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 These interventions abolished the depolarization-induced and L-type Ca(2+) channel-depende

22 While depolarization-induced aortic contraction was unchanged

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

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

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

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

27 All sensors reported differences in muscle depolarization induced by a voltage-gated Ca(2+)-channel

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

29 Depolarization induced by elevated extracellular K(+) re

30 The depolarization induced by exogenous acetylcholine was no

31 Estradiol increases membrane depolarization induced by GABA(A) receptor activation in

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

33 Cell membrane depolarization induced by increased potassium concentrat

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

35 ate transporter blocker, suggesting that the depolarization induced by L-lactate can also occur by di

36 ould be responsible for AP activation during depolarization induced by TCWs.

37 onduction block and reentry arising from the depolarization induced by TCWs.

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

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

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

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

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

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

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

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

46 ires both muscarinic receptor activation and depolarization-induced Ca(2+) influx during the ramp.

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

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

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

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

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

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

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

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

55 important regulatory feedback loops linking depolarization-induced Ca(2+) signaling at these sites t

56 provide new insights into canonical forms of depolarization-induced Ca(2+) signaling occurring at jun

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

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

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

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

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

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

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

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

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

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

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

68 Depolarization-induced Ca2+ release was independent of e

69 Depolarization-induced Ca2+ release was not detected dur

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

71 The depolarization-induced calcium increase is dependent on

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

73 Depolarization-induced calcium influx in dorsal root gan

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

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

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

77 ding delayed channel inactivation, prolonged depolarization-induced calcium rise, impaired interneuro

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

79 Depolarization-induced calcium signaling increased the e

80 Compared to WT, muscle strength and depolarization-induced calcium transients in RyR1Q1970fs

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

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

83 Depolarization-induced capacitance changes increased wit

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

85 Depolarization-induced capacitance increases in most cas

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

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

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

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

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

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

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

93 Depolarization-induced changes in phosphatidylserine and

94 Depolarization-induced changes in the regulome revealed

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

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

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

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

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

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

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

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

103 18beta-glycyrrhetinic acid or La3+, blocked depolarization-induced currents.

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

105 Depolarization-induced degradation of the p35 regulatory

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

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

108 nvestigated whether the peak total spreading depolarization-induced depression duration of a recordin

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

110 Remarkably, both depolarization-induced dopamine vesicle hyperacidificati

111 Depolarization-induced down-regulation of sGC activity w

112 e translated uORFs were sufficient to confer depolarization-induced, eIF4G2-dependent translational c

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

114 Depolarization-induced elevation of nuclear CaM also was

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

116 Here, we identify novel crosstalk between depolarization-induced entry of Ca2+ and lysosomal catio

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

118 Visualizing depolarization-induced exocytic and endocytic membrane t

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

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

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

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

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

124 Depolarization-induced FM1-43 uptake in photoreceptor sy

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

126 Depolarization-induced glutamate release from hippocampa

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

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

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

130 Mitochondrial depolarization induced Gp78-dependent expression of the

131 Depolarization-induced gradients of fluorescence between

132 This depolarization-induced hyperacidification is mediated by

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 Depolarization-induced long-term potentiation is blocked

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

155 Depolarization-induced LTD did not occlude the conventio

156 the bioenergetic demand of neural activity, depolarization-induced mitochondrial ATP production was

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

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

159 tivation of other E3 ligases in mitochondria depolarization-induced mitophagy process.

160 kin phosphorylation and enhances the rate of depolarization-induced mitophagy, independently of ULK1.

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

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

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

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

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

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

167 3beta (GSK3beta) significantly increased the depolarization-induced nuclear localization of NFATc4.

168 Spreading depolarizations induced only hyperaemic responses (794%

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

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

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

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

173 t each of these interactions is required for depolarization-induced phosphorylation of the CREB nucle

174 EIF2AK1 knockdown enhances mitochondrial depolarization-induced PINK1 stabilization and phosphory

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

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

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

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

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

180 insensitivity to dendrotoxin, and a lack of depolarization-induced presynaptic facilitation, indicat

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

182 to increase Oma1 activity and necessary for depolarization-induced proteolysis.

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

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

185 Pharmacological and depolarization-induced reduction of inwardly rectifying

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

202 These depolarization-induced shape changes are not fragmentati

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

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

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

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

207 The depolarization-induced slowing was blocked by incubating

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

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

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

211 ive allosteric modulator) did not affect the depolarization-induced spike frequency in nRT neurons.

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

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

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

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

216 induced suppression of inhibition (DSI) and depolarization induced suppression of excitation (DSE),

217 CB1R participates in both depolarization induced suppression of inhibition (DSI) a

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

219 Depolarization-induced suppression of excitation (DSE) a

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

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

222 Depolarization-induced suppression of excitation (DSE) a

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

224 Depolarization-induced suppression of excitation (DSE) i

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

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

227 Depolarization-induced suppression of excitation (DSE) i

228 )-CBD is ~10 times more potent at inhibiting depolarization-induced suppression of excitation (DSE),

229 deletion from VTA dopamine neurons prevents depolarization-induced suppression of excitation (DSE),

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

231 ices and assessed Cb1R activity by measuring depolarization-induced suppression of excitation (DSE).

232 1)-dependent short-term synaptic plasticity (depolarization-induced suppression of excitation [DSE])

233 Depolarization-induced suppression of excitation and inh

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

235 echanisms controlling two different outputs, depolarization-induced suppression of excitation and spi

236 echanisms controlling two different outputs, depolarization-induced suppression of excitation and spi

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

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

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

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

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

242 However, CCK+ inputs undergo depolarization-induced suppression of inhibition (DSI) a

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

244 Depolarization-induced suppression of inhibition (DSI) i

245 Depolarization-induced suppression of inhibition (DSI) i

246 Depolarization-induced suppression of inhibition (DSI) i

247 Depolarization-induced suppression of inhibition (DSI) i

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

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

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

251 Depolarization-induced suppression of inhibition (DSI) i

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

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

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

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

256 This endocannabinoid-mediated depolarization-induced suppression of inhibition (DSI) w

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

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

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

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

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

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

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

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

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

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

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

268 e inhibition produced by exogenous agonists, depolarization-induced suppression of inhibition protoco

269 Using a depolarization-induced suppression of inhibition protoco

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

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

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

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

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

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

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

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

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

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

280 in kinase A-dependent pathway, whereas early depolarization-induced suppression of inhibition-initiat

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

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

283 This depolarization-induced suppression of spontaneous releas

284 CB1-mediated depolarization-induced suppression of synaptic inhibitio

285 Furthermore, potassium depolarization induced the tyrosine phosphorylation of b

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

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

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

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

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

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

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

293 1.2, and reduced intravascular pressure- and depolarization-induced vasoconstriction.

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

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

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