ライフサイエンスコーパス: synapse elimination

1 tnatal life is a competitive process called 'synapse elimination'.

2 nhibitor that regulates complement-dependent synapse elimination.

3 c vesicles available for fusion and increase synapse elimination.

4 synapse formation rather than an increase in synapse elimination.

5 within the spinal cord, appears to modulate synapse elimination.

6 t lysosomal activity is a central feature of synapse elimination.

7 ed motor neuron activity and delay postnatal synapse elimination.

8 dendritic branching, synapse maturation, and synapse elimination.

9 within the spinal cord, ultimately delaying synapse elimination.

10 ys earlier at P10, however, had no effect on synapse elimination.

11 tners during synaptogenesis and by selective synapse elimination.

12 developmental periods of microglial-mediated synapse elimination.

13 cise synaptic connectivity through selective synapse elimination.

14 d function, and have even been implicated in synapse elimination.

15 apses is most prominent during the period of synapse elimination.

16 ment may represent a widespread mechanism of synapse elimination.

17 uscle connectivity, and it directly promotes synapse elimination.

18 uts are strongly favoured competitors during synapse elimination.

19 otor endplates, strongly resembling neonatal synapse elimination.

20 ions at each neuromuscular junction regulate synapse elimination.

21 Synapses are lost during developmental synapse elimination.

22 ed a mathematical model of activity-mediated synapse elimination.

23 serine (PS) is a neuronal cue for microglial synapse elimination.

24 at protect synapses from complement-mediated synapse elimination.

25 pokinesia, survival, microgliosis, and brain synapse elimination.

26 re translated at specific time points during synapse elimination.

27 s potential regulators of astrocyte-mediated synapse elimination.

28 implicate the ubiquitin-proteasome system in synapse elimination.

29 C4A) gene expression are linked to excessive synapse elimination.

30 rally restricted, and transiently reversible synapse elimination.

31 by 5-HT2A receptors for experience-dependent synapse elimination.

32 atidylserine signaling to glial phagocytosis synapse elimination.

33 cient in complement C3 and C4 do not exhibit synapse elimination.

34 2A receptors is necessary and sufficient for synapse elimination.

35 would also be abnormal without C1q-mediated synapse elimination.

36 ortical activity, induces microglia-mediated synapse elimination.

37 hagocytes orchestrating experience-dependent synapse elimination.

38 rosine kinase as a key regulator of inactive synapse elimination.

39 tch that serves as a determinant of inactive synapse elimination.

40 stages and reduced afterward, suggesting DA synapse elimination.

41 synapse formation, only ERK is required for synapse elimination.

42 of target myofiber contractile properties on synapse elimination.

43 a patients, which is suggestive of increased synapse elimination.

44 and axons proposing tSCs as key effectors of synapse elimination.

45 ell as synaptic glia influence the course of synapse elimination.

46 onnections are removed in a process known as synapse elimination.

47 deficient in CX3CL1 have profound defects in synapse elimination.

48 portant structural correlates of the rate of synapse elimination.

49 stochastic model of tSC and vacancy mediated synapse elimination.

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

51 l autonomous, postsynaptic activity leads to synapse elimination.

52 on of Mdm2 as well as PSD-95 degradation and synapse elimination.

53 of motor inputs at NMJs during developmental synapse elimination.

54 crotubule stabilization delays neuromuscular synapse elimination.

55 of neuronal circuits predominantly involves synapse elimination.

56 roBDNF and mature BDNF (mBDNF) play roles in synapse elimination.

57 ts involves substantial experience-dependent synapse elimination.

58 h p75(NTR) and sortilin signaling attenuated synapse elimination.

59 t C3 is necessary for the effect of SRPX2 on synapse elimination.

60 whereas mBDNF infusion substantially delayed synapse elimination.

61 conversion of proBDNF to mBDNF may regulate synapse elimination.

62 le autism-linked genes in activity-dependent synapse elimination.

63 event MEF2-induced PSD-95 ubiquitination and synapse elimination.

64 inhibits MEF2-induced PSD-95 degradation and synapse elimination.

65 neuronal activity) contribute to the rate of synapse elimination.

66 protective role for activated CaMKII against synapse elimination.

67 c spines, suggesting a deficit in excitatory synapse elimination.

68 2 (MEF2) transcription factors induce robust synapse elimination.

69 Activity-dependent, polyneuronal synapse elimination (ADPSE) is a programmed, regressive

70 tients, inhibited postnatal retinogeniculate synapse elimination, an effect similar to the ADLTE trun

71 loping CNS synapses during periods of active synapse elimination and are required for normal brain wi

72 es, for changes in the timecourse of in vivo synapse elimination and assayed both thrombin activity a

73 s or OSN degeneration, but rather from rapid synapse elimination and axon pruning in the target olfac

74 uncover a novel facet of GABA in regulating synapse elimination and axon pruning.

75 or addressing the role of neural activity in synapse elimination and axon refinement.

76 erve as signals for increased glial-mediated synapse elimination and early loss of brain function in

77 e current limitations of studying microglial synapse elimination and evaluate evidence supporting eit

78 t H2-D(b) in K(b)D(b)(-/-) mice rescues both synapse elimination and eye-specific segregation despite

79 , presynaptic involvement in this process of synapse elimination and formation in the adult is unknow

80 ion of exogenous NMDA at the NMJ accelerates synapse elimination and increases muscle calcium levels

81 nd functions in neuronal development, normal synapse elimination and intracellular metabolism.

82 however, the molecular mechanisms directing synapse elimination and its timing remain elusive.

83 rcuit development by concurrently regulating synapse elimination and maturation of remaining contacts

84 nt role of REM sleep in experience-dependent synapse elimination and neuronal activity reduction.

85 or the interpretation of previous studies on synapse elimination and offer insight into the failure o

86 lopmental period, after the time when normal synapse elimination and pruning has occurred.

87 Synapse elimination and resulting lethality are rescued

88 Synapse elimination and strengthening are central mechan

89 s in the development of excitatory circuits, synapse elimination and strengthening are important proc

90 at miR-188-5p rescued the Abeta1-42-mediated synapse elimination and synaptic dysfunctions.

91 tion are thought to drive this developmental synapse elimination and tested as key parameters in quan

92 emphasizing that the contribution of C1q to synapse elimination appears to be dependent on context.

93 is intermuscular difference in the timing of synapse elimination appears to result from local differe

94 avoidance, self/non-self discrimination, and synapse elimination are essential for proper function of

95 echanisms that coordinate synaptogenesis and synapse elimination are poorly understood.

96 spase-3 deficiency blocks activity-dependent synapse elimination, as evidenced by reduced engulfment

97 in C3 exhibit large sustained defects in CNS synapse elimination, as shown by the failure of anatomic

98 ing postsynaptic sites during the process of synapse elimination at developing () and reinnervated ad

99 tant role for myelinating glia in regulating synapse elimination at the mouse NMJ, where loss of a si

100 to mediate neurite retraction in neurons and synapse elimination at the neuromuscular junction.

101 ficient to cause a robust delay in postnatal synapse elimination at the NMJ across all muscle groups

102 se a novel "synaptic takeover" mechanism for synapse elimination at the vertebrate NMJ, where withdra

103 asc155, suggesting that glial cells regulate synapse elimination, at least in part, through modulatio

104 variation in the timing of the developmental synapse elimination between muscles and show that the mu

105 ed axons and synaptic debris produced during synapse elimination, but also engulf unwanted synapses t

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

107 C4A promotes synapse elimination by microglia in preclinical models;

108 This can provide a potential rescue from synapse elimination by uncorrelated activity and also in

109 ivity that, in turn, modulates neuromuscular synapse elimination, by using mutant mice lacking connex

110 ippocampal neuron and microglia co-cultures, synapse elimination can be partially prevented by blocki

111 tly to maintain excitatory synapses and that synapse elimination caused by the absence of NLs and LRR

112 lization to GABAergic nuclei is required for synapse elimination, consistent with DVE-1 regulation of

113 guishing between two potential mechanisms of synapse elimination, culling and scavenging.

114 er regressive changes such as cell death and synapse elimination, decreases in cell size affect spina

115 AM10 phenocopies Cx3cr1(-/-) and Cx3cl1(-/-) synapse elimination defects.

116 icroglial activation and microglia-dependent synapse elimination dependent on neuronal secretion of h

117 Caspase-3 deficiency results in defects in synapse elimination driven by both spontaneous and exper

118 d role for a SATB family member in directing synapse elimination during circuit remodeling, likely th

119 he key role of transcriptional regulation in synapse elimination during development and reveal parall

120 tivation as a key step in activity-dependent synapse elimination during development and synapse loss

121 echanism regulating presynaptic activity and synapse elimination during development, and suggest that

122 o the lateral superior olive (LSO) undergoes synapse elimination during development.

123 The phenomenon of synapse elimination during developmental stages of the n

124 l component of nervous system development is synapse elimination during early postnatal life, a proce

125 In mice, C4 mediated synapse elimination during postnatal development.

126 in microglia demonstrated protection against synapse elimination following WNV infection and decrease

127 At the neuromuscular junction, where synapse elimination has been analysed in detail, muscle

128 This synapse elimination has been extensively studied at the

129 Synapse elimination has been extensively studied at the

130 Complement-mediated synapse elimination has emerged as an important process

131 , whether activity is strictly necessary for synapse elimination has not been resolved directly.

132 neuroglia, resulting in complement-mediated synapse elimination in AD models.

133 tein C1q, contributes to complement-mediated synapse elimination in both developmental and disease mo

134 SPARC triggers a cell-autonomous program of synapse elimination in cholinergic neurons that likely o

135 scues PSD-95 ubiquitination, degradation and synapse elimination in Fmr1 KO neurons.

136 This work reveals detailed mechanisms of synapse elimination in health and a developmental brain

137 Synaptogenesis and synapse elimination in humans appear to be heterochronou

138 enhancer factor 2 (MEF2) induces excitatory synapse elimination in mouse neurons, which requires fra

139 e absence of Wallerian degeneration resemble synapse elimination in neonatal muscle.

140 omplement overactivation mediates microglial synapse elimination in neurological diseases such as Alz

141 synapse engulfment, we demonstrate increased synapse elimination in patient-derived neural cultures a

142 s from neurons to glial phagocytes sculpting synapse elimination in response to critical period exper

143 Here, we examined the functional basis of synapse elimination in the apical dendrites of L2/3 neur

144 regulates complement activity and microglial synapse elimination in the brain and that diminished Npt

145 nction as a regulator of complement-mediated synapse elimination in the brain during development.

146 eal a novel role for astrocytes in mediating synapse elimination in the developing and adult brain, i

147 of the peripheral immune response, mediates synapse elimination in the developing CNS.

148 been shown to be required for developmental synapse elimination in the mouse visual thalamus as well

149 Synapse elimination in the newborn period in vivo is del

150 f the classical complement cascade, mediates synapse elimination in the postnatal mouse dorsolateral

151 cule H2-D(b) is necessary and sufficient for synapse elimination in the retinogeniculate system.

152 glial activation and complement C3-dependent synapse elimination in vivo.

153 ribosome-bound mRNAs in motor neurons during synapse elimination in vivo.

154 with neural metabolism increased the rate of synapse elimination in vivo.

155 h generates considerable cellular debris, is synapse elimination, in which many axonal branches are p

156 haviors evident in wild type neonates during synapse elimination, including an affinity for the posts

157 viding evidence for a novel, complement- and synapse elimination-independent role for C1q in CNS agin

158 Furthermore, the model showed that synapse elimination is accelerated by enhanced synaptic

159 In support of the idea that synapse elimination is activity dependent, it is slowed

160 aged 28, 29 and 30 days (when developmental synapse elimination is complete).

161 This synapse elimination is dependent on signaling by CX3CR1,

162 Synapse elimination is documented through light-level, u

163 We found no evidence that synapse elimination is facilitated by a lack of activity

164 culate synapse of QKI mice reveal that while synapse elimination is initially normal at P14, it is si

165 During scavenging, synapse elimination is neuronal-driven, and the neuronal

166 Thus, although synapse elimination is occurring in most EOMs and somite

167 MEF2-dependent synapse elimination is rescued in Fmr1 KO neurons by acu

168 This phenomenon, known as synapse elimination, is thought to result from competiti

169 TAT1, a substrate of JAK2, mediates inactive synapse elimination; JAK2 signaling is critical for phys

170 ination and suggest that complement-mediated synapse elimination may become aberrantly reactivated in

171 nd that Brg1 is required for dendritic spine/synapse elimination mediated by the ASD-associated trans

172 lts, or at later timepoints in regeneration, synapse elimination must also remove convergent synaptic

173 sis, including the regulation of cell death, synapse elimination, neurogenesis, and neuronal surveill

174 unwanted synapses thereby actively promoting synapse elimination non-cell autonomously.

175 in forming paranodal axo-glial junctions, as synapse elimination occurred normally in mice lacking th

176 A phase of net synapse elimination occurs late in childhood, earlier in

177 udies have yet to demonstrate how microglial synapse elimination occurs.

178 Synapse elimination offers an opportunity to understand

179 xpression normally peak during the period of synapse elimination, our findings identify axon-tethered

180 Mice lacking NF-L recapitulated the delayed synapse elimination phenotype observed in mice lacking N

181 Postnatal synapse elimination plays a critical role in sculpting a

182 elopmental mechanisms of complement-mediated synapse elimination potentially driving disease progress

183 l aspects of postnatal maturation, including synapse elimination, proceeded normally in the absence o

184 tivity has been implicated in initiating the synapse elimination process cell-autonomously, the cellu

185 We therefore conclude that the synapse elimination process is synapse-wide, removing no

186 the disassembly of synaptic sites during the synapse elimination process, we surveyed the distributio

187 Axon pruning and synapse elimination promote neural connectivity and syna

188 activity-dependent and activity-independent synapse elimination provide insights into mechanisms und

189 ctivity imposed upon the two nerves promotes synapse elimination, provided that their relative spikes

190 In developing muscle, synapse elimination reduces the number of motor axons th

191 protect synapses against complement-mediated synapse elimination remains unknown.

192 ssion, a proposed physiological correlate of synapse elimination, requires caspase-3 and the mitochon

193 This process helps to mediate synapse elimination, requires the MEGF10 and MERTK phago

194 O) mice would exhibit defects in neocortical synapse elimination resulting in enhanced excitatory syn

195 rring in the motor neuron translatome during synapse elimination, revealing rapid and dynamic respons

196 between this process and naturally occurring synapse elimination suggest that short-lived target deri

197 t of ganglion cell axon loss and retino-dLGN synapse elimination, suggesting that, in the primate, ey

198 postnatal life occurs through the process of synapse elimination: Supernumerary axon inputs are gradu

199 tnatal life, neuromuscular junctions undergo synapse elimination that is modulated by patterns of mot

200 pporting Schwann cells during the process of synapse elimination that occurs after reinnervation.

201 l that microglia expressing TWEAK facilitate synapse elimination through a novel, non-phagocytic mech

202 ociate with excitatory synapses resulting in synapse elimination through a process that requires NMDA

203 ergoing lamina-specific arbor retraction and synapse elimination to arrive at their mature, restricte

204 c conversion of proBDNF to mBDNF accelerated synapse elimination via activation of p75 neurotrophin r

205 neurons drives cell-autonomous, compensatory synapse elimination via CaMKIV-dependent transcription.

206 ular recording showed that the neuromuscular synapse elimination was accelerated in muscles from Cx40

207 The disruption of synapse elimination was associated with a delay in synap

208 her CSMD1 is involved in complement-mediated synapse elimination, we examined Csmd1-knockout mice and

209 The model reliably reproduced synapse elimination whereas equal or random probability

210 We observed that exogenous proBDNF promoted synapse elimination, whereas mBDNF infusion substantiall

211 ly (by 8 days postnatally) in the process of synapse elimination (which is complete by 20 days postna

212 ile brain, critical period experience drives synapse elimination, which is transiently reversible.

213 loss of Schwann cell processes from sites of synapse elimination, with a time course similar to that