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 EPSCs and eliminated spines, indicative of a synapse elimination.

3 otor endplates, strongly resembling neonatal synapse elimination.

4 ions at each neuromuscular junction regulate synapse elimination.

5 Synapses are lost during developmental synapse elimination.

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

7 crotubule stabilization delays neuromuscular synapse elimination.

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

9 ts involves substantial experience-dependent synapse elimination.

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

11 whereas mBDNF infusion substantially delayed synapse elimination.

12 conversion of proBDNF to mBDNF may regulate synapse elimination.

13 l autonomous, postsynaptic activity leads to synapse elimination.

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

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

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

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

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

19 protective role for activated CaMKII against synapse elimination.

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

21 2 (MEF2) transcription factors induce robust synapse elimination.

22 c vesicles available for fusion and increase synapse elimination.

23 synapse formation rather than an increase in synapse elimination.

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

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

26 ed motor neuron activity and delay postnatal synapse elimination.

27 dendritic branching, synapse maturation, and synapse elimination.

28 within the spinal cord, ultimately delaying synapse elimination.

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

30 tners during synaptogenesis and by selective synapse elimination.

31 cise synaptic connectivity through selective synapse elimination.

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

33 of motor inputs at NMJs during developmental synapse elimination.

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

35 ment may represent a widespread mechanism of synapse elimination.

36 uscle connectivity, and it directly promotes synapse elimination.

37 uts are strongly favoured competitors during synapse elimination.

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

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

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

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

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

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

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

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

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

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

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

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

50 Synapse elimination and resulting lethality are rescued

51 Synapse elimination and strengthening are central mechan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

75 This synapse elimination has been extensively studied at the

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

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

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

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

80 Synaptogenesis and synapse elimination in humans appear to be heterochronou

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

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

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

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

85 Synapse elimination in the newborn period in vivo is del

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

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

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

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

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

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

92 Synapse elimination is documented through light-level, u

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

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

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

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

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

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

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

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

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

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

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

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

105 Postnatal synapse elimination plays a critical role in sculpting a

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

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

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

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

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

111 Axon pruning and synapse elimination promote neural connectivity and syna

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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