca2+ release was independent of e

60 Depolarization-induced Ca2+ release was not detected dur

61 contrast, GLTs show neither spontaneous nor depolarization-induced Ca2+ transients, but do release C

62 alcium (1 mM EGTA) Ringer solution inhibited depolarization-induced calcium increases but not the cal

63 Depolarization-induced calcium influx in dorsal root gan

64 in both PC12 cells and hippocampal neurons, depolarization-induced calcium influx stimulates ERK act

65 Galanin inhibited gastrin, Bay K8644, and K+ depolarization-induced calcium mobilization and entry as

66 milar to those present in the SR lumen after depolarization-induced calcium release cause the dissoci

67 sion is typically triggered by postsynaptic, depolarization-induced calcium rises, whereas long-term

68 Depolarization-induced calcium signaling increased the e

69 This potentiation of depolarization-induced calcium transients was blocked by

70 In this report, we demonstrate the depolarization-induced, calcium-dependent phosphorylatio

71 Depolarization-induced capacitance changes increased wit

72 Elimination of Ca2+ current blocked depolarization-induced capacitance changes.

73 Depolarization-induced capacitance increases in most cas

74 ariable amount of rapid endocytosis followed depolarization-induced capacitance increases.

75 e following: 1) increased exocytosis (serial depolarization-induced capacitance), 2) enhanced voltage

76 protein kinase C were not implicated in the depolarization-induced CGRP increases.

77 Membrane depolarization-induced changes in [Ca2+]i were larger an

78 al whole-cell recording technique to monitor depolarization-induced changes in C(m) in the different

79 xamined the effects of TNFalpha on AMPA- and depolarization-induced changes in cytosolic Ca(2+) in cu

80 Here, we report direct measurements of depolarization-induced changes in intramitochondrial tot

81 Depolarization-induced changes in phosphatidylserine and

82 Here we examine whether depolarization-induced charge movement causes a conforma

83 lcholine receptor (M2R) was found to exhibit depolarization-induced charge movement-associated curren

84 The other channel is an outwardly rectifying depolarization induced Cl- channel (ORDIC) that is disti

85 ltures by heterocellular coupling leading to depolarization-induced conduction slowing and by direct

86 irect link between Na(+)(o) inhibition and a depolarization-induced conformational change, most likel

87 Our results demonstrate that depolarization-induced conformational changes in the ort

88 firmed that nifedipine progressively dilated depolarization-induced constrictions in MAs but not MVs.

89 es by the SERCA pump inhibitor thapsigargin, depolarization-induced constrictions in MVs were blocked

90 18beta-glycyrrhetinic acid or La3+, blocked depolarization-induced currents.

91 volved in appetite and "natural reward." The depolarization-induced decrease in inhibitory tone to LH

92 Depolarization-induced degradation of the p35 regulatory

93 Here, we show that BDNF mediates depolarization-induced dendritic growth and branching in

94 ical neurons, it was effective in inhibiting depolarization-induced dendritic growth, suggesting that

95 reting dense core granules and an absence of depolarization-induced dopamine release.

96 Remarkably, both depolarization-induced dopamine vesicle hyperacidificati

97 Depolarization-induced down-regulation of sGC activity w

98 de suppression of GABA release caused by the depolarization-induced elevation of [Ca(+)](i) in DGCs (

99 Depolarization-induced elevation of nuclear CaM also was

100 The early development of depolarization-induced elevations of [Ca2+]i several hou

101 t complex was promptly disassembled upon the depolarization-induced entry of Ca2+ into intact nerve e

102 K(+) (Kv) channel Kv2.1 (KCNB1) facilitates depolarization-induced exocytosis in INS 832/13 cells an

103 comolar concentrations, alpha-LT potentiates depolarization-induced exocytosis often without evidence

104 t, knockdown of MEF2D significantly enhanced depolarization-induced expression of Bdnf exon I.

105 down of MEF2C significantly impairs membrane depolarization-induced expression of Bdnf exon IV.

106 Similar results were obtained for depolarization-induced expression of the immediate early

107 Depolarization-induced FM1-43 uptake in photoreceptor sy

108 Expression of RyR1 restored depolarization-induced global Ca(2+) release in intact m

109 Depolarization-induced glutamate release from hippocampa

110 These data suggest that most depolarization-induced glutamate release in immature hip

111 PDC decreased depolarization-induced glutamate release in P14 slices b

112 Most depolarization-induced glutamate release was Ca2+-depend

113 Mitochondrial depolarization induced Gp78-dependent expression of the

114 Depolarization-induced gradients of fluorescence between

115 This depolarization-induced hyperacidification is mediated by

116 al neurons, NMDA receptor activation but not depolarization induced importin nuclear translocation.

117 ies impulse conduction in the heart, and its depolarization-induced inactivation is essential in cont

118 disrupted spindling, which in turn is due to depolarization-induced inactivation of the low-threshold

119 ace expression and accelerated recovery from depolarization-induced inactivation.

120 Both nifedipine and Y-27632 prevented the depolarization-induced increase in myocardin expression.

121 The ROK inhibitor, Y-27632, prevented depolarization-induced increase in SMMHC/SM alpha-actin

122 ent protein kinase in vitro and in situ, the depolarization-induced increase in their state of phosph

123 indicating that calcium influx mediated the depolarization-induced increase in this current.

124 Depolarization-induced increases in [Ca](mito) were spat

125 t only type III taste cells show significant depolarization-induced increases in C(m), which were cor

126 -dependent kinase inhibitor, KN93, prevented depolarization-induced increases in c-fos expression wit

127 llations occurred, at least in part, through depolarization-induced increases in Ca2+ entry.

128 itive whole-cell Ca2+ currents and increases depolarization-induced increases of intracellular Ca2+ l

129 ase A or C had any significant effect on the depolarization-induced inhibition of EPSCs.

130 it has a major impact on the organization of depolarization-induced intracellular Ca(2+) signaling in

131 Our aim was to test the hypothesis that depolarization-induced intracellular pH (pH(i)) shifts i

132 spiration, membrane potential (DeltaPsi) and depolarization-induced K+ efflux.

133 The rate of recovery of [Ca2+]i following a depolarization-induced load was increased by low [fura-2

134 ia CP-AMPARs is selectively depressed during depolarization-induced long-term depression (DiLTD), a p

135 t postsynaptic form of long-term depression (depolarization-induced long-term depression, DiLTD) at i

136 nstationary variance analysis indicated that depolarization-induced LTD correlated with a reduction i

137 Depolarization-induced LTD did not occlude the conventio

138 ouse cortical neurons, we observed increased depolarization-induced mitochondrial calcium uptake.

139 prolin homologous protein 1 (WAVE1) controls depolarization-induced mitochondrial movement into dendr

140 cells increased mitofusin levels and reduced depolarization-induced mitophagy, whereas siRNA knockdow

141 ut not Mfn2, was required for Gp78-dependent depolarization-induced mitophagy.

142 /C current, consistent with an initial rapid depolarization-induced NBCe1 activation, and then a subs

143 sm of inhibitory channels and a mechanism of depolarization-induced neurite outgrowth.

144 P depletion, we first identified features of depolarization-induced neuronal [Ca(2+)]c transients tha

145 ered by tetrodotoxin, an agent that inhibits depolarization-induced neurotransmitter release.

146 3beta (GSK3beta) significantly increased the depolarization-induced nuclear localization of NFATc4.

147 Spreading depolarizations induced only hyperaemic responses (794%

148 nto a state that is distinct from the normal depolarization-induced open state.

149 perated Ca(2+) channels, directly suppresses depolarization-induced opening of the voltage-gated Ca(2

150 mitochondria, but did not sensitize them to depolarization-induced Parkin translocation.

151 ion of dopamine caused a prolongation of the depolarization-induced pause and an increase in the dura

152 K(+) depolarization-induced PKC translocation entirely mirror

153 ed the role of calcineurin in other forms of depolarization-induced plasticity.

154 ptic stimulation was followed 30 ms later by depolarization-induced postsynaptic action potentials.

155 rm of inhibitory synaptic plasticity, termed depolarization-induced potentiation of inhibition, in ro

156 reveal a new form of retrograde plasticity, depolarization-induced potentiation of inhibition.

157 l as the recovery of baseline function after depolarization-induced presynaptic silencing.

158 Furthermore, removal of depolarization induced rapid cytoplasm-to-nuclear transl

159 Whole-cell patch-clamp recordings revealed a depolarization-induced, rapidly activating and rapidly i

160 arge sTDPs and leTDPs is the spontaneous and depolarization-induced regenerative calcium potentials (

161 but neither type II nor type I cells exhibit depolarization-induced regulated exocytosis to release t

162 The agonist 2R,4R-APDC inhibited depolarization-induced release of [3H]d-aspartate from c

163 DCG-IV also powerfully inhibited depolarization-induced release of [3H]D-aspartate from r

164 synaptic vesicle exocytosis, GRAB regulates depolarization-induced release of dopamine from PC12 cel

165 lication of 2-arachidonoylglycerol(2-AG) and depolarization-induced release of endogenous cannabinoid

166 r of dendrites, and knockdown of Sp4 blocked depolarization-induced remodeling.

167 spersion, and an increased susceptibility to depolarization-induced repetitive activity.

168 Buffering of the depolarization-induced rise in [Ca(2+)](i) was also obse

169 -permeable, non-selective cation channel via depolarization-induced rise in [Ca(2+)]i.

170 was employed to test the effect of NO on the depolarization-induced rise in [Ca2+]i.

171 id-binding protein resulted in inhibition of depolarization-induced secretion in a manner identical t

172 By contrast, depolarization-induced secretion was unaffected, arguing

173 s transfected with met-BDNF-GFP showed lower depolarization-induced secretion, while constitutive sec

174 l SCAMP2 caused dose-dependent inhibition of depolarization-induced secretion.

175 ceptors and protein phosphatase 2B prevented depolarization-induced Ser-845 dephosphorylation but had

176 oteasome system, as was shown previously for depolarization-induced silencing, implicating the degrad

177 erties (kainate receptors) failed to prevent depolarization-induced silencing.

178 This depolarization-induced slow current (DISC) is attenuated

179 This current, called depolarization-induced slow current (DISC), is triggered

180 The depolarization-induced slowing was blocked by incubating

181 NA (siRNA) specific for myocardin attenuated depolarization-induced SMMHC/SM alpha-actin transcriptio

182 We examined the ionic mechanisms mediating depolarization-induced spike activity in pancreatic beta

183 a modulation of light evoked, as well as the depolarization-induced spike firing pattern of ganglion

184 otential, input resistance, spike threshold, depolarization-induced spike frequency increase, current

185 l, but not white matter NG2(+) cells, elicit depolarization-induced spikes that are akin to immature

186 s in all cells tested and reduced light- and depolarization-induced spiking.

187 Whereas Y-27632 decreased basal and depolarization-induced SRF enrichment in the SMMHC/SM al

188 THC blocked depolarization-induced suppression of EPSCs evoked at 0.

189 tes retrograde synaptic depression including depolarization-induced suppression of excitation (DSE) a

190 Depolarization-induced suppression of excitation (DSE) a

191 ice showed enhanced endocannabinoid-mediated depolarization-induced suppression of excitation (DSE) a

192 Depolarization-induced suppression of excitation (DSE) a

193 o forms of eCB-mediated synaptic plasticity, depolarization-induced suppression of excitation (DSE) a

194 We found that depolarization-induced suppression of excitation (DSE) i

195 This depolarization-induced suppression of excitation (DSE) i

196 Depolarization-induced suppression of excitation (DSE) i

197 Depolarization-induced suppression of excitation (DSE) i

198 eatures coincided with a rescued hippocampal depolarization-induced suppression of excitation (DSE),

199 Depolarization-induced suppression of excitation and inh

200 urons, CRIP1a overexpression attenuated both depolarization-induced suppression of excitation and inh

201 de messenger with DSI in the hippocampus and depolarization-induced suppression of excitation in the

202 ssion of inhibition" (DSI)] and excitatory ("depolarization-induced suppression of excitation") affer

203 ses, as it occurred without increases in the depolarization-induced suppression of excitation.

204 ated inhibition of EPSC and the eCB-mediated depolarization-induced suppression of excitation.

205 a(9)-THC and during endocannabinoid-mediated depolarization-induced suppression of excitation.

206 oids by a rat CA1 pyramidal cell during this depolarization-induced suppression of inhibition (DSI) e

207 Depolarization-induced suppression of inhibition (DSI) i

208 Depolarization-induced suppression of inhibition (DSI) i

209 Depolarization-induced suppression of inhibition (DSI) i

210 Depolarization-induced suppression of inhibition (DSI) i

211 We report that CUS led to impairment of depolarization-induced suppression of inhibition (DSI) i

212 etrograde endocannabinoid signaling, namely, depolarization-induced suppression of inhibition (DSI) i

213 rt that MAGL(-)/(-) mice exhibited prolonged depolarization-induced suppression of inhibition (DSI) i

214 Depolarization-induced suppression of inhibition (DSI) i

215 Here, we show that depolarization-induced suppression of inhibition (DSI) i

216 s to inhibit neurotransmitter release during depolarization-induced suppression of inhibition (DSI) o

217 We used the retrograde signal process called depolarization-induced suppression of inhibition (DSI) t

218 We investigated depolarization-induced suppression of inhibition (DSI) u

219 A similar depolarization-induced suppression of inhibition (DSI) w

220 d inhibitory synaptic activity and augmented depolarization-induced suppression of inhibition (DSI),

221 C depolarization ACh triggered a presynaptic depolarization-induced suppression of inhibition (DSI),

222 This process, depolarization-induced suppression of inhibition (DSI),

223 Three eCB-mediated responses were examined: depolarization-induced suppression of inhibition (DSI),

224 duce GABAergic transmission-a process called depolarization-induced suppression of inhibition (DSI).

225 suppresses IPSCs through a process known as depolarization-induced suppression of inhibition (DSI).

226 on to study the calcium (Ca2+) dependence of depolarization-induced suppression of inhibition (DSI).

227 ippocampal pyramidal cells, a process called depolarization-induced suppression of inhibition (DSI).

228 dent form of short-term plasticity, that is, depolarization-induced suppression of inhibition (DSI).

229 grade synaptic mediators of the phenomena of depolarization-induced suppression of inhibition or exci

230 m currents in LH neurons and a CB1R-mediated depolarization-induced suppression of inhibition that is

231 ase by demonstrating significantly prolonged depolarization-induced suppression of inhibition when su

232 f a hippocampal CA1 pyramidal neuron-termed "depolarization-induced suppression of inhibition" (DSI).

233 ng from principal cells to both inhibitory ["depolarization-induced suppression of inhibition" (DSI)]

234 We have investigated the phenomenon of 'depolarization-induced suppression of inhibition' (DSI)

235 nduced elevation of [Ca(+)](i) in DGCs (DSI: depolarization-induced suppression of inhibition).

236 tic firing could also overcome even complete depolarization-induced suppression of inhibition, indica

237 etrograde signalling molecules that underlie depolarization-induced suppression of inhibition, or DSI

238 in dendrites, our results revealed that the depolarization-induced suppression of inhibition, the en

239 Here, we show that three classes of depolarization-induced suppression of inhibition-express

240 s to Purkinje cells after the termination of depolarization-induced suppression of inhibition.

241 This leads to depolarization-induced suppression of inhibitory (DSI) a

242 This depolarization-induced suppression of spontaneous releas

243 CB1-mediated depolarization-induced suppression of synaptic inhibitio

244 Furthermore, potassium depolarization induced the tyrosine phosphorylation of b

245 Instead, depolarization-induced Thr-840 dephosphorylation was pre

246 se findings now add NF-kappaB to the list of depolarization-induced transcription factors in pancreat

247 male DRG neurons, IP3 (100 mum) potentiated depolarization-induced transients produced by extracellu

248 of Mfn2 in mouse cardiac myocytes prevented depolarization-induced translocation of Parkin to the mi

249 While strong depolarization-induced uptake of HRP suppressed evoked r

250 f the aqueous pore, the mechanistic basis of depolarization-induced 'use-dependent' lidocaine block r

251 CCt and 92CCt both inhibited pressure- and depolarization-induced vasoconstriction, although CCt wa

252 1.2, and reduced intravascular pressure- and depolarization-induced vasoconstriction.

253 crease in both pressure (myogenic tone)- and depolarization-induced vasoconstriction.

254 in the formation of LDCV-like structures and depolarization-induced VGF secretion.

255 One remaining enigma was the basis for depolarization-induced weakness in hypokalaemic periodic