ライフサイエンスコーパス: neurotransmitter release

1 exocytosis to maintain SV pool size and thus neurotransmitter release.

2 nd splice variants adapted to the demands on neurotransmitter release.

3 the magnitude of Ca(2+) currents (I(Ca)) and neurotransmitter release.

4 directional delivery of SVs between sites of neurotransmitter release.

5 1 and the SNARE complex cooperate to trigger neurotransmitter release.

6 phoproteins fundamental to the regulation of neurotransmitter release.

7 de more complete spatiotemporal control over neurotransmitter release.

8 ponent of the SNARE complex, which underlies neurotransmitter release.

9 rough local estrogen synthesis or inhibitory neurotransmitter release.

10 h regulation of cell firing and heterologous neurotransmitter release.

11 +) influx to trigger action potential-evoked neurotransmitter release.

12 t1), an SV protein essential for synchronous neurotransmitter release.

13 t7), and spontaneous (Doc2a/Doc2b) phases of neurotransmitter release.

14 ing a previously unrecognized role of 5RK in neurotransmitter release.

15 action potential (AP) has a strong impact on neurotransmitter release.

16 channel clusters for reliable and modifiable neurotransmitter release.

17 ut affecting normal fluctuations of synaptic neurotransmitter release.

18 minant of the functions of Syt C2 domains in neurotransmitter release.

19 ncluding axonal elongation and branching and neurotransmitter release.

20 n within the approximately 1-ms timescale of neurotransmitter release.

21 ity, intracellular [Ca(2+) ] regulation, and neurotransmitter release.

22 x assembly together with Munc13-1 to mediate neurotransmitter release.

23 synaptic plasticity consistent with enhanced neurotransmitter release.

24 us contribution of L-type Ca(2+) channels to neurotransmitter release.

25 ial widening that could account for enhanced neurotransmitter release.

26 cleave SNARE proteins nor impair spontaneous neurotransmitter release.

27 RIM at the active zone cytomatrix to promote neurotransmitter release.

28 and proposed a potential role in regulating neurotransmitter release.

29 rpotentials did not alter calcium current or neurotransmitter release.

30 awn mutants harbor a significant increase in neurotransmitter release.

31 (Ca(v)) channels to trigger Ca(2+)-dependent neurotransmitter release.

32 nct from the fast sensors that mediate rapid neurotransmitter release.

33 nnels, allowing calcium to enter and trigger neurotransmitter release.

34 unctionally important for SNARE assembly and neurotransmitter release.

35 nge IL-18, the extent proportional to opioid neurotransmitter release.

36 membranes, which could potentially regulate neurotransmitter release.

37 decrease (long-term depression, LTDGABA) of neurotransmitter release.

38 ing the balance among the different modes of neurotransmitter release.

39 including protein and hormone secretion and neurotransmitter release.

40 activates protein kinase C (PKC) to increase neurotransmitter release.

41 h often follow APs, affect calcium entry and neurotransmitter release.

42 tion of nearby synapses to further stimulate neurotransmitter release.

43 fluxes, neuronal or muscle excitability, and neurotransmitter release.

44 besity effect over those with loss of single neurotransmitter release.

45 chain expression, which prevented vesicular neurotransmitter release.

46 nent of the exocytic machinery that controls neurotransmitter release.

47 ulates Glutamate receptor A1 trafficking and neurotransmitter release.

48 ction potential initiation, propagation, and neurotransmitter release.

49 se machinery, but dramatically impaired fast neurotransmitter release.

50 ical functions including membrane fusion and neurotransmitter release.

51 SNARE protein cleavage leading to a loss of neurotransmitter release.

52 serotonin neurons, where they act to inhibit neurotransmitter release.

53 s contraction rate and timing through phasic neurotransmitter release.

54 soforms to phosphorylate targets and enhance neurotransmitter release.

55 h subsequent action potential evokes greater neurotransmitter release.

56 potent homeostatic reduction in presynaptic neurotransmitter release.

57 plasticity that is associated with enhanced neurotransmitter release.

58 in essential for synaptic vesicle fusion and neurotransmitter release.

59 um influx to exocytosis, thereby suppressing neurotransmitter release.

60 mains, C2A and C2B, act as Ca(2+) sensors of neurotransmitter release.

61 25, forms the essential fusion machinery for neurotransmitter release.

62 anges in the Ca(2+) channel subtypes driving neurotransmitter release.

63 ritical to its central role in orchestrating neurotransmitter release.

64 c side through uniform downscaling of evoked neurotransmitter release.

65 sion pore, leading to an increased amount of neurotransmitter release.

66 e expressed in axons, where it downregulates neurotransmitter release.

67 vate SNARE proteins, which are essential for neurotransmitter release.

68 vesicular exocytosis and activity-dependent neurotransmitter release.

69 than not, action potentials fail to trigger neurotransmitter release.

70 the synaptic cleft to modulate photoreceptor neurotransmitter release.

71 s functional APP domain promoting excitatory neurotransmitter release.

72 First, presynaptic DCAF12 promotes evoked neurotransmitter release.

73 that restores synaptic function by adjusting neurotransmitter release.

74 Munc13-1 plays a crucial role in neurotransmitter release.

75 aptobrevin, allowing exquisite regulation of neurotransmitter release.

76 rocessing of ISVAID did not alter excitatory neurotransmitter release.

77 contraction, audition, hormone secretion and neurotransmitter release.

78 stinct mechanisms for evoked and spontaneous neurotransmitter release.

79 ex firing frequencies and tune the amount of neurotransmitter released.

80 aptic vesicle exocytosis and thereby enhance neurotransmitter release?

81 f secretory machines determine properties of neurotransmitter release?

82 eal a suppressing action of Cplx3/4 on tonic neurotransmitter release, a facilitating action on evoke

83 profound increases in evoked and spontaneous neurotransmitter release, a high frequency of spontaneou

84 crease in the basal frequency of spontaneous neurotransmitter release, a higher basal number of funct

85 ling" maintained the relative differences in neurotransmitter release across all inputs around a home

86 n which caused uniform downscaling of evoked neurotransmitter release across all inputs through decre

87 ulation and support an ultrafast recovery of neurotransmitter release after low-frequency depression.

88 d presynaptic vesicle fusion, and changes in neurotransmitter release, all of which contribute to dif

89 The eCBs mediates inhibition of neurotransmitter release and acts as a major homeostatic

90 ynaptic glutamate receptors (GluRs) modulate neurotransmitter release and are physiological targets f

91 n implicated in spontaneous and asynchronous neurotransmitter release and compete with Syt1 for bindi

92 cent glutamate indicators (iGluSnFRs) enable neurotransmitter release and diffusion to be visualized

93 effector protein that decreases spontaneous neurotransmitter release and enhances evoked release.

94 del of SYT1 and SYT7 mediating all phases of neurotransmitter release and facilitation is not applica

95 sary for normal postsynaptic responsivity to neurotransmitter release and for normal coordinated larv

96 d protein of 25kDa (SNAP-25B), which disrupt neurotransmitter release and have been implicated in neu

97 They facilitate presynaptic neurotransmitter release and modulate mechanisms control

98 stingly, shawn mutants also harbor increased neurotransmitter release and neurodegeneration.

99 ates PTP and the PKC activator PDBu enhances neurotransmitter release and occludes PTP.

100 pling between the reliability of presynaptic neurotransmitter release and postsynaptic responsiveness

101 Exogenous Mel inhibits neurotransmitter release and promotes sleep in wild-type

102 Complexin activates Ca(2+)-triggered neurotransmitter release and regulates spontaneous relea

103 +) channel-mediated current, which increases neurotransmitter release and rhythmic firing activity of

104 el synthesis) causes substantially increased neurotransmitter release and shortened sleep duration, a

105 utamatergic synapses of CH and SR supporting neurotransmitter release and synaptic plasticity.

106 entral nervous system, with key roles during neurotransmitter release and synaptic plasticity.

107 cal role of presynaptic ER in the control of neurotransmitter release and will help frame future inve

108 ponding postsynaptic sites through increased neurotransmitter release and, consequently, promotes the

109 lo-1 gain-of-function mutants in locomotion, neurotransmitter release, and calcium-mediated asymmetri

110 Ca(2+) channel responsible for synchronized neurotransmitter release, and found that channel abundan

111 Gi/o, they limit cAMP accumulation, diminish neurotransmitter release, and induce neuronal hyperpolar

112 ynapses with an initially low probability of neurotransmitter release, and may inform strategies to r

113 ion to the nerve terminal suggests a role in neurotransmitter release, and overexpression inhibits re

114 hannels, decreased and desynchronized evoked neurotransmitter release, and rendered evoked and sponta

115 c contribution of VGCCs to calcium dynamics, neurotransmitter release, and short-term facilitation re

116 ene expression and protein levels, glutamate neurotransmitter release, and, consequently, reduced spo

117 s, but presynaptic mechanisms regulating the neurotransmitter release apparatus remain largely enigma

118 i did not alter calcium channel responses or neurotransmitter release appreciably.

119 notypes, specific alterations in spontaneous neurotransmitter release are a key factor to account for

120 Long-term changes of neurotransmitter release are critical for proper brain f

121 n, implying that trans-synaptic increases in neurotransmitter release are not necessary for the posts

122 so demonstrate that neuronal maintenance and neurotransmitter release are regulated by Stx1 through i

123 tic vesicle numbers and modifies presynaptic neurotransmitter release as an effector of neuromodulato

124 release from intracellular stores can drive neurotransmitter release as well as subsequent signallin

125 -binding protein involved in endocytosis and neurotransmitter release, as a novel IRP-interacting tra

126 vity inhibits presynaptic calcium signal and neurotransmitter release, assigning synaptic defects to

127 Action potentials trigger neurotransmitter release at active zones, specialized re

128 RIBEYE severely impaired fast and sustained neurotransmitter release at bipolar neuron/AII amacrine

129 inhibition, resulting in the suppression of neurotransmitter release at both excitatory and inhibito

130 protein RIM-BP2 has diversified functions in neurotransmitter release at different central murine syn

131 s, in controlling presynaptic morphology and neurotransmitter release at excitatory synapses.

132 are often subjected to bursts of very brief neurotransmitter release at high frequencies.

133 t increase in presynaptic calcium levels and neurotransmitter release at individual glutamatergic ter

134 Munc13 proteins are essential regulators of neurotransmitter release at nerve cell synapses.

135 Neurons communicate through Ca(2+)-dependent neurotransmitter release at presynaptic active zones (AZ

136 vesicle number, indicating that it augments neurotransmitter release at presynaptic level.

137 eal a selective role for presynaptic RIM1 in neurotransmitter release at prominent basal ganglia syna

138 pled G protein-coupled receptors can inhibit neurotransmitter release at synapses via multiple mechan

139 amp recording, we showed that TMEM16B alters neurotransmitter release at the hippocampal-LS synapse,

140 trograde, homeostatic control of presynaptic neurotransmitter release at the neuromuscular junction i

141 tional transitions play an important role in neurotransmitter release at the neuronal synapse.

142 Efficient neurotransmitter release at the presynaptic terminal req

143 on rapid, temporally precise, and sustained neurotransmitter release at the ribbon synapses of senso

144 s to hyperpolarization of the cell, reducing neurotransmitter release at the synapse.

145 er segment, metabolism in the cell body, and neurotransmitter release at the synaptic terminal.

146 superficial layers consistent with enhanced neurotransmitter release at these synapses.

147 nsmembrane protein 2 (PRRT2), a regulator of neurotransmitter release, at glycine-305 was previously

148 Prior to entering neurons and blocking neurotransmitter release, BoNT/A recognizes motoneurons

149 not only the proximal Ca(2+) sensor for fast neurotransmitter release but also serves to clamp sponta

150 nal localization required for the control of neurotransmitter release, but also suggests that, in add

151 powerful tool to elucidate the mechanism of neurotransmitter release, but it is important to underst

152 re it contributes to action potential-evoked neurotransmitter release, but it is not expressed mid-ax

153 s not required for immediate potentiation of neurotransmitter release, but necessary to sustain poten

154 eceptor) proteins mediate evoked synchronous neurotransmitter release, but the molecular mechanisms m

155 hat presynaptic afterpotentials should alter neurotransmitter release by affecting the electrical dri

156 a topic of some debate; genetic ablation of neurotransmitter release by deletion of the Munc18-1 gen

157 uces a retrograde enhancement of presynaptic neurotransmitter release by increasing the size of the r

158 te calcium-dependent cellular events such as neurotransmitter release by limiting calcium influx.

159 inding contributes to enabling regulation of neurotransmitter release by Munc13-1.

160 ynapses, RIM-BP2 has a substantial impact on neurotransmitter release by promoting vesicle docking/pr

161 ile another posits that alpha-syn attenuates neurotransmitter release by restricting synaptic vesicle

162 naptotagmins (Syts) act as Ca(2+) sensors in neurotransmitter release by virtue of Ca(2+)-binding to

163 Maps of the synapses made and neurotransmitters released by all neurons in model syste

164 However, the neurotransmitters released by cortical ChAT(+) neurons a

165 unterbalanced compensatory plasticity of two neurotransmitters released by different terminals of the

166 espite accumulating evidence indicating that neurotransmitters released by the sympathetic nervous sy

167 synapses, RIM-BP2 loss has a mild effect on neurotransmitter release, by only regulating Ca(2+)-secr

168 itized to neurobiological processes, such as neurotransmitter release, calcium signaling, and gene ex

169 Neurotransmitter release can be synchronous and occur wi

170 eals three aspects of neuronal interactions: neurotransmitter release, cell firing, and dopamine-rece

171 ts of neuronal communication simultaneously: neurotransmitter release, cell firing, and identificatio

172 Facilitation can enhance neurotransmitter release considerably and can profoundly

173 peroxide (H2 O2 ) modified the properties of neurotransmitter release depending on the route of HRP u

174 Neurotransmitter release depends on a complex interplay

175 Neurotransmitter release depends on the SNARE complex fo

176 Neurotransmitter release depends on voltage-gated Na(+)

177 the primary interface, which strongly impair neurotransmitter release, disrupt and enhance synaptotag

178 eract with presynaptic proteins and regulate neurotransmitter release downstream of Ca(2+) influx.

179 exocytosis accounts for the potentiation of neurotransmitter release driven by betaARs.

180 presynaptic local protein synthesis controls neurotransmitter release during long-term plasticity in

181 Ca(2+)-evoked release, RIM uniquely controls neurotransmitter release efficiency.

182 oregulates synapse number and probability of neurotransmitter release, emerging as a potential therap

183 eurotransmission requires precise control of neurotransmitter release from axon terminals.

184 r excitation generates patterns of staggered neurotransmitter release from different MNTB axons resul

185 lar calcium dynamics, neuronal excitability, neurotransmitter release from mouse brain slices, and br

186 on of VGCCs, a phenomenon known to influence neurotransmitter release from neurons.

187 ensures efficient action potential-triggered neurotransmitter release from presynaptic active zones (

188 onal communication across synapses relies on neurotransmitter release from presynaptic active zones (

189 Fast neurotransmitter release from ribbon synapses via Ca(2+)

190 ne potential fluctuations at the soma affect neurotransmitter release from synaptic boutons.

191 processing by the nervous system depends on neurotransmitter release from synaptic vesicles (SVs) at

192 Potentiation of neurotransmitter release from the active synaptic inputs

193 nate a neuronal signal and enable subsequent neurotransmitter release from the presynaptic neuron.

194 iour in an open-field assay, and depended on neurotransmitter release from VMHdm(SF1) neurons.

195 though glutamate is known to be an important neurotransmitter released from baroreceptor afferent syn

196 gmin-2, the fastest Ca2+ sensor for synaptic neurotransmitter release, from parvalbumin neurons in mi

197 ms, loss of SNAP-25 or Syb2 severely impairs neurotransmitter release; however, complete loss of func

198 1 acts as the Ca(2+) sensor for synchronous neurotransmitter release; however, the mechanism by whic

199 central nervous system or to facilitation of neurotransmitter release if expressed at presynaptic sit

200 nsorineural hearing loss and prevents normal neurotransmitter release in IHCs and colocalization of p

201 e no published studies investigating in vivo neurotransmitter release in M1 during dyskinesia.

202 ecular understanding of CaV2.1 regulation of neurotransmitter release in mammalian CNS synapses.

203 he roles of Stx1 in neuronal maintenance and neurotransmitter release in mice with constitutive or co

204 sicle docking, priming, and Ca(2+)-triggered neurotransmitter release in mouse neurons.

205 main of Cav1.4 Ca(2+) channels that regulate neurotransmitter release in photoreceptors in the retina

206 tion converted synchronous into asynchronous neurotransmitter release in projections from cerebellar

207 aseline transmission and enhance presynaptic neurotransmitter release in response to diminished posts

208 e the absence of a requirement for regulated neurotransmitter release in the assembly of early neuron

209 le of VACCs in the regulation of spontaneous neurotransmitter release (in the absence of a synchroniz

210 Acute dynamin inhibition impairs neurotransmitter release, in agreement with the protein'

211 ells a prime signaling molecule to transform neurotransmitter release into activity-dependent myelina

212 SIGNIFICANCE STATEMENT: Neurotransmitter release involves fusion of synaptic ves

213 Spontaneous neurotransmitter release is a fundamental property of sy

214 2 voltage-gated calcium channels for driving neurotransmitter release is broadly conserved.

215 IFICANCE STATEMENT In presynaptic terminals, neurotransmitter release is dynamically regulated by the

216 Neurotransmitter release is mediated by the fast, calciu

217 Neurotransmitter release is orchestrated by synaptic pro

218 stem (CNS) synapses, action potential-evoked neurotransmitter release is principally mediated by CaV2

219 Synchronous neurotransmitter release is triggered by Ca(2+) binding

220 ls that STAT3 signaling, but not fast-acting neurotransmitter release, is required for leptin action

221 nce and relapse, being the components of the neurotransmitter release machinery good candidates for t

222 ribes reconstitution assays to study how the neurotransmitter release machinery triggers Ca(2+)-depen

223 and postsynaptic compartments, organizes the neurotransmitter release machinery, and provides a frame

224 tions with synaptic vesicle proteins and the neurotransmitter release machinery, and that beta-/alpha

225 is an essential component of the presynaptic neurotransmitter release machinery.

226 Neurotransmitter release may occur either in response to

227 ation causes rapid pumping, suggesting tonic neurotransmitter release may regulate pumping.

228 Thus, defects in excitatory neurotransmitter release may represent a general and con

229 Non-regulated neurotransmitter release might be prevented by alphaSNAP

230 roperties are key for the precise control of neurotransmitter release, muscle contraction and cell ex

231 ar 200 pm oAbeta(42) concentrations increase neurotransmitter release, number of docked vesicles, pos

232 hibitory activities of alphaSNAP ensure that neurotransmitter release occurs through the highly-regul

233 a rapidly tunable substrate for potentiating neurotransmitter release over both acute and chronic tim

234 ee genes converge onto the syntaxin-mediated neurotransmitter release pathway, which was previously i

235 cross the postsynaptic membrane, rather than neurotransmitter release per se, a result consistent wit

236 active zone protein Munc13 is essential for neurotransmitter release, playing key roles in vesicle d

237 esicles that maintain spontaneous and evoked neurotransmitter release preserve their identity during

238 usly distributed Cac is highly predictive of neurotransmitter release probability at individual AZs a

239 uman leaky RyR2 mutation, R176Q (RQ), alters neurotransmitter release probability in mice and signifi

240 studies suggest that spontaneous and evoked neurotransmitter release processes are maintained by syn

241 studies suggest that spontaneous and evoked neurotransmitter release processes are maintained by syn

242 suggest that stimulus-evoked and spontaneous neurotransmitter release processes are mechanistically d

243 t glutamatergic synapses rescues the altered neurotransmitter release properties characterizing LKB1-

244 ular mechanisms whereby mitochondria control neurotransmitter release properties in a bouton-specific

245 synaptic factors that establish and modulate neurotransmitter release properties is crucial to unders

246 Neurotransmitter release properties play a key role in d

247 mitochondria at presynaptic boutons dictates neurotransmitter release properties through Mitochondria

248 ) channels confers broad capacity for tuning neurotransmitter release properties to maintain neural c

249 Despite their central role in determining neurotransmitter release properties, little is known abo

250 ividual synapses vary significantly in their neurotransmitter release properties, which underlie comp

251 amics play an important role in establishing neurotransmitter release properties.

252 spontaneous vesicle fusion and asynchronous neurotransmitter release, regulate vesicle priming, medi

253 ant of syntaxin could only minimally restore neurotransmitter release relative to Munc13-1 rescue.

254 Although synchronous neurotransmitter release relies on both P/Q- and N-type

255 isms underlying asynchronous and spontaneous neurotransmitter release remain elusive.

256 onship between neuronal impulse activity and neurotransmitter release remains elusive.

257 Neurotransmitter release requires formation of trans-SNA

258 Assembly of SNARE complexes that mediate neurotransmitter release requires opening of a 'closed'

259 Neurotransmitter release requires the formation of solub

260 function of GPCRs is to inhibit presynaptic neurotransmitter release, requiring ligand-activated rec

261 Cplx3/4 on Ca(2+)-dependent tonic and evoked neurotransmitter release, respectively, and a regulatory

262 etrograde signal(s) that control presynaptic neurotransmitter release, resulting in synaptic potentia

263 release, and rendered evoked and spontaneous neurotransmitter release sensitive to the slow Ca(2+) bu

264 both transsynaptic adhesion and presynaptic neurotransmitter release.SIGNIFICANCE STATEMENT Despite

265 ed contribution of P/Q- and N-types VGCCs to neurotransmitter release.SIGNIFICANCE STATEMENT In presy

266 chanism controlling vesicle availability and neurotransmitter release.SIGNIFICANCE STATEMENT Mechanis

267 phase alter calcium entry, which can affect neurotransmitter release significantly.

268 in the distal axon (>150 mum) and triggered neurotransmitter release similar to regular spiking.

269 unique arrangement of excitatory inputs and neurotransmitter release sites on starburst amacrine cel

270 Surprisingly, spontaneous neurotransmitter release, synaptic strength, the time co

271 k in coordination to regulate key aspects of neurotransmitter release, synaptic transmission, and syn

272 f release.SIGNIFICANCE STATEMENT Spontaneous neurotransmitter release that occurs independent of pres

273 In addition to blocking neurotransmitter release, this approach will have broad

274 xpression of dSol-1 is sufficient to enhance neurotransmitter release through a DKaiR1D-dependent mec

275 Neurons dynamically regulate neurotransmitter release through many processes known co

276 the synapse in order to continuously adjust neurotransmitter release to a level matching current mus

277 Synaptotagmin 1 (Syt1) synchronizes neurotransmitter release to action potentials (APs) acti

278 le docking and positions Syt1 to synchronize neurotransmitter release to Ca(2+) influx.

279 proteins and lipid membranes to synchronize neurotransmitter release to calcium (Ca(2+)) influx.

280 ty of presynaptic dopamine terminals to tune neurotransmitter release to meet the demands of neuronal

281 gnaling that precisely increases presynaptic neurotransmitter release to restore baseline synaptic st

282 Collectively these changes lead to sustained neurotransmitter release under conditions that would oth

283 elate devices and demonstrate measurement of neurotransmitter release upon electrical stimulation of

284 ofmeister series and the cellular process of neurotransmitter release via exocytosis and provide a be

285 ion occurs when an action potential triggers neurotransmitter release via the fusion of synaptic vesi

286 wo transgenic mouse models in which exocytic neurotransmitter release was impaired via conditional ex

287 A-mediated IPSCs, although the net effect of neurotransmitter release was to increase the firing of m

288 a genetic screen for suppressors of reduced neurotransmitter release, we identified a mutation in Ca

289 ddition, this mechanism can act to stabilize neurotransmitter release when the presynaptic resting po

290 ommunication at chemical synapses occurs via neurotransmitter release whereas electrical synapses uti

291 may be involved in activation of synchronous neurotransmitter release, whereas both conformations may

292 t beta-hydroxybutyrate causes an increase in neurotransmitter release, which is dependent upon the Tr

293 nsitivity to extracellular calcium-dependent neurotransmitter release, which leads to minimal neuromu

294 is protein, resulting in loss of synchronous neurotransmitter release with a concomitant increase in

295 1) acts as a Ca(2+) sensor that synchronizes neurotransmitter release with Ca(2+) influx during actio

296 Presynaptic boutons support neurotransmitter release with nanoscale precision at sub

297 has been a powerful approach for disrupting neurotransmitter release within defined circuitry, but t

298 luR agonists act presynaptically to increase neurotransmitter release without affecting postsynaptic

299 s spontaneous and activates Ca(2+)-triggered neurotransmitter release, yet the molecular mechanisms a

300 ive zone (AZ) are critical factors governing neurotransmitter release; yet, these fundamental synapti