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

1 including protein and hormone secretion and neurotransmitter release.

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

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

4 tion of nearby synapses to further stimulate neurotransmitter release.

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

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

7 chain expression, which prevented vesicular neurotransmitter release.

8 rough local estrogen synthesis or inhibitory neurotransmitter release.

9 nent of the exocytic machinery that controls neurotransmitter release.

10 ulates Glutamate receptor A1 trafficking and neurotransmitter release.

11 ction potential initiation, propagation, and neurotransmitter release.

12 h regulation of cell firing and heterologous neurotransmitter release.

13 ical functions including membrane fusion and neurotransmitter release.

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

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

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

17 s contraction rate and timing through phasic neurotransmitter release.

18 soforms to phosphorylate targets and enhance neurotransmitter release.

19 h subsequent action potential evokes greater neurotransmitter release.

20 l function to regulate neuronal survival and neurotransmitter release.

21 on presynaptic neuron terminals to modulate neurotransmitter release.

22 brane of presynaptic terminals, facilitating neurotransmitter release.

23 d in neurons, the chimera slowed the rate of neurotransmitter release.

24 ion to function as a clamp on SNARE-mediated neurotransmitter release.

25 e expression and trafficking, and modulating neurotransmitter release.

26 ectional, homeostatic control of presynaptic neurotransmitter release.

27 quantify the spatio-temporal fluctuations of neurotransmitter release.

28 enger, which ultimately enhances presynaptic neurotransmitter release.

29 wnstream Ca(2+) -dependent processes such as neurotransmitter release.

30 r genetically induced changes in spontaneous neurotransmitter release.

31 to be involved in the modulation of synaptic neurotransmitter release.

32 ork sheds light on fundamental mechanisms of neurotransmitter release.

33 function as Ca(2+) sensors for asynchronous neurotransmitter release.

34 It has roles in both SV trafficking and neurotransmitter release.

35 ion pathway that enhances axon outgrowth and neurotransmitter release.

36 eurons, which was found to cause a defect in neurotransmitter release.

37 d RIM2, localizes to synapses, and modulates neurotransmitter release.

38 aberrant calcium homeostasis, and imbalanced neurotransmitter release.

39 s underlying the homeostatic potentiation of neurotransmitter release.

40 Syt-1, which is regulated by Wnts, modulates neurotransmitter release.

41 lize to the endocytic periactive zone during neurotransmitter release.

42 oupling, decreases the reliability of evoked neurotransmitter release.

43 vesicle fusion with the plasma membrane and neurotransmitter release.

44 l synaptic protein with a regulatory role in neurotransmitter release.

45 in, to return to the pool of vesicles during neurotransmitter release.

46 (Syt1) is a major Ca(2+)-sensor that evokes neurotransmitter release.

47 tials (APs), and in some cases the extent of neurotransmitter release.

48 modulation of presynaptic calcium influx and neurotransmitter release.

49 play activating and inhibitory functions in neurotransmitter release.

50 e presynaptic plasma membrane and subsequent neurotransmitter release.

51 ng and recycling, and consequently attenuate neurotransmitter release.

52 entials trigger synchronous and asynchronous neurotransmitter release.

53 ing insulin secretion, GLUT4 exocytosis, and neurotransmitter release.

54 the regulation of neuronal functions such as neurotransmitter release.

55 n implicated in asynchronous and spontaneous neurotransmitter release.

56 , stabilizing AP repolarization and limiting neurotransmitter release.

57 rine cells and involved in the regulation of neurotransmitter release.

58 increases derived from GlyT2 activity after neurotransmitter release.

59 (SV) exocytosis, while enhancing stimulated neurotransmitter release.

60 mbrane, accounting for the fast component of neurotransmitter release.

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

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

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

64 channel clusters for reliable and modifiable neurotransmitter release.

65 ut affecting normal fluctuations of synaptic neurotransmitter release.

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

67 ncluding axonal elongation and branching and neurotransmitter release.

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

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

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

71 synaptic plasticity consistent with enhanced neurotransmitter release.

72 ial widening that could account for enhanced neurotransmitter release.

73 cleave SNARE proteins nor impair spontaneous neurotransmitter release.

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

75 and proposed a potential role in regulating neurotransmitter release.

76 rpotentials did not alter calcium current or neurotransmitter release.

77 awn mutants harbor a significant increase in neurotransmitter release.

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

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

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

81 membranes, which could potentially regulate neurotransmitter release.

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

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

84 aptic vesicle exocytosis and thereby enhance neurotransmitter release?

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

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

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

88 atially and temporally resolved detection of neurotransmitter release across a single pheochromocytom

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

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

91 We show that Futsch regulates neurotransmitter release and active zone density.

92 endent functions in neuronal maintenance and neurotransmitter release and complete SNARE complex form

93 ty was associated with an increased level of neurotransmitter release and dependent on intrinsic glia

94 f PRRT2 protein may lead to altered synaptic neurotransmitter release and dysregulated neuronal excit

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

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

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

98 d throughout the nervous system and regulate neurotransmitter release and hence synaptic transmission

99 plasma membrane undergo rapid fusion during neurotransmitter release and how this process is spatial

100 tudies demonstrate that Wnt signalling tunes neurotransmitter release and identify Syt-1 as a target

101 They facilitate presynaptic neurotransmitter release and modulate mechanisms control

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

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

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

105 lcium with strontium to promote asynchronous neurotransmitter release and produce quantal events.

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

107 M-BPs decelerated action-potential-triggered neurotransmitter release and rendered it unreliable, the

108 mbly mediates synaptic vesicle fusion during neurotransmitter release and requires that the target-SN

109 ptic boutons, calcium (Ca(2+)) triggers both neurotransmitter release and short-term synaptic plastic

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

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

112 ls (LGICs) have long been proposed to affect neurotransmitter release and to tune the neural circuit

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

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

115 twork output usually results from changes in neurotransmitter release and/or membrane conductance.

116 nd thus contribute to neuronal excitability, neurotransmitter release, and calcium-induced gene regul

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

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

119 allergic reactions, gastric acid secretion, neurotransmitter release, and inflammation.

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

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

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

123 es, aberrant calcium homeostasis, imbalanced neurotransmitter release, and ultimately with neuronal d

124 elded crucial insights into the mechanism of neurotransmitter release, and working models for the fun

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

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

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

128 Unravelling principles underlying neurotransmitter release are key to understand neural si

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

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

131 er and highlight the key role of spontaneous neurotransmitter release as a mediator of functional and

132 rine synapses, RIM-BPs are not essential for neurotransmitter release as such, but are selectively re

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

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

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

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

137 on of alpha-neurexins dramatically decreased neurotransmitter release at excitatory synapses in cultu

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

139 ings indicate that Synaptotagmin 2 regulates neurotransmitter release at human peripheral motor nerve

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

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

142 one (CAZ) controls the strength and speed of neurotransmitter release at synapses in response to acti

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

144 f release-ready synaptic vesicles to support neurotransmitter release at synapses.

145 highly potent bacterial proteins that block neurotransmitter release at the neuromuscular junction b

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

147 Fast synchronous neurotransmitter release at the presynaptic active zone

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

149 ulate vesicle fusion, a required process for neurotransmitter release at the synapse.

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

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

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

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

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

155 la, deletion of RIM-BPs dramatically reduces neurotransmitter release, but little is known about RIM-

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

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

158 Ca(2+) triggers fast synchronous neurotransmitter release by binding to synaptotagmin-1,

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

160 ports calcium domain cooperativity and tunes neurotransmitter release by equalizing Pr for docked SVs

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

162 2+) sensor synaptotagmin-1 (syt-1) regulates neurotransmitter release by interacting with anionic pho

163 In calcium, synaptotagmin-1 triggers neurotransmitter release by interacting with membranes.

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

165 Controlling neurotransmitter release by modulating the presynaptic c

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

167 tely 30% and decrease spontaneous and evoked neurotransmitter release by nearly 50%.

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

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

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

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

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

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

174 Facilitation can enhance neurotransmitter release considerably and can profoundly

175 l endpoint: voxel-level temporal patterns of neurotransmitter release ("DA movies") in individual sub

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

177 Neurotransmitter release depends on the SNARE complex fo

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

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

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

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

182 HT neuron firing through 5-HT autoreceptors, neurotransmitter release, enzymatic degradation, and reu

183 es glial activation, cytokine production and neurotransmitter release following brain injury.

184 hows that miR-8 is important for spontaneous neurotransmitter release frequency and quantal content.

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

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

187 eport the development of a method to measure neurotransmitter release from exocytosis events at indiv

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

189 al source of Ca(2+) ions that trigger evoked neurotransmitter release from presynaptic boutons.

190 y to axons and enhances axonal outgrowth and neurotransmitter release from presynaptic terminals.

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

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

193 rsal motor nucleus neurones and dysregulates neurotransmitter release from synaptic inputs and that t

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

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

196 ting muscle excitation-contraction coupling, neurotransmitter release, gene expression, and hormone s

197 ncluding the influx of extracellular Ca(2+), neurotransmitter release, gene transcription, and synapt

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

199 ins have central roles in evoked synchronous neurotransmitter release; however, it is unknown how the

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

201 ozygous NRXN1 mutations selectively impaired neurotransmitter release in human neurons without changi

202 ial STXBP1 loss of function robustly impairs neurotransmitter release in human neurons, and suggest t

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

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

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

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

207 st that it is essential for Ca(2+)-triggered neurotransmitter release in mouse hippocampal neuronal s

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

209 -synuclein (alphaS) is a protein involved in neurotransmitter release in presynaptic terminals, and w

210 The SNARE complex mediates neurotransmitter release in response to presynaptic Ca(2

211 The probabilistic nature of neurotransmitter release in synapses is believed to be o

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

213 genes encoding synaptic proteins involved in neurotransmitter release in the mPFC.

214 , supporting a role for H2S in Ca(2+)-evoked neurotransmitter release in these cells.

215 Glutamate is the fast excitatory neurotransmitter released in the NTS by vagal afferents,

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

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

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

219 SIGNIFICANCE STATEMENT: Neurotransmitter release involves fusion of synaptic ves

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

221 Neurotransmitter release is mediated by the fast, calciu

222 Neurotransmitter release is orchestrated by synaptic pro

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

224 lthough the importance of a SNARE complex in neurotransmitter release is widely accepted, there exist

225 lved in the regulation of SV trafficking and neurotransmitter release, is one of the presynaptic subs

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

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

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

229 ase, likely through the interaction with the neurotransmitter release machinery.

230 apsins are key components of the presynaptic neurotransmitter release machinery.

231 mains of Ca(V)2.2 known to interact with the neurotransmitter release machinery.

232 fect that completely reversed the deficit in neurotransmitter release magnitude at LEMS model NMJs.

233 Neurotransmitter release may occur either in response to

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

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

236 al trigger for cellular processes, including neurotransmitter release, muscle contraction, and gene e

237 toneurons results from a high probability of neurotransmitter release onto multiple postsynaptic cont

238 fective as a result of a high probability of neurotransmitter release onto multiple release sites and

239 y 11; however, a compensatory enhancement of neurotransmitter release onto these neurons maintains no

240 for fundamental synaptic operations, such as neurotransmitter release or postsynaptic AMPAR insertion

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

242 many release sites (N), high probability of neurotransmitter release (Pr), and large quantal size (Q

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

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

245 apses as a function of stimulus strength and neurotransmitter release probability, which, together wi

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

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

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

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

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

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

252 mitochondria at presynaptic boutons dictates neurotransmitter release properties through Mitochondria

253 eostasis plays a critical role in specifying neurotransmitter release properties, but the mechanisms

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

255 rongly inhibit spontaneous as well as evoked neurotransmitter release, providing genetic evidence for

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

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

258 isms underlying asynchronous and spontaneous neurotransmitter release remain elusive.

259 Neurotransmitter release requires the formation of solub

260 Ultrafast neurotransmitter release requires tight colocalization o

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

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

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

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

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

269 register with the corresponding presynaptic neurotransmitter release sites.

270 alcium-binding protein, which is involved in neurotransmitter release, sorting, and exocytosis.

271 stinct roles for GIT1 and GIT2 in regulating neurotransmitter release strength, with GIT1 as a specif

272 haker mutations cause a dramatic increase in neurotransmitter release, suggesting that Shaker is pred

273 ound heterozygotes of these alleles impaired neurotransmitter release, synapse morphology, and homeos

274 r proteins critical for proper glutamatergic neurotransmitter release, synaptic transmission, and sho

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

276 on the homeostatic modulation of presynaptic neurotransmitter release, termed presynaptic homeostasis

277 e and novel mechanism by which SYT regulates neurotransmitter release: The ring acts as a spacer to p

278 ignaling affect neuronal firing patterns and neurotransmitter release, this is an unreported cellular

279 heral nervous system and is known to inhibit neurotransmitter release through inhibition of the forma

280 Neurons dynamically regulate neurotransmitter release through many processes known co

281 oteins that are indispensable in controlling neurotransmitter release through SNARE and synaptic vesi

282 ongly influencing rhythmicity and triggering neurotransmitter release throughout the central nervous

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

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

285 of SV pool sizes serves to adapt presynaptic neurotransmitter release to chronic silencing of network

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

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

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

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

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

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

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

293 s have slightly stimulatory or no effects on neurotransmitter release, whereas a poor-clamp mutant in

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

295 has a key role in regulating the process of neurotransmitter release, which is associated with the m

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

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

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

299 t roles in the control of synaptogenesis and neurotransmitter release, yet their regulation is poorly

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