ライフサイエンスコーパス: synapse

1 e. AMPA, NMDA, and kainate receptors) at the synapse.

2 ed plasticity at the Kenyon cell-MBONalpha'3 synapse.

3 g and exclusion of CD45 phosphatase from the synapse.

4 network that is polarized at the immunologic synapse.

5 ry but rather at the afferent-central neuron synapse.

6 urnover and maintenance of the immunological synapse.

7 amate receptors at the visual system's first synapse.

8 he majority of synaptic transmission at this synapse.

9 exclusively on the postsynaptic side of the synapse.

10 the question-the site of BDNF release at the synapse.

11 er-409 helps restrict GluK1 targeting to the synapse.

12 that safeguard cytoskeleton dynamics at the synapse.

13 d dopamine neurons from axoaxonic reciprocal synapses.

14 R-dependent insertion of GluA1 at stimulated synapses.

15 lation of GABAARs and gephyrin at inhibitory synapses.

16 networks predominantly via their perisomatic synapses.

17 etermine the fundamental properties of these synapses.

18 plasmalemma, making asymmetric and symmetric synapses.

19 oncomitant upregulation of NMDA-only, silent synapses.

20 and the mechanisms they use to interact with synapses.

21 sion at adult hippocampal temporoammonic-CA1 synapses.

22 al were associated with generation of silent synapses.

23 ependent short-term plasticity of electrical synapses.

24 at hippocampal Schaffer collateral (SC)-CA1 synapses.

25 interactions through chemical and electrical synapses.

26 in initiating plastic changes in biological synapses.

27 1 neurons without affecting their excitatory synapses.

28 of neurotransmitter release in mammalian CNS synapses.

29 ontrol transmitter release at specific brain synapses.

30 ptical microscopic resolution to study human synapses.

31 complex spikes and depressing parallel fibre synapses.

32 nveyed via a pathway involving as few as two synapses.

33 ance instructs the integrity and function of synapses.

34 R-dependent EPSP amplification at ventral SC synapses.

35 ation at hippocampal Schaffer collateral-CA1 synapses.

36 ten bidirectional interactions with neuronal synapses.

37 amatergic signalling only at olivocerebellar synapses.

38 of AMPARs during homeostatic scaling down of synapses.

39 ted to the deleterious actions of AbetaOs on synapses.

40 the postsynaptic terminal forming functional synapses.

41 e of long-term potentiation of glutamatergic synapses.

42 RIM isoform present at photoreceptor ribbon synapses.

43 clude each other during development of calyx synapses.

44 y support microscale alterations of adjacent synapses.

45 euroligin 1 (NLGN1) dominating at excitatory synapses.

46 omimetic mutant impeded GluK1 trafficking to synapses.

47 e recruitment of previously active or silent synapses.

48 sed the remaining approximately 40% of PV-IR synapses.

49 of excitatory corticostriatal glutamatergic synapses.

50 insight into compound fusion at ribbon-style synapses.

51 sed the confinement of GABAARs at inhibitory synapses.

52 correlated with functional asymmetry at the synapse [3, 4].

53 e tissue contains a high density of chemical synapses, about 1 per microm(3) in the mammalian cerebra

54 nhibitory synapses and facilitate inhibitory synapse adaptations.

55 he loss of dendritic outgrowth and number of synapses after treatment with a PERK activator, tunicamy

56 n that binds the receptors in the APC/T cell synapse and causes increased proliferation of T cells an

57 ents in nerve terminals of the neuromuscular synapse and improves the innervation of muscles.

58 m depression of parallel fiber-Purkinje cell synapse and induction of long-term plasticity (LTP) in M

59 urotransmission relies on maintenance of the synapse and meeting the energy demands of neurons.

60 48 (K48) of ubiquitin, is a key mechanism in synapse and neural circuit remodeling.

61 after granule fusion, actin recovers at the synapse and no further secretion is observed.

62 ate transmission at this first-order sensory synapse and that limiting Ca(2+) accumulation in the ter

63 and AP-evoked Ca(2+) entry were impaired at synapses and (2) AP propagation was severely compromised

64 in the ability of cerebellar neurons to form synapses and an increased number of dendritic spines tha

65 s are the main fast transduction elements at synapses and are critical for the expression of plastici

66 city are associated with Abeta localizing to synapses and binding of soluble Abeta aggregates to syna

67 ctors, support myelin production, and remove synapses and cellular debris, as well as participating i

68 eby alleviating amyloid-beta-induced loss of synapses and cognitive decline in Alzheimer's disease mi

69 ntal difference between photoreceptor ribbon synapses and conventional chemical synapses in synaptic

70 inhibition of transmission at direct pathway synapses and D1-mediated activation of motor activity.

71 Neurons communicate through chemical synapses and electrical synapses (gap junctions).

72 porter function at excitatory and inhibitory synapses and facilitate inhibitory synapse adaptations.

73 ects are associated with Abeta localizing to synapses and genetic ablation of APP prevents both Abeta

74 taneous release at excitatory and inhibitory synapses and heterogeneity of the mechanisms of release

75 ligomers are significantly more bioactive on synapses and microglia than the HMW species from which t

76 Disrupting synapses and motor maps by infusions of anisomycin (ANI)

77 t1 is weakly coexpressed at these inhibitory synapses and must be genetically inactivated together wi

78 h neuroligin 2 (NLGN2) limited to inhibitory synapses and neuroligin 1 (NLGN1) dominating at excitato

79 65) as markers of, respectively, Ia afferent synapses and presynaptic inhibition (P-boutons) on retro

80 Inner hair cells, auditory synapses and spiral ganglion neurons are all present aft

81 After nerve transection, Ia afferent synapses and stretch reflexes are permanently lost, even

82 of individual release sites in small central synapses and their activity-dependent modulation.

83 hibit distinct maturation patterns of silent synapses and thus provided instructive animal models to

84 d body to lateral superior olive glycinergic synapse, and the basket/stellate cell-Purkinje GABAergic

85 hways, lateral diffusion of proteins between synapses, and chloride transporter function at excitator

86 , enhances the formation of effective immune synapses, and improves antileukemic activity in vivo in

87 to those that induce plasticity at chemical synapses, and offer the possibility that calcium-regulat

88 center function requires mapping cell types, synapses, and peptidergic networks.

89 t Ca(2+) sensor at fast-releasing inhibitory synapses, and show that Syt1 and Syt2 can redundantly co

90 ons comprised approximately 60% of all PV-IR synapses, and Type I PV-IR synapses from putative thalam

91 SynEM removes the burden of manual synapse annotation for large densely mapped connectomes.

92 Neuronal synapses are adhesions specialized for communication and

93 precision of APs when they reach each of the synapses are fundamentally important for information pro

94 synapses supports the idea that AD-diseased synapses are intrinsically defective in LTP.

95 The formation and function of synapses are tightly orchestrated by the precise timing

96 To begin filling this gap, SNc glutamatergic synapses arising from pedunculopotine nucleus (PPN) neur

97 atergic neurotransmission is unnecessary for synapse assembly and maintenance.

98 s Abeta receptors mediating an inhibition of synapse assembly, plasticity, and learning.

99 nching of axons, as well as the formation of synapses between neurons.

100 ed and stabilized by chemical and electrical synapses between them.

101 ld standard for reliable identification of a synapse, but offers only limited molecular discriminatio

102 t loss of approximately 50% of glutamatergic synapses, but not inhibitory synapses, in culture.

103 Microglia control excitatory synapses, but their role in inhibitory neurotransmission

104 analyses to probe the architecture of ribbon synapses by perturbing the function of RIM-binding prote

105 can 4 induces formation of active excitatory synapses by recruiting AMPA glutamate receptors to the p

106 ion that the recruitment of new receptors to synapses by surface diffusion is a critical mechanism fo

107 nce and, by establishing precisely localized synapses, calibrates cognitive function.

108 However, the exact mechanism through which synapses can rapidly recruit new AMPARs during early LTP

109 exocytosis calcium sensor at inner hair cell synapses changes along the mammalian cochlea such that t

110 e levels, maintenance of striatal excitatory synapses, clearance of Htt aggregates and preserves body

111 The postsynaptic proteome of excitatory synapses comprises 1,000 highly conserved proteins that

112 ngs supporting a special role for excitatory synapses connecting pyramidal neurons of the hippocampus

113 mal in Cabp2(LacZ/LacZ) mice, as were ribbon synapse counts.

114 olved in early neuronal oxidative stress and synapse damage, ultimately leading to neurodegeneration

115 of noise, leakage of plasticity to adjacent synapses degrades the recognition of sparse static patte

116 ired recordings from adult bullfrog auditory synapses demonstrate that CP-AMPARs mediate a major comp

117 by electron microscopy termed the electrical synapse density (ESD) [5].

118 This was linked with greater axodendritic synapse density and ultrastructural characteristics of e

119 y, causes a dramatic increase or decrease in synapse density, whereas genetic deletions of neuroligin

120 acking the NTD exhibit increased mobility in synapses, depress synaptic transmission and are unable t

121 mechanism underlying hippocampal inhibitory synapse development.

122 ates in the cytoplasm in neurons to suppress synapse differentiation in vivo.

123 ces known architectural features of cortical synapse distributions.

124 s completely ineffective for most excitatory synapses due to spine electrical compartmentalization.

125 of the pathological role of Abeta and tau in synapse dysfunction, several questions remain as to how

126 nd activity refine cortical circuits through synapse elimination, but little is known about the activ

127 EPSCs and eliminated spines, indicative of a synapse elimination.

128 nce of reactive astrocytes in the tripartite synapse following TBI.

129 The energy consumption within the analogue synapses for each iteration is 1,000 x (20 x) lower comp

130 t developmental origins influence fine-scale synapse formation and microcircuit assembly of neocortic

131 relates to a coordinated inhibitory chemical synapse formation between sparsely labelled interneurons

132 neuroligins are generally not essential for synapse formation in CA1 pyramidal neurons but shape syn

133 ubiquitin-signaling network that suppresses synapse formation in the brain.

134 Despite their apparent behavioral rescue, synapse formation in these fish was significantly altere

135 Here we find that electrical synapse formation in vivo requires an intracellular scaf

136 Wnts are known regulators of synapse formation, and our data reveal that Wnt5a inhibi

137 tal alteration in dendritic arborization and synapse formation, our findings provide new insights int

138 Given the key roles of astrocytes in synapse formation, plasticity, and function, we sought t

139 roles of Celsr3 and Vangl2 in glutamatergic synapse formation.

140 uggest that they do not play a major role in synapse formation.SIGNIFICANCE STATEMENT Human neuroligi

141 ith an RNA-binding protein, FMRP, to promote synapse formation; and Top3beta gene deletion has been l

142 h raises the question of how thalamocortical synapses formed in M1 in the mouse compare with those in

143 ata reveal that Wnt5a inhibits glutamatergic synapses formed via Celsr3.

144 rst direct evidence to support the idea that synapses from AD brain are intrinsically defective in LT

145 Astrocytes depressed excitatory synapses from basolateral amygdala via A1 adenosine rece

146 In both laminar zones, Type II PV-IR synapses from interneurons comprised approximately 60% o

147 nd truth, we show that our algorithm detects synapses from muxFM data alone as successfully as human

148 we study frequency-invariant transmission at synapses from Purkinje cells to deep cerebellar nuclei a

149 60% of all PV-IR synapses, and Type I PV-IR synapses from putative thalamocortical terminals compris

150 Synapses from the dentate gyrus (DG) to the CA3 area of

151 receptor activation and enhanced inhibitory synapses from the lateral subdivision of the central amy

152 However, how OGT regulates excitatory synapse function is largely unknown.

153 rol the balance of excitatory and inhibitory synapse function remain poorly understood; no proteins t

154 reas genetic deletions of neuroligins impair synapse function with only minor effects on synapse numb

155 e in synapses numbers, but strongly impaired synapse function.

156 ate through chemical synapses and electrical synapses (gap junctions).

157 cant biological pathways related to neurons, synapses, genic intolerance, membrane transport, epileps

158 In contrast, disrupting chemical synapses has no effect on the electrical coupling.

159 Dendritic spine and synapse impairments are features of many neurological di

160 cruitment of LAT to the T-cell immunological synapse in data acquired by iPALM providing 10 nm isotr

161 in is believed to exert toxic effects at the synapse in dementia with Lewy bodies and other alpha-syn

162 the basket/stellate cell-Purkinje GABAergic synapse in the cerebellum.

163 The calyx of Held synapse in the mammalian medial nucleus of the trapezoid

164 These connections form the first synapse in the somatosensory pathway.

165 of synaptic stimulation on Tau pathology and synapses in in vivo and in vitro models of AD and fronto

166 ts that gamma-2 is associated with AMPARs at synapses in lamina II but excluded from those at C-fiber

167 ominance and reduces the density of thalamic synapses in layer 4 of the mouse primary visual cortex (

168 glutamatergic transmission, indicating that synapses in mature animals require MAGUKs for anchoring

169 to deep cerebellar nuclei and at vestibular synapses in mice.

170 We measured 6920 synapses in mouse motor and sensory cortices using three

171 the housekeeping of heavily used and strong synapses in response to the increased neuronal activity

172 or ribbon synapses and conventional chemical synapses in synaptic vesicle exocytosis.SIGNIFICANCE STA

173 At most synapses in the brain, short-term plasticity dynamically

174 imbalance between excitatory and inhibitory synapses in the cerebral cortex.

175 that CP-AMPAR-mediated maturation of silent synapses in the NAc is a signature of drug-context assoc

176 be wide ranging, holding for large and small synapses in the neocortex and brainstem.

177 es in synaptic strength at prefrontal cortex synapses in the nucleus accumbens.

178 ic plasticity in D1- versus D2-MSN GABAergic synapses in the ventral pallidum could explain the diffe

179 f glutamatergic synapses, but not inhibitory synapses, in culture.

180 e at both central and peripheral cholinergic synapses, including the neuromuscular junction.

181 s present largely in a nonaggregated form at synapses, indicating that cytosolic forms of the protein

182 ained by structural synaptic plasticity, how synapses integrate spaced stimuli and decode them into s

183 Here we demonstrate that LTD at adult TA-CA1 synapses involves JAK-STAT signaling, but unlike SC-CA1

184 f auditory and vestibular organs, the ribbon synapse is required for the precise encoding of a wide r

185 The excitatory glutamatergic synapse is the principal site of communication between c

186 PA-type glutamate receptor (AMPAR) number at synapses is a major mechanism for controlling synaptic s

187 Synaptic strength at excitatory synapses is determined by the presence of glutamate rece

188 Mapping neural circuits across defined synapses is essential for understanding brain function.

189 tic plasticity and homeostatic regulation of synapses is established to be input specific.

190 The formation of functional spine synapses is thought to be critically dependent on presyn

191 ulators may induce at neighboring non-active synapses is thought to be detrimental for the specificit

192 s, mostly of presynaptic origin and in large synapses, is upregulated already after a few hours of sl

193 zation of GABAARs and gephyrin at inhibitory synapses, leading to reductions in the efficacy of GABAe

194 Prolonged activation of these synapses leads to initial depression, which is followed

195 structural synaptic plasticity at the single-synapse level after distinct patterns of stimulation in

196 or reduces tau and APP cleavage, ameliorates synapse loss and augments long-term potentiation, result

197 nd underscore the persistent impact of MD on synapse loss in the developing visual cortex.

198 ctive for GluN2B-containing NMDARs, reverses synapse loss when applied after Tat.

199 AbetaO-induced neuronal oxidative stress and synapse loss.

200 cits when compared to control, such as: less synapses, lower dendritic arborization and reduced spine

201 The number of inhibitory synapses made by CCK(+)VGlut3(+) basket cells and the in

202 CTTNBP2 (synapse maintenance) and REEP3 (vesicle trafficking) are

203 mal models to examine the role of NAc silent synapse maturation in cocaine-conditioned place preferen

204 e novel insights into the role of Unc-104 in synapse maturation.

205 ery of neurotransmitters across the T-B-cell synapse may be advantageous in the face of infection.

206 Drugs that rescue synapses may improve neurocognitive function in HAND.SIG

207 Furthermore, the plasticity of electrical synapses may play an important role in regulation of sta

208 nderstanding how microglia respond to active synapse modification in the visual cortex.SIGNIFICANCE S

209 al. build a stacked yet flexible artificial synapse network using layer-by-layer solution processing

210 The three-dimensional artificial synapse networks enable a direct emulation of correlated

211 he conserved kinase SRPK79D to ensure normal synapse number and behavior.

212 und that neuroligin deletions did not affect synapse numbers but differentially impaired excitatory o

213 synapse function with only minor effects on synapse numbers, raising fundamental questions about the

214 s caused no change or only a small change in synapses numbers, but strongly impaired synapse function

215 m synaptic depression at hippocampal CA3-CA1 synapses (O-GlcNAc LTD).

216 tracking AMPA receptor (AMPAR) diffusion at synapses observed a large mobile extrasynaptic AMPAR poo

217 The sensorimotor synapse of Aplysia expresses different forms of long-ter

218 icant role in cortical computations, but how synapses of functionally defined cortical networks are a

219 hesion kinase (FAK) rescued SERT function in synapses of KI mice, demonstrating that constitutive act

220 These neurons project to, synapse on, and positively regulate noradrenergic neuron

221 minals, which, in turn, form inhibitory-like synapses on auditory efferent somata.

222 Remarkably, LTMRs form synapses on between four and 11 LTMR-RZ interneuron subt

223 otentiation (t-SP) of cortical glutamatergic synapses on nucleus accumbens core medium spiny neurons,

224 ural preservation after crush of Ia afferent synapses on regenerating motoneurons and decreased presy

225 and calbindin-labeled putative Renshaw cell synapses on their soma and proximal dendrites.

226 ss the hippocampal fissure to preferentially synapse onto early-born DGCs.

227 xamined the effects of CHL at auditory nerve synapses onto bushy cells in the mouse anteroventral coc

228 rganization of muscle and cutaneous afferent synapses onto immature rat lamina I spino-parabrachial n

229 neurons make functionally diverse inhibitory synapses onto principal neurons.

230 Loss of synapses or alteration of synaptic activity is associate

231 r LRP4, enabling deeper understanding of how synapse organization is coordinated.

232 hether MDGAs act selectively or suppress the synapse organizing function of multiple NLs.

233 betaOs decrease astrocyte ability to protect synapses, our results unravel a new mechanism underlying

234 g-initiated mechanisms underlying electrical synapse plasticity are similar to those that induce plas

235 hosphorylated alpha-synuclein aggregation in synapses (pre > pre + post > postsynaptic) was observed.

236 Both the synapse promoting and synapse suppressing effects of Mef

237 nd SAP102 differentially regulate excitatory synapse properties in the NAc.

238 ans-synaptic signaling network that controls synapse properties, which thereby determines the precise

239 hat alterations in PIP2 at the immunological synapse regulate cortical actin in CTLs, providing a pot

240 Thus, the mechanical properties of B cell synapses regulate antigen extraction, suggesting that di

241 ibution in axons and beta cleavage of APP at synapses remain largely unknown.

242 vity is increasingly recognized, identifying synapses remains challenging relative to the routine cha

243 s and binding of soluble Abeta aggregates to synapses requires the expression of APP.

244 volves JAK-STAT signaling, but unlike SC-CA1 synapses, requires rapid gene transcription.

245 s relieve depressive symptoms by forming new synapses resulting in increased excitatory drive.

246 reduces excitatory but increases inhibitory synapse size and strength, altering the E/I ratio in cor

247 able to function on both a highly localized, synapse-specific level and on a larger, spatial scale th

248 However, despite these defects, C9orf72 synapses still retain the ability to express presynaptic

249 eins that regulate excitatory and inhibitory synapse strength in a coordinated reciprocal manner have

250 rxs) and neuroligins (NLs) are essential for synapse structure, stability, and function, and reduced

251 The IHC ribbon synapse structure, synaptic Ca(2+) currents, and otoferl

252 ampal neurons and relate this to measures of synapse structure.

253 Our analysis of hundreds of synapses supports the idea that AD-diseased synapses are

254 Both the synapse promoting and synapse suppressing effects of Mef2c deletion required n

255 ism known for HHL is loss of inner hair cell synapses (synaptopathy).

256 lamocortical boutons typically form a single synapse, thalamocortical boutons in S1 usually formed mu

257 patient-derived placodal neurons make fewer synapses than control cells.

258 riming mechanism at the photoreceptor ribbon synapse that is independent of the formation of a RIM-Mu

259 Here, we show at the calyx synapse that synaptotagmin-7-dependent asynchronous rele

260 eurexins are recognized as key organizers of synapses that are essential for normal brain function.

261 ular profiling of the diverse populations of synapses that compose those networks.

262 novel type of plasticity at CA1 hippocampal synapses that is expressed by the activation of GluA3-co

263 Scaling was selective, sparing synapses that were large and lacked recycling endosomes.

264 ll corpse/phagocyte interactions (phagocytic synapses) that impinge on host immunity, with a main emp

265 Upon ligand-receptor binding at synapses the receptor is cleaved in its transmembrane do

266 Synapses, the fundamental unit in neuronal circuits, are

267 pike-timing-dependent plasticity (STDP) at a synapse: the connection from neuron A to neuron B is str

268 assembly of viral components at virological synapses, thereby facilitating cell-to-cell viral transm

269 n renders spike initiation more sensitive to synapse timing than dendritic location.

270 ly controlled by neuronal activity, in which synapse to nucleus signalling, mediated via NMDAR and L-

271 ed, neurons can transport RNAs to sites near synapses to locally produce proteins.

272 y information, each make multiple en passant synapses to MB output neurons (MBONs) in each compartmen

273 ls and sign-inverting chemical (glycinergic) synapses to modulate OFF cone cell bipolar terminals; th

274 macrine cell uses sign-conserving electrical synapses to modulate ON cone bipolar cell terminals and

275 ostatic, adaptive response of auditory nerve synapses to reduced activity.

276 that the capacity of presynaptic cholinergic synapses to respond to stimulation by elevating presynap

277 thereby determines the precise responses of synapses to spike patterns in a neuron and circuit and w

278 anism by which slow-wave activity might bias synapses towards weakening, while preserving the synapti

279 uller understanding of how changes at single synapses translate to an entire population of neurons.

280 Activity at synapses triggers insertion of GLUT4 into the axonal pla

281 localization precision at single hippocampal synapses under physiological conditions.

282 eviously that, at mouse photoreceptor ribbon synapses, vesicle priming is Munc13 independent.

283 ely eliminating and maintaining newly formed synapses via dendritic calcium spike-dependent mechanism

284 ninfected CD4(+) T cells through virological synapses (VS) has been found to require greater amounts

285 f a lipid probe and trapping of receptors at synapses), we show that Pc detected and localized tempor

286 previous studies at the T cell immunological synapse, we quantitatively assess the structure and dyna

287 KCC2 is highly localized to excitatory synapses where it regulates spine morphogenesis and AMPA

288 brain plasticity has tended to focus on the synapse, where well-described activity-dependent mechani

289 ynaptic transmission, or silenced excitatory synapses, whereas more prolonged (24 hr) firing depresse

290 naptic release at the first central auditory synapse, which may contribute to perceptual deficits in

291 responses by selectively regulating specific synapses, which indicates that animal behavior results f

292 rtical boutons in S1 usually formed multiple synapses, which means they can be identified with high p

293 s actin meshwork at the T cell immunological synapse, whose structure has been shown to be important

294 MCs also synapse with GABAergic interneurons that mediate feed-fo

295 the idea that bipolar cells might be able to synapse with reintroduced photoreceptors, thereby restor

296 amacrine cell also makes direct glycinergic synapses with certain RGCs, but it is not well establish

297 nges in the strength or number of excitatory synapses with MCs but was instead associated with increa

298 However, AII amacrine cells avoid making synapses with numerous RGC types that co-stratify with t

299 the stratum lacunosum-moleculare, which form synapses with presynaptic entorhinal cortex afferents.

300 lect pairs promote excitatory and inhibitory synapses, with neuroligin 2 (NLGN2) limited to inhibitor