ライフサイエンスコーパス: nerve terminal

1 y and compared them to the mechanisms in the nerve terminal.

2 t anterograde, transport in the axon and the nerve terminal.

3 -endocytic sorting steps likely occur in the nerve terminal.

4 ing anterograde DCV transport in the axon or nerve terminal.

5 ynaptic release sites within the presynaptic nerve terminal.

6 results in approximately 10(6) free ATPs per nerve terminal.

7 naptic action potential (AP) waveform at the nerve terminal.

8 nly) complex, as might be found in a central nerve terminal.

9 to cannabinoid type 1 receptors on the motor nerve terminal.

10 ocytosis at the active zone of a presynaptic nerve terminal.

11 central nervous system and Drosophila motor nerve terminal.

12 s (DCVs) as they circulate in and out of the nerve terminal.

13 minode and in regulating excitability of the nerve terminal.

14 egulates the presynaptic excitability of the nerve terminal.

15 minode and in regulating excitability of the nerve terminal.

16 s such as TMEM16a in GPCR-activation of itch nerve terminals.

17 oxins (BoNTs) possess unique specificity for nerve terminals.

18 S) contained the densest accumulation of MCH nerve terminals.

19 interacting with polarity-specific afferent nerve terminals.

20 ich inhibit neurotransmission at cholinergic nerve terminals.

21 exocytic machinery component SNAP25 in motor nerve terminals.

22 of synaptic vesicles and degeneration of the nerve terminals.

23 of continuous NET uptake and release at the nerve terminals.

24 degeneration and regeneration of peripheral nerve terminals.

25 of tubulovesicular structures at presynaptic nerve terminals.

26 y transient Ca(2+) elevations in presynaptic nerve terminals.

27 at develop progressive degeneration of motor nerve terminals.

28 ly represents specific uptake in sympathetic nerve terminals.

29 ransmitter release at human peripheral motor nerve terminals.

30 ght (NF-L) protein in distal axons and motor nerve terminals.

31 studies to quantify presynaptic cholinergic nerve terminals.

32 regulator of SV replenishment in presynaptic nerve terminals.

33 vestibular hair cells to postsynaptic calyx nerve terminals.

34 orrelates directly with the levels of Htt at nerve terminals.

35 ated protein 25 (SNAP-25) within presynaptic nerve terminals.

36 d an endocytic deficit specific to aminergic nerve terminals.

37 enhance glutamate release at cerebrocortical nerve terminals.

38 during high-frequency stimulation in central nerve terminals.

39 o a role in vesicle-related processes within nerve terminals.

40 ing showed that both proteins are present at nerve terminals.

41 encodes a probable vesicular transporter in nerve terminals.

42 through non-Orai mechanisms but is absent at nerve terminals.

43 n of action potentials (APs) in auditory CNS nerve terminals.

44 e action potential (AP)-driven exocytosis at nerve terminals.

45 tic transmission and the normal structure of nerve terminals.

46 al activity and pH regulation in presynaptic nerve terminals.

47 KR and its physiological modulation in small nerve terminals.

48 as a sign of acute activation of nociceptive nerve terminals.

49 ial cells decipher the strength of competing nerve terminals.

50 ges the proportion of presynaptically silent nerve terminals.

51 still formed in the absence of glutamatergic nerve terminals.

52 s level is modulated by neuronal activity in nerve terminals.

53 roteolytic conversion of proBDNF to mBDNF at nerve terminals.

54 tion sites, S76 and T181, of syndapin I from nerve terminals.

55 e differentiation and stabilization of motor nerve terminals.

56 monstrate that RyR1 plays a role in VICaR in nerve terminals.

57 cytosis) to efficiently retrieve membrane at nerve terminals.

58 and presynaptic Ca(2+) transients at single nerve terminals.

59 d protection from cytotoxicity in live mouse nerve terminals.

60 during high intensity stimulation in central nerve terminals.

61 and active zone components from the soma to nerve terminals.

62 he proper biogenesis of synaptic vesicles at nerve terminals.

63 DI and CDF, which has not been determined in nerve terminals.

64 sitization of ryanodine channels in afferent nerve terminals.

65 , vesicles are retrieved and recycled within nerve terminals.

66 t these TRCs may have synaptic contacts with nerve terminals.

67 e rate of transmitter uptake at serotonergic nerve terminals.

68 y regulator of synaptic vesicle recycling at nerve terminals.

69 e-induced action potential discharge in itch nerve terminals.

70 ation of BoNT/C1 ad with diaphragmatic motor nerve terminals.

71 re and are characterized by poorly arborized nerve terminals.

72 deficits in transporter export to axons and nerve terminals.

73 ynaptic myofiber surface and phagocytosis of nerve terminals.

74 ivity-driven Ca(2+) influx and exocytosis at nerve terminals.

75 on activity-dependent Ca(2+) entry into the nerve terminal, a behaviorally important neuromodulator

76 ited Ca(2+)syntillas (scintilla, spark, in a nerve terminal, a SYNaptic structure) in WT, but not in

77 n, the influx of Ca(2+) into the presynaptic nerve terminal activates a Ca(2+) sensor for vesicle fus

78 in triggering the regeneration of peripheral nerve terminals affected by other forms of neurodegenera

79 nent of glutamate release in cerebrocortical nerve terminals after blocking Na(+) channels with tetro

80 The increase in FDG6P in nerve terminals agreed well with the increase in cortica

81 pathogenic role remains unclear, in healthy nerve terminals alpha-synuclein undergoes a cycle of mem

82 In normal nerve terminals, alpha-synuclein is present in an equili

83 raction were similar for axosomatic auditory nerve terminals, although rostral auditory nerve termina

84 icle, we review the role of synuclein at the nerve terminal and in membrane remodeling.

85 ovides for reliable transmission between the nerve terminal and muscle fiber.

86 d pathway stabilizes AZ specification at the nerve terminal and that such a novel function is indepen

87 ects the synaptic strength of each competing nerve terminal and the state of synaptic competition.

88 assoon staining showed a punctate pattern in nerve terminals and axons at the nascent NMJ on embryoni

89 rial function, mitochondria supplying ATP to nerve terminals and boosting synaptic and cognitive func

90 Q-induced action potential discharge at itch nerve terminals and bouts of scratching by about 50%.

91 rimarily on their highly specific binding to nerve terminals and cleavage of SNARE proteins.

92 M) are closely associated with enteric motor nerve terminals and electrically coupled to smooth muscl

93 and functional bridges between enteric motor nerve terminals and gastrointestinal smooth muscle cells

94 Parkinson's disease, is distributed both at nerve terminals and in the cell nucleus.

95 o reduction in the density of SV proteins in nerve terminals and increased synaptic fatigue under hig

96 nin gene-related peptide (CGRP) from sensory nerve terminals and insulin from isolated pancreatic isl

97 e mutant form of SYT1 correctly localizes to nerve terminals and is expressed at levels that are appr

98 ted calcium channels localize to presynaptic nerve terminals and mediate key events including synapto

99 an vesicles just being exocytosed, occurs at nerve terminals and non-neuronal secretory cells.

100 lomeruli, releasing GABA and DA onto sensory nerve terminals and postsynaptic neurons.

101 abeled neuronal proteins were transported to nerve terminals and secreted, and then appeared in CSF.

102 rds a relationship between its generation at nerve terminals and structural synaptic pathology.

103 ave shown that silencing is achieved both at nerve terminals and the soma and is independent of membr

104 Immune cells at peripheral nerve terminals and within the spinal cord release media

105 s critical for targeting mitochondria to the nerve terminal, and a disruption in mitochondrial fissio

106 ) RyR1 plays a role in VICaR in hypothalamic nerve terminals; and (ii) a neuronal alteration accompan

107 ogenous, nonvesicular glycine/GABA levels in nerve terminals are 5-7 mm, and that vesicular transport

108 Presynaptic nerve terminals are formed from preassembled vesicles th

109 -dependent mechanisms.SIGNIFICANCE STATEMENT Nerve terminals are highly specialized regions of a neur

110 We found that a fraction of nerve terminals are kept in a presynaptically silent sta

111 insic bioenergetic capacities of presynaptic nerve terminals are maintained in these symptomatic AD m

112 pinephrine released locally from sympathetic nerve terminals are significantly increased in the acute

113 ol, as well as on SV distribution within the nerve terminal, are virtually abolished in mouse SynI kn

114 to sustain cellular function and identifies nerve terminals as critical sites of proper metabolic co

115 cal defects were largely restricted to motor nerve terminals, as the ultrastructure of motoneuron som

116 ism for axons to independently functionalize nerve terminals at great distances from cellular somata.

117 the Drosophila brain, LRP4 localizes to the nerve terminals at or near active zones.

118 ecific effects were found on the presynaptic nerve terminals at the neuromuscular junction level, but

119 raction-induced injury occurs at or near the nerve terminal axon.

120 beta-catenin specifically in muscles, motor nerve terminals became extensively defasciculated and ar

121 ted endocytosis and synaptic transmission at nerve terminals, but its potential role in synaptic deve

122 otoxicity has been characterized in cochlear nerve terminals, but much less is known about whether ex

123 for localizing presynaptic Ca(2+) influx to nerve terminals, but the role of the second mechanism re

124 to profoundly impact information transfer at nerve terminals by controlling both vesicle priming and

125 SR), a G-protein-coupled receptor present in nerve terminals, by several specific agonists increased

126 eveal new mechanisms by which neuroendocrine nerve terminal Ca(2+) can be controlled in the brain.

127 rsts last seconds; however, the increases in nerve terminal Ca(2+) driven by neuropeptides can persis

128 e both capable of evoking large increases in nerve terminal Ca(2+) Increases in Ca(2+) driven by spik

129 xert powerful and long-lasting regulation of nerve terminal Ca(2+) independently from actions at the

130 ing in brain slices from mice to address how nerve terminal Ca(2+) is controlled in gonadotropin-rele

131 es, in particular when different presynaptic nerve terminals compete for the control of the same syna

132 ential-triggered Ca(2+) influx in inhibitory nerve terminals, consistent with the deficits in synapti

133 SCs phagocytose nerve terminals contacting the muscle fiber.

134 cles in gamma-aminobutyric acid (GABA)-ergic nerve terminals contain labeling for both VGLUT3 and the

135 Nerve terminals contain multiple sites specialized for t

136 y nerve terminals, although rostral auditory nerve terminals contained a greater concentration of syn

137 (tens of seconds) endocytosis in calyx-type nerve terminals containing conventional active zones and

138 ing that glutamate is enriched in inhibitory nerve terminals containing VGLUT3 compared to those lack

139 We determined the resting pH of the nerve terminal cytosol to be 7.30 +/- 0.02, and observed

140 ted dopaminergic neuronal loss, dopaminergic nerve terminal damage and behavioral deficits caused by

141 red to be normal at the stages when synaptic nerve terminals degenerated.

142 ular and molecular mechanisms of presynaptic nerve terminal degeneration.

143 ments leads to elevated BMP signaling within nerve terminals, driving excessive synaptic growth.

144 Thus, remodeling of the nerve terminal during the period of target absence does

145 calcium (Ca(2+)) accumulating in presynaptic nerve terminals during repetitive action potentials.

146 hydrolase that degrades 2-AG in presynaptic nerve terminals-elevates 2-AG levels and suppresses the

147 rate, which is actively transported into the nerve terminal, eliciting vesicular depletion and revers

148 We show that neurotrophin stimulation of nerve terminals elicits new bclw transcripts that are im

149 ason we examined the timing of supernumerary nerve terminal elimination at synapses in extraocular mu

150 ng presynaptic Ca(2+) rises and increases in nerve terminal excitability.

151 We have previously shown that nerve terminals exposed to spider or snake presynaptic n

152 ynaptic vesicles (SVs) from live hippocampal nerve terminals expressing vesicle-associated membrane p

153 Thus, it appears that the chorda tympani nerve terminal field defaults to its early postnatal fie

154 when the nerves were cut, the chorda tympani nerve terminal field expanded to a volume four times lar

155 red peripheral axons, and the chorda tympani nerve terminal field organization in the nucleus of the

156 tent reduction of the labeled chorda tympani nerve terminal field volume and density in the NTS follo

157 se surprising results suggest that gustatory nerve terminal fields remain plastic well into adulthood

158 rda tympani and greater superficial petrosal nerve terminal fields were 1.4x and 1.6x larger than age

159 ns that rely on hyperactivity of cholinergic nerve terminals for 25 years.

160 organizes the differentiation of excitatory nerve terminals formed onto them.

161 The nerve terminals found in the body wall of Drosophila mel

162 during elimination: their processes separate nerve terminals from each other and from the muscle fibe

163 dings suggest a more severe loss of striatal nerve terminal function compared with neuronal cell bodi

164 ion of subcellular components of sympathetic nerve terminal function does not occur simultaneously.

165 Thus, GnRH nerve terminal function is controlled over disparate tim

166 gy efficiency can be viewed as one aspect of nerve terminal function, in balance with others, because

167 ed, immediate rescue of deficits in dopamine nerve-terminal function in animals with a history of hig

168 ular mechanisms of catecholamine handling in nerve terminals has not been investigated.

169 and Protein-kinase C (PKC) signaling in the nerve terminal have been widely implicated in the short-

170 rried by the vagus nerve, and vagal afferent nerve terminals have been well defined in animals.

171 these metabolic responses in mitochondria in nerve terminals have not been determined.

172 known neuronal metabolites, were compared in nerve terminals, homogenate, and cortex of anesthetized

173 We report, for the first time, a nerve terminal impairment in SV trafficking selectively

174 dependence of exocytosis on Ca(2+) entry at nerve terminals implies that voltage control of both Ca(

175 igated the excitability of the calyx of Held nerve terminal in dysmyelinated auditory brainstems usin

176 estion using the calyx of Held (CH), a large nerve terminal in the auditory brainstem in mice.

177 Using the calyx of Held, a giant nerve terminal in the mouse brainstem, we evaluated the

178 Relaxin-3 colocalized with synaptophysin in nerve terminals in all septal areas, and ultrastructural

179 Hence, we investigated isolated nerve terminals in brain slices by transecting hippocamp

180 s of metabolism in excitatory and inhibitory nerve terminals in mammalian systems.

181 in (aS) is a protein abundant in presynaptic nerve terminals in Parkinson disease (PD) and is a major

182 to the cytosol and function, for example, in nerve terminals in short-term synaptic plasticity.

183 3 receptors, increased glutamate release at nerve terminals in some LHb neurons.

184 tonin and norepinephrine, respectively, into nerve terminals in the brain.

185 Methamphetamine damages monoamine-containing nerve terminals in the brains of both animals and human

186 P2X2 -IR identifies probable vagal nerve terminals in the central (Ce) subnucleus in the in

187 These findings demonstrate that nerve terminals in the corneal epithelium of mice and gu

188 explore the structure and neurochemistry of nerve terminals in the corneal epithelium of mice and gu

189 s released from synaptic vesicles of certain nerve terminals in the hippocampus during neuronal activ

190 marker for dopamine production, in GABAergic nerve terminals in the median eminence suggested that ra

191 absence of tyrosine hydroxylase in GABAergic nerve terminals in the median eminence suggests that onl

192 to presynaptic gamma-aminobutyric acidergic nerve terminals in the NAcSh originating from the dorsal

193 ia, increase in tyrosine hydroxylase in both nerve terminals in the SAT and sympathetic ganglia neuro

194 other GPCRs) leads to activation of the itch nerve terminals in the skin, but previous studies have f

195 nt in synaptic vesicles in acetylcholinergic nerve terminals in the striatum.

196 The degeneration of nerve terminals in Ub(G76V)-GFP-Syb2 mice was preceded b

197 in clinical development for mapping cardiac nerve terminals in vivo using PET.

198 Nerve terminals in which dynamin 1 and 3 have been repla

199 euronal activity when ATP consumption within nerve terminals increases drastically.

200 Voltage-gated Ca(2+) channels in presynaptic nerve terminals initiate neurotransmitter release in res

201 specially prominent for cholinergic C-bouton nerve terminal input onto motor neurons in affected C1q-

202 output processes: olfactory receptor neuron nerve terminals (input) and mitral/tufted cell apical de

203 anes with high endocytic activity, including nerve terminals involved in neurotransmitter recycling,

204 ents show that the buffering capacity of the nerve terminal is markedly lower for Sr(2+) than for Ca(

205 ervous system development, axon branching at nerve terminals is an essential step in the formation of

206 lation of acetylcholine receptors (AChRs) at nerve terminals is critical for signal transmission at t

207 The control of neurotransmitter release at nerve terminals is of profound importance for neurologic

208 numerous neurological diseases, its role at nerve terminals is poorly understood.

209 at direct uptake and oxidation of glucose in nerve terminals is substantial under resting and activat

210 gest that the overshoot pool exists at every nerve terminal, is of limited size arising from vesicles

211 the uptake and phosphorylation of glucose in nerve terminals isolated from rats infused with the gluc

212 esynaptic proteins in resting and stimulated nerve terminals isolated from the brains of Wistar rats.

213 iated primary neurons, we show that at small nerve terminals K(+) channels constrain the peak voltage

214 equency stimulation (HFS) of the presynaptic nerve terminal leads to a PcTx1-sensitive increase in in

215 Abnormal accumulation of Abeta at nerve terminals leads to synaptic pathology and ultimate

216 at many terminals, including the calyx-type nerve terminal, led to a well accepted "principle" that

217 ow and rapid forms of vesicle endocytosis at nerve terminals, likely by functioning downstream of Ca(

218 The remaining two mutants displayed a nerve terminal localization but did not support efficien

219 %, respectively; (2) after correcting for DA nerve terminal loss, DA uptake per VMAT2 transport site

220 ns can perturb either axonal arborization or nerve terminal maturation, depending on the stage of del

221 Nerve terminals may use all available vesicles to maximi

222 nsidered that rapid AGAb uptake at the motor nerve terminal membrane might attenuate complement-media

223 clearance of anti-ganglioside antibodies by nerve terminals might also be of sufficient magnitude to

224 peroxidation, we investigated the effect of nerve terminal mitochondrial dysfunction on airway senso

225 TMEM184b is necessary for normal peripheral nerve terminal morphology and maintenance.

226 e being enveloped in a single large afferent nerve terminal, named the calyx, and by the expression o

227 increases the rate of exocytosis in isolated nerve terminals, neuromuscular junctions, neuroendocrine

228 Degeneration of motor nerve terminals occurs in amyotrophic lateral sclerosis

229 leus, as well as to additional expression in nerve terminals of cortical projections to RA from the l

230 we have performed live Ca(2+) imaging in the nerve terminals of gonadotropin-releasing hormone neuron

231 ELKS is required for normal Ca(2+) influx at nerve terminals of inhibitory hippocampal neurons.

232 component of the clearance occurred at motor nerve terminals of neuromuscular junctions, from where a

233 cord, especially in motor neurons and motor nerve terminals of the neuromuscular junction (NMJ), whe

234 ed in neurons, such as motoneurons and motor nerve terminals of the neuromuscular junction (NMJ).

235 al accumulation of intermediate filaments in nerve terminals of the neuromuscular synapse and improve

236 Consistent with previous reports, olfactory nerve terminals onto both cell types had a high release

237 ferent subunit combinations can be placed on nerve terminals or soma/dendrites in the ventral tegment

238 ransmitter concentrations inside presynaptic nerve terminals, or the dynamics of vesicle refilling af

239 sine hydroxylase-immunolabeled (sympathetic) nerve terminals originating from the superior cervical g

240 s ranged in distribution from 3 to 111 motor nerve terminals per unit.

241 m the activation of MLCK, based on increased nerve terminal phospho-MLC immunostaining, with 100 Hz b

242 a tripartite synapse that is formed by motor nerve terminals, postjunctional muscle membranes, and te

243 hat resulting protein inactivation disrupted nerve terminal processes and impaired neurotransmission.

244 ce that during action potential (AP) firing, nerve terminals rely on the glucose transporter GLUT4 as

245 neurotrophins affect synapses, particularly nerve terminals, remains unclear.

246 clear presence of the protein in inhibitory nerve terminals revealed by immunohistochemistry.

247 s of a tripartite synapse with a presynaptic nerve terminal, Schwann cells that ensheathe the termina

248 cytosis kinetics at hippocampal and cortical nerve terminals show a bi-phasic dependence on electrica

249 ich are expressed at a majority of mammalian nerve terminals, show two types of Ca2+-dependent feedba

250 mportant function for TMEM184b in peripheral nerve terminal structure, function, and the axon degener

251 Synaptophysin and sybII form a complex in nerve terminals, suggesting this interaction may have a

252 Localization to the nerve terminal suggests a role in neurotransmitter relea

253 cate that alpha-SYN, present in dopaminergic nerve terminals supplying the subependymal zone, acts as

254 n's vast number of synapses, the presynaptic nerve terminal, synaptic cleft, and postsynaptic special

255 In a presynaptic nerve terminal, synaptic strength is determined by the p

256 In a nerve terminal, synaptic vesicle docking and release are

257 In a presynaptic nerve terminal, synaptic vesicle exocytosis is restricte

258 bles of cortical and hippocampal presynaptic nerve terminals (synaptosomes) from commonly used mouse

259 tripartite motor synapse consisting of motor nerve terminal, terminal Schwann cells (tSCs) and postsy

260 The calyx of Held is a giant nerve terminal that forms a glutamatergic synapse in the

261 n in this study reveals defects in the motor nerve terminal that may compensate for the muscle hypere

262 synaptogenesis at the calyx of Held, a large nerve terminal that selectively innervates the cell body

263 clearance mechanisms are present in central nerve terminals that regulate intracellular free calcium

264 ase neuropeptides and neurotransmitters from nerve terminals that regulate vascular, innate, and adap

265 addressed this apparent conflict at a large nerve terminal, the calyx of Held in rat brainstem, in w

266 depolarization at a large mammalian central nerve terminal, the rat calyx of Held, we report for the

267 As BoNTs act in the cytosol of nerve terminals, the entry into an appropriate compartme

268 t neuroblastoma cell line and isolated mouse nerve terminals, the N-terminal beta-amyloid fragment pr

269 yperexcitability near axon branch points and nerve terminals, thereby leading to uncontrolled movemen

270 ral neuropathy, such as depletion of sensory nerve terminals, thermal hypoalgesia, and nerve conducti

271 cryptin, promotes the assembly of inhibitory nerve terminals through integrin receptors.

272 What causes a motor nerve terminal to degenerate remains unknown.

273 indicate that pathogenic Htt acts locally at nerve terminals to alter trafficking between endosomal c

274 e that pathogenic Htt can act locally within nerve terminals to disrupt synaptic endosomal signaling

275 Complexin functions at presynaptic nerve terminals to inhibit spontaneous SNARE-mediated sy

276 We show that SCs in mice lead nerve terminals to prepatterned AChRs.

277 At inhibitory nerve terminals, up- or downregulation of VAMP4 causes a

278 stem in structural plasticity of presynaptic nerve terminals using an in vitro model of classical con

279 functional properties of ion channels at the nerve terminals, using electrophysiology, dynamic Na(+)

280 Neuronal transmitters are released from nerve terminals via the fusion of synaptic vesicles with

281 tabotropic glutamate receptors on inhibitory nerve terminals was attenuated, allowing modulation of G

282 The percentage of primary auditory nerve terminals was larger in caudal AVCN, whereas non-p

283 ence or presence of transmitter glutamate in nerve terminals, we developed a new method to count func

284 Three morphologies for these nerve terminals were identified.

285 Properties of presumed optic nerve terminals were investigated in the optic tectum us

286 is is unlikely to be due to an effect at the nerve terminals, where chloride channels may play a more

287 s, neurites, axons, and dendrites but not at nerve terminals, where peptidergic neurotransmission occ

288 ion of potassium ion channels at presynaptic nerve terminals, where they modulate excitability and th

289 rogressive adult-onset degeneration of motor nerve terminals, whereas GFP-Syb2 and Ub(G76V)-GFP-Synta

290 Es suggests a sorting/degradation pathway in nerve terminals wherein the role of AEs is similar to th

291 cularly at the last axon heminode before the nerve terminal, which regulates the presynaptic excitabi

292 We tested this in calyx of Held nerve terminals, which allow simultaneous recording of p

293 ry transduction in cutaneous primary sensory nerve terminals, which converts thermal stimuli into dep

294 LC3-positive autophagosomes generated in the nerve terminals, which then underwent retrograde transpo

295 ddressed this issue at the rat calyx of Held nerve terminal with capacitance measurements.

296 23)I-MIBG demonstrated stable storage at the nerve terminal with resistance to a NET inhibitor chase,

297 phology and neurochemistry, and suggest that nerve terminals with different sensory modalities can be

298 GRP- and IB4-immunoreactive primary afferent nerve terminals without noticeable expression on glial c

299 tress in the microenvironment of cholinergic nerve terminals would diminish cholinergic transmission

300 number of available vesicles for release and nerve terminals would have to distinguish the recycling