ライフサイエンスコーパス: synaptic vesicle

1 SNAREpins participate in the fusion of each synaptic vesicle.

2 nd increasing the readily releasable pool of synaptic vesicles.

3 complex, and contained dense-core and clear synaptic vesicles.

4 properties that reflect storage in different synaptic vesicles.

5 d the size of the readily releasable pool of synaptic vesicles.

6 of glutamate molecules stored inside single synaptic vesicles.

7 c proteins enabling the continued release of synaptic vesicles.

8 terminals' cytoplasm and tethers hundreds of synaptic vesicles.

9 egeneration of the axon terminal and loss of synaptic vesicles.

10 ritical for the recycling and maintenance of synaptic vesicles.

11 cellular Ca(2+) and diminution of releasable synaptic vesicles.

12 onal differences in loading of dopamine into synaptic vesicles.

13 taneous or action-potential evoked fusion of synaptic vesicles.

14 mulate serotonergic accumulation in cortical synaptic vesicles.

15 ng the large number of v-SNAREs available in synaptic vesicles.

16 veled a nonuniform distribution of VGLUT3 in synaptic vesicles.

17 of synapses relies on efficient recycling of synaptic vesicles.

18 minals and facilitates glutamate uptake into synaptic vesicles.

19 g with curvature with time constants 0.23 s (synaptic vesicles), 3.3 s (chromaffin vesicles), and 9.1

20 Synaptic vesicles accumulate and exocytose at ensheathme

21 Synaptic vesicles accumulate neurotransmitters, enabling

22 These results show that bridging the synaptic vesicle and plasma membranes is a central funct

23 of Munc13-1 (C(1)C(2)BMUNC(2)C) bridges the synaptic vesicle and plasma membranes through interactio

24 rmation of trans-SNARE complexes between the synaptic vesicle and plasma membranes, which likely unde

25 uced size of mossy fiber boutons, with fewer synaptic vesicles and altered synaptic transmission.

26 s, is expressed at presynaptic membranes and synaptic vesicles and associates with synaptic component

27 It is unclear how autophagy of synaptic vesicles and components of presynaptic active z

28 NT Zn(2+) is present along with glutamate in synaptic vesicles and coreleased during synaptic transmi

29 als in lobule V of CB (1) -KO contained less synaptic vesicles and lower vesicle density; by contrast

30 known protein markers of neurodegeneration, synaptic vesicles and mitochondrial integrity.

31 enhanced the number of releasable GABAergic synaptic vesicles and morphological synapses.

32 esides on abundant vesicles that differ from synaptic vesicles and resemble trafficking endosomes.

33 reflection fluorescence microscopy to image synaptic vesicles and ribbons in retinal bipolar cells o

34 sly decreasing the number of VGLUT3-positive synaptic vesicles and the amount of VGLUT3 per synapses.

35 emerging concept in neuroscience states that synaptic vesicles and the molecular machinery underlying

36 c vesicles, which determines the contents of synaptic vesicles and the strength of synaptic transmiss

37 in the proteins RIBEYE and piccolino, tether synaptic vesicles and their delivery likely involves act

38 ecrease in the accumulation of release-ready synaptic vesicles and their release probability caused b

39 branches with discontinuous distributions of synaptic vesicles, and further the Pearson value of colo

40 xchanger, facilitated glutamate loading into synaptic vesicles, and increased quantal size of asynchr

41 elease of neurotransmitters and protons from synaptic vesicles, and is supported by direct data from

42 n navigation for synaptogenesis, but whether synaptic vesicles are functionally employed in circuit f

43 Synaptic vesicles are indispensable for neuronal communi

44 Thus, when large numbers of synaptic vesicles are released during high-frequency syn

45 A large number of synaptic vesicles are released during high-frequency syn

46 Here, we showed that when a large number of synaptic vesicles are released during high-frequency syn

47 A large number of synaptic vesicles are released during high-frequency syn

48 electron microscopy, we find an increase in synaptic vesicles at Dscam2 mutant active zones, providi

49 associated with the release and recycling of synaptic vesicles at nerve terminals, as well as with th

50 are characterized by a small accumulation of synaptic vesicles at points of contact with nerve fibers

51 er-resolution microscopy, is positioned with synaptic vesicles at the boundary.

52 g of L-type Ca(2+) channels to release-ready synaptic vesicles at the presynaptic active zone, which

53 ytosis and/or the presynaptic trafficking of synaptic vesicles back to the nonready releasable pool.

54 ance for both normal protein function (e.g., synaptic vesicle binding) and dysfunction (e.g., mitocho

55 Synaptic vesicle biogenesis must be concurrent with axon

56 apses, the fast and indefatigable release of synaptic vesicles by IHCs is controlled by otoferlin, a

57 loss reduces the readily releasable pool of synaptic vesicles by up to 75%.

58 The synaptic vesicle Ca(2+) sensor Synaptotagmin binds Ca(2+

59 ons are macromolecular scaffolds that tether synaptic vesicles close to release sites in nonspiking n

60 A significant higher amount of synaptic vesicles close to the active zone in lobule V a

61 KIF1A motor in promoting axonal transport of synaptic-vesicle components for presynaptic assembly and

62 size of the readily releasable pool (RRP) of synaptic vesicles, consistent with the isoproterenol-ind

63 l a novel role of uPA as an activator of the synaptic vesicle cycle in cerebral cortical neurons via

64 domain contributes to the regulation of the synaptic vesicle cycle in IHCs are still incompletely un

65 roton and chloride concentrations during the synaptic vesicle cycle to ensure normal synaptic transmi

66 nscriptional markers of proteins involved in synaptic vesicle cycle were selectively altered, and the

67 sponses, as well as pathways responsible for synaptic vesicle cycle, long-term potentiation and depre

68 eiotropic role of otoferlin in the hair cell synaptic vesicle cycle, notably in triggering both ultra

69 ating at the presynapse, separately from the synaptic vesicle cycle, which clears activated receptors

70 KO) mouse, we studied the impact of NAMPT on synaptic vesicle cycling in the neuromuscular junction (

71 it sustains the ATP production required for synaptic vesicle cycling.

72 /-) mice, but not in Syb1(lew/lew) mice; (2) synaptic vesicle density was markedly reduced in Syb1(le

73 -bisphosphate (PI-4,5-P(2) ) is critical for synaptic vesicle docking and fusion and generation of th

74 associated protein SNAP25 is a key player in synaptic vesicle docking and fusion and has been associa

75 as it recruits Ca(2+) channels and activates synaptic vesicle docking and priming via Munc13-1.

76 In another step, both RIM and Munc13 mediate synaptic vesicle docking and priming.

77 lead to corresponding disruptive effects on synaptic vesicle docking, priming, and Ca(2+)-triggered

78 We show that cell depolarization increases synaptic vesicle dopamine content prior to release via v

79 l excitatory neurotransmitter glutamate into synaptic vesicles, driven by membrane potential.

80 RBM3 knockdown altered synaptic vesicle dynamics and changed the neuronal activ

81 .SIGNIFICANCE STATEMENT Mechanisms governing synaptic vesicle dynamics during recycling remain poorly

82 We demonstrate long-term imaging of synaptic vesicle dynamics in cultured neurons as well as

83 ime-dependent changes in global activity, in synaptic vesicle dynamics, in synapse size, and in synap

84 ur measurements show that an isolated single synaptic vesicle encapsulates about 8000 glutamate molec

85 in A1), have also highlighted disruptions in synaptic vesicle endocytosis (SVE) as a significant cont

86 ssibility that PDLIM1 may be involved in the synaptic vesicle endocytosis and/or the presynaptic traf

87 animals were physiologically tested using a synaptic vesicle endocytosis assay and FM4-64 dye showin

88 n, syt1 acted as an essential determinant of synaptic vesicle endocytosis time course by delaying the

89 a major presynaptic phosphatase that couples synaptic vesicle endocytosis to the dephosphorylation of

90 t HDAC activity may oppose Kismet to promote synaptic vesicle endocytosis.

91 Loss of NAMPT impaired synaptic vesicle endocytosis/exocytosis in the NMJs.

92 s influenced by the protein association with synaptic vesicles, especially for membrane proteins.

93 Synaptic vesicle exocytosis and endocytosis are tightly

94 mouse models suggest a role for otoferlin in synaptic vesicle exocytosis and endocytosis, it is uncle

95 vous system, using VGLUT-pHluorin to monitor synaptic vesicle exocytosis and retrieval in intact anim

96 pre-synaptic HCN channels alter the rate of synaptic vesicle exocytosis and thereby enhance neurotra

97 arge six-C2-domain protein, is essential for synaptic vesicle exocytosis at auditory hair cell ribbon

98 To capture synaptic vesicle exocytosis at cultured mouse hippocampa

99 ny yeast orthologs have established roles in synaptic vesicle exocytosis in the mammalian brain.

100 otagmins are calcium-sensing proteins of the synaptic vesicle exocytosis machinery, and changes in Sy

101 ptotagmin (syt) 1, a major Ca(2+)-sensor for synaptic vesicle exocytosis, drove the formation of an i

102 lytic cleavage of host proteins required for synaptic vesicle exocytosis.

103 effectors, the exocyst, are dispensable for synaptic vesicle exocytosis.

104 vealed an acid efflux mechanism reliant upon synaptic vesicle exocytosis.

105 napses and conventional chemical synapses in synaptic vesicle exocytosis.SIGNIFICANCE STATEMENT RAB3A

106 ts: narrow intercellular cleft, keratinocyte synaptic vesicles expressing synaptophysin and synaptota

107 Stabilized boutons rapidly recruited synaptic vesicles, followed by accumulation of postsynap

108 IFICANCE STATEMENT Despite the importance of synaptic vesicles for neurons, little is known about how

109 e of FM1-43, a dye that is incorporated into synaptic vesicles, from EC synaptic terminals using two

110 dues of synapsin I, which critically impacts synaptic vesicle function.

111 Synaptic vesicles fuse at morphological specializations

112 Neurotransmitter-laden synaptic vesicles fuse with the plasma membrane on cue w

113 Synaptic vesicles fuse with the plasma membrane to relea

114 Upon Ca(2+) influx, synaptic vesicles fuse with the presynaptic plasma membr

115 e progress in the molecular understanding of synaptic vesicle fusion and its control.

116 large multifunctional protein essential for synaptic vesicle fusion and neurotransmitter release.

117 a role for synucleins in the enhancement of synaptic vesicle fusion and turnover.

118 of the SNARE four-helix bundle that mediates synaptic vesicle fusion and used it to study vesicle fus

119 rich tapestry of molecular players governing synaptic vesicle fusion at highly specialized release si

120 ed that modulation of the energy barrier for synaptic vesicle fusion boosts release rates supralinear

121 eous fusion, with the protein serving as the synaptic vesicle fusion clamp at Drosophila synapses.

122 Synaptic vesicle fusion is coupled to swift retrieval of

123 tagmin that promote Ca(2+) activation of the synaptic vesicle fusion machinery.

124 ctions with SNAP-25, a core component of the synaptic vesicle fusion machinery.

125 unc18-1 (Stxbp1), a presynaptic organizer of synaptic vesicle fusion, is a powerful mechanism to regu

126 the protein is involved in the regulation of synaptic vesicle fusion, signifying the importance of al

127 In contrast, after single synaptic vesicle fusion, syt1 acted as an essential dete

128 has been extensively studied in its role in synaptic vesicle fusion.

129 promoted the influx of calcium necessary for synaptic vesicle fusion.

130 release machinery triggers Ca(2+)-dependent synaptic vesicle fusion.

131 ARE folding and assembly, thereby regulating synaptic vesicle fusion.

132 They mediate the priming step that renders synaptic vesicles fusion-competent, and their genetic el

133 lly found in the surrounding tissues such as synaptic vesicle genes in the brain endothelium and card

134 The synaptic vesicle glycoprotein 2A (SV2A) can be used to i

135 dy examined the density of all synapses with synaptic vesicle glycoprotein 2A (SV2A) in Parkinson dis

136 sted directly in vivo. Here, we investigated synaptic vesicle glycoprotein 2A (SV2A) levels and their

137 PET) and [(11)C]UCB-J, a radioligand for the synaptic vesicle glycoprotein 2A (SV2A), were used to st

138 The use of synaptic vesicle glycoprotein 2A radiotracers with PET i

139 best with 1TC BP (ND) Conclusion: The novel synaptic vesicle glycoprotein 2A tracer, (18)F-SynVesT-1

140 phenyl)pyrrolidin-2-one) is a PET tracer for synaptic vesicle glycoprotein 2A, which may be a marker

141 anti-SV2, a monoclonal antibody that labels synaptic vesicle glycoprotein SV2.

142 ted by the release of neurotransmitters from synaptic vesicles in response to stimulation or through

143 of SVPs, leading to ectopic accumulation of synaptic vesicles in the proximal axon.

144 exocytosis, as well as the replenishment of synaptic vesicles, in IHCs was not affected.

145 Regulated exocytosis of synaptic vesicles is substantially faster than of endocr

146 urotransmitter and neuropeptide release from synaptic vesicles, is a critical PKC-2 effector in AFD.

147 Our studies demonstrate that SREBP regulates synaptic vesicle levels by interacting with tetraspanins

148 slight increase in the mutants' avidity for synaptic vesicle-like membranes can be detected, most of

149 test this, we used fusion proteins to track synaptic vesicle localization and membrane fusion in zeb

150 act in overlapping and independent stages of synaptic vesicle localization and release.SIGNIFICANCE S

151 We found that RIM modulates synaptic vesicle localization in the proximity of the ac

152 P) is both necessary and sufficient to cause synaptic vesicle loss.

153 pecific scaling of several components of the synaptic vesicle machinery, including the vesicular glut

154 Expression of the synaptic vesicle marker SV2 was significantly increased

155 ion, kismet mutants exhibit reduced VGLUT, a synaptic vesicle marker, at stimulated but not resting s

156 ogyrins 1 and 3 constitute a major family of synaptic vesicle membrane proteins.

157 ned release sites and endocytic retrieval of synaptic vesicle membranes.

158 sphorylated Synapsin1 and CREB, which affect synaptic vesicle mobilization and gene transcription, re

159 ates neurotransmitter release by restricting synaptic vesicle mobilization and recycling.

160 can ensure release of neurotransmitters from synaptic vesicles much faster: in a 10th of a millisecon

161 e membrane and formation of fusion-competent synaptic vesicles near voltage-gated Ca(2+) channels.

162 Synaptic vesicles need to be recycled and refilled rapid

163 requency synaptic transmission; accordingly, synaptic vesicles need to be recycled and refilled rapid

164 requency synaptic transmission; accordingly, synaptic vesicles need to be recycled rapidly to repleni

165 Synapsin-1 thereby bidirectionally regulates synaptic vesicle numbers and modifies presynaptic neurot

166 l that the neuromodulator-induced control of synaptic vesicle numbers was largely dependent on synaps

167 dulator receptors bidirectionally controlled synaptic vesicle numbers within nerve terminals.

168 WT mice, while nCLCa-only mice had increased synaptic vesicle numbers, restoring normal neurotransmis

169 ltra-small amounts of glutamate and to study synaptic vesicle physiology, pathogenesis, and drug trea

170 Mice with only nCLCb had a reduced synaptic vesicle pool and impaired neurotransmission com

171 errogation of the link between this putative synaptic vesicle pool heterogeneity and neurotransmissio

172 repertoire of specific phospholipids and the synaptic vesicle pool in adult Drosophila photoreceptors

173 We also found that synaptic vesicle pool recovery from depletion was sensit

174 ion with the presynaptic plasma membrane and synaptic vesicle pool replenishment in the IHC active zo

175 However, activity-dependent augmentation of synaptic vesicle pool size relies exclusively on the act

176 hila photoreceptor (PR) degeneration and the synaptic vesicle pool through a transcriptional-translat

177 autophagy, which in turn limits the size of synaptic vesicle pools and influences the kinetics of ac

178 ocess engaged by neural activity to regulate synaptic vesicle pools for optimal synaptic responses, l

179 g role for this feedback loop in maintaining synaptic vesicle pools in the adult brain.

180 urons, little is known about how the size of synaptic vesicle pools is maintained under basal conditi

181 dentifies a new mechanism for the control of synaptic vesicle pools, and a new, nonapoptotic function

182 k identifies a new mechanism for controlling synaptic vesicle pools, and a novel, nonapoptotic, presy

183 se-3 cascade and autophagy in the control of synaptic vesicle pools.

184 f activity-induced depletion and recovery of synaptic vesicle pools.

185 itution assays, we find that the delivery of synaptic vesicle precursors (SVPs) to en passant synapse

186 ransporters of cargos, such as mitochondria, synaptic vesicle precursors, neurotransmitter receptors,

187 An increase in the number of synaptic vesicles primed for exocytosis accounts for the

188 -specific RIM variants are not essential for synaptic vesicle priming at photoreceptor ribbon synapse

189 nventional chemical synapses with respect to synaptic vesicle priming mechanisms.

190 it adds the neuronal Munc13 proteins and the synaptic vesicle priming process that they control to th

191 and plasma membranes, which likely underlies synaptic vesicle priming to a release-ready state.

192 und that a Na(+)/H(+) exchanger expressed on synaptic vesicles promotes vesicle filling with glutamat

193 elease is triggered by Ca(2+) binding to the synaptic vesicle protein Synaptotagmin 1, while asynchro

194 Here, we examined the distribution of the synaptic vesicle protein Synaptotagmin 2a (Syt2a) during

195 esin-3 KIF1A known for its fast shuffling of synaptic vesicle protein transport vesicles in axons.

196 ed to protein domains as we show for another synaptic vesicle protein, synaptophysin 1.

197 sicular and extravesicular interactions with synaptic vesicle proteins and the neurotransmitter relea

198 Unlike other widely expressed synaptic vesicle proteins such as vSNAREs and synaptotag

199 ses capable of responding to local damage of synaptic vesicle proteins within minutes and to be criti

200 We compared synaptic vesicle proteins, endo- and exocytosis cofactor

201 racts with glutamatergic, but not GABAergic, synaptic vesicle proteins.

202 hospho-tau species with their synaptogyrin-3 synaptic vesicle receptor replace excessive production a

203 eurons mitigates TDP-43 dependent defects in synaptic vesicle recycling and improves locomotion.

204 unrecognized linkage between the pathway of synaptic vesicle recycling and the properties of exocyto

205 ormation, synaptic activity, plasticity, and synaptic vesicle recycling at distinct developmental and

206 etic ablation of GLUT4 leads to an arrest of synaptic vesicle recycling during sustained AP firing, s

207 Synaptic vesicle recycling is essential for maintaining

208 However, how neuronal activity regulates synaptic vesicle recycling is largely unknown.

209 We examined synaptic vesicle recycling pathways at complexin null ne

210 Synaptic vesicle recycling studies suggested functional

211 ion in zebrafish larvae and found defects in synaptic vesicle recycling, abnormal synaptic ribbons, a

212 a phosphoinositide phosphatase implicated in synaptic vesicle recycling, results in PD.

213 d in clathrin-mediated endocytosis (CME) and synaptic vesicle recycling.

214 ial may elicit temporally highly coordinated synaptic vesicle release at tens of active zones, thereb

215 Antipsychotics blocked synaptic vesicle release during efficacy but enhanced th

216 ns induced by amphetamine (AMPH), we blocked synaptic vesicle release from these neurons using Cre-in

217 air synaptic transmission and plasticity and synaptic vesicle release kinetics.

218 c vesicles, which leads to increased initial synaptic vesicle release probability and abnormal short-

219 er expression, and membrane conductances and synaptic vesicle release properties consistent with poss

220 e that Fife organizes active zones to create synaptic vesicle release sites within nanometer distance

221 mouse hippocampal synapses via inhibition of synaptic vesicle release.

222 e' structure, where ion channels cluster and synaptic vesicles release their neurotransmitters(2).

223 acking nCLCa or nCLCb were both defective in synaptic vesicle replenishment.

224 +))-evoked release of neurotransmitters from synaptic vesicles requires mechanisms both to prevent un

225 wing brief intense activity, VAMP4-dependent synaptic vesicle retrieval supports a pool of vesicles t

226 sicle recycling studies suggested functional synaptic vesicle retrieval.

227 demonstrate that Ca(2+) is not essential for synaptic vesicle retrieval.

228 egregation of the readily releasable pool of synaptic vesicles (RRP) in sub-pools that are differenti

229 re critical "trans" interactions between the synaptic vesicle SNARE protein synaptobrevin 2 and the p

230 usion between proteoliposomes containing the synaptic vesicle SNARE synaptobrevin (with or without th

231 d, their synaptic terminals contain numerous synaptic vesicles, some of which are ribbon associated,

232 thout interference from cotransmitting small synaptic vesicles (SSVs) with the use of a fluorogen-act

233 the expression level of active zone (AZ) and synaptic vesicle (SV) components.

234 knock-in Ca(2+) channels, and Ca(2+) channel-synaptic vesicle (SV) coupling distance using Ca(2+) che

235 VAPA and VAPB are involved in modulating the synaptic vesicle (SV) cycle.

236 Synaptic vesicle (SV) endocytosis is coupled to exocytos

237 We further show that the rate of synaptic vesicle (SV) endocytosis is differentially affe

238 Synaptic vesicle (SV) exocytosis is mediated by SNARE pr

239 SV2A, has a number of potential roles in the synaptic vesicle (SV) life cycle.

240 romalin functions as a negative regulator of synaptic vesicle (SV) pool size in Drosophila neurons.

241 ses (NCL) CLN4 is caused by mutations in the synaptic vesicle (SV) protein CSPalpha.

242 re activity.SIGNIFICANCE STATEMENT SV2A is a synaptic vesicle (SV) protein, the absence or dysfunctio

243 Mechanisms regulating the turnover of synaptic vesicle (SV) proteins are not well understood.

244 The regulated turnover of synaptic vesicle (SV) proteins is thought to involve the

245 est alpha-syn as a physiologic attenuator of synaptic vesicle (SV) recycling, mechanisms are unclear.

246 hed isoform has been shown to participate in synaptic vesicle (SV) recycling.

247 ansporters (VGLUT) accumulate glutamate into synaptic vesicles (SV) and thereby regulate quantal size

248 brain function requires proper targeting of synaptic-vesicle (SV) and active-zone components for pre

249 ins Piccolo and Bassoon triggers the loss of synaptic vesicles (SVs) and compromises synaptic integri

250 of neurotransmitters from readily releasable synaptic vesicles (SVs) at the active zone.

251 tem depends on neurotransmitter release from synaptic vesicles (SVs) at the presynaptic active zone.

252 Synaptic vesicles (SVs) can be pooled across multiple sy

253 is sustained by endocytosis and refilling of synaptic vesicles (SVs) locally within the presynapse.

254 a wide range of axonal organelles as well as synaptic vesicles (SVs) relative to vGlut1(+) stable pre

255 role in synaptic transmission by recruiting synaptic vesicles (SVs) to become available for release,

256 t of the three functionally defined pools of synaptic vesicles (SVs) were quantified.

257 tobrevin2), a core SNARE protein residing on synaptic vesicles (SVs), forms helix bundles with syntax

258 their affinity to intracellular partners and synaptic vesicles (SVs).

259 all-molecule neurotransmitters packaged into synaptic vesicles (SVs).

260 diate fast and temporally precise release of synaptic vesicles (SVs).

261 Conversely, a second pool of synaptic vesicles that cannot be released by a single st

262 s in location or cytoskeletal association of synaptic vesicles, the release of different transmitters

263 bility that Syt1 rings could pre-form on the synaptic vesicle to facilitate docking.

264 reby non-phosphorylated synapsin-1 "latches" synaptic vesicles to presynaptic clusters at the active

265 rotein 25 (SNAP25), VAMP2 mediates fusion of synaptic vesicles to release neurotransmitters.

266 results demonstrate that the recruitment of synaptic vesicles to release sites is rapid and reversib

267 teins that functionally interact to localize synaptic vesicles to release sites, ensuring neurotransm

268 the presynaptic terminal requires docking of synaptic vesicles to the active zone membrane and format

269 st exocytosis and endocytosis and recruiting synaptic vesicles to the active zone.

270 ein regions (IDPs and IDRs, respectively) in synaptic vesicle trafficking and exocytosis and in overa

271 ation causes activity-induced locomotion and synaptic vesicle trafficking defects, while TBC1D24R360H

272 or alpha-tocopherol as indicated by restored synaptic vesicle trafficking levels and sustained behavi

273 way that differs from the well-characterized synaptic vesicle trafficking pathway but is also essenti

274 s a reactive oxygen species sensor mediating synaptic vesicle trafficking rates that, when dysfunctio

275 rosophila, where TBC1D24/Skywalker regulates synaptic vesicle trafficking.

276 ment utilizes a "waterfall" mechanism gating synaptic vesicle transport polarity by promoting anterog

277 e transcripts associated with cell adhesion, synaptic vesicle transport, regulation of membrane poten

278 During neurotransmission, synaptic vesicles undergo multiple rounds of exo-endocyt

279 bulk endocytosis, the primary mechanism for synaptic vesicle uptake during intense neuronal stimulat

280 urons, the loading of neurotransmitters into synaptic vesicles uses energy from proton-pumping vesicu

281 Retrieval of synaptic vesicles via endocytosis is essential for maint

282 Glutamate is loaded into synaptic vesicles via the vesicular glutamate transporte

283 In each animal >=425 ASIs were measured and synaptic vesicles were counted in ~100 synapses/mouse.

284 synaptic transmission, when large numbers of synaptic vesicles were fused, the rapid buildup of presy

285 l excitatory neurotransmitter glutamate into synaptic vesicles, whereas closely related proteins use

286 ective axon growth and impaired autophagy of synaptic vesicles, which can be rescued by constitutivel

287 e control of neurotransmitter transport into synaptic vesicles, which determines the contents of syna

288 racterized by increased fusion propensity of synaptic vesicles, which leads to increased initial syna

289 sensor is placed into a solution of isolated synaptic vesicles, which stochastically rupture at the s

290 ation or through the spontaneous fusion of a synaptic vesicle with the presynaptic plasma membrane.

291 planted interneurons that are unable to fill synaptic vesicles with GABA migrate and integrate into t

292 lly using spikes that trigger the release of synaptic vesicles with low probability.

293 Neurotransmitter release involves fusion of synaptic vesicles with the plasma membrane in response t

294 Fusion of secretory granules and synaptic vesicles with the plasma membrane is driven by

295 s neurotransmitter release via the fusion of synaptic vesicles with the presynaptic membrane, driven

296 f an action potential, through the fusion of synaptic vesicles with the presynaptic membrane.

297 regulate the binding affinity of alphaS for synaptic vesicles without altering the structural proper

298 hment rate of the readily releasable pool of synaptic vesicles without changes in their probability o

299 Zn(2+) in these cultures, we did detect the synaptic vesicle Zn(2+) transporter ZnT3 and found it to

300 n between synaptic markers in the active and synaptic vesicle zones.