Glia Engulf Degenerating Axons during Developmental Axon Pruning

Watts, Ryan J.; Schuldiner, Oren; Perrino, John; Larsen, Camilla; Luo, Liqun

doi:10.1016/j.cub.2004.03.035

Cited by 211 publications

(223 citation statements)

References 34 publications

(3 reference statements)

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“…There has been no evidence that glial cells are involved in the IPB mossy fiber pruning, but a recent in vitro time-lapse imaging shows that EphB-containing vesicles on the hippocampal neurons are pinched off by neighboring glial cells expressing Ephrin-Bs (Lauterbach and Klein 2006). These results suggest that the EphB/Ephrin-B mediated IPB pruning might be facilitated by glial cells, as has been clearly shown in the small-scale pruning in vertebrates and the pruning in Drosophila (Awasaki and Ito 2004;Bishop et al 2004;Watts et al 2004). In addition, it remains to be clarified whether semaphorin signaling involves similar downstream pathways, and how it coordinates with Ephrin-B/EphB reverse signaling to mediate the stereotyped pruning of the IPB.…”

Section: Pruning and Deathmentioning

confidence: 95%

Guidance Molecules in Axon Pruning and Cell Death

Vanderhaeghen¹,

Cheng²

2010

Cold Spring Harbor Perspectives in Biology

114

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Axon pruning and neuronal cell death constitute two major regressive events that enable the establishment of fully mature brain architecture and connectivity. Although the cellular mechanisms for these two events are thought to be distinct, recent evidence has indicated the direct involvement of axon guidance molecules, including semaphorins, netrins, and ephrins, in controlling both processes. Here, we review how axon guidance cues regulate regressive events in paradigmatic models of neural development, from early control of apoptosis of neural progenitors, to later maintenance of neuronal survival and stereotyped pruning of axonal branches. These new findings are also discussed in the context of neural diseases and the potential links between axon pruning and degeneration. REGRESSIVE EVENTS IN NEURONAL DEVELOPMENT

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Section: Pruning and Deathmentioning

confidence: 95%

Guidance Molecules in Axon Pruning and Cell Death

Vanderhaeghen¹,

Cheng²

2010

Cold Spring Harbor Perspectives in Biology

114

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“…Presumably, axon collaterals could just retract in a distal to proximal manner, whereas the axonal contents are recycled to other parts of the axon (Riley, 1981); however, no direct evidence has been shown to account for this in the vertebrate CNS. Alternatively, the axon collaterals may degenerate in a process resembling classic Wallerian degeneration (Jones and Powell, 1969;Rosenthal and Taraskevich, 1977) as was observed for stereotyped pruning in Drosophila (Watts et al, , 2004Broadie, 2004;Marin et al, 2005). At the vertebrate NMJ, however, it seems that neither retraction nor classic Wallerian degeneration was observed (Bishop et al, 2004).…”

Section: Introductionmentioning

confidence: 93%

Stereotyped Axon Pruning via Plexin Signaling Is Associated with Synaptic Complex Elimination in the Hippocampus

et al. 2005

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Plexin signaling is required for stereotyped pruning of long axon collaterals in the vertebrate CNS; however, a cellular basis for plexins on stereotyped pruning has not been determined. Using quantitative electron microscopy and immunocytochemistry, we found that infrapyramidal mossy fiber axon collaterals form transient synaptic complexes with basal dendrites of CA3 pyramidal cells in the early postnatal mouse hippocampus. At later postnatal ages, these synaptic complexes stop maturing and are removed before stereotyped pruning by a mechanism that does not involve axon degeneration and glial cell engulfment. In knock-out mice that lack plexin-A3 signaling, the synaptic complexes continue to mature, and, as a result, the collaterals are not pruned. Thus, our results suggest that intact plexin-A3 signaling contributes to synaptic complex elimination, which is associated with stereotyped axon pruning.

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“…Cite this article as Cold Spring Harb Perspect Biol 2010;2:a001925 contexts during neuronal development, including: axonal pruning (Watts et al 2004); various aspects of axon guidance (Campbell and Holt 2001;DiAntonio et al 2001;Bloom et al 2007;Lewcock et al 2007); synapse formation (DiAntonio et al 2001;Nakata et al 2005); synapse maintenance (DiAntonio et al 2001;Aravamudan and Broadie 2003;Ehlers 2003;Speese et al 2003); and synapse elimination (Ding et al 2007) (reviewed in DiAntonio and Hicke 2004). Acute treatment with the proteosome inhibitor lactacystin blocks axogenesis in dorsal root ganglion cells (Klimaschewski et al 2006).…”

Section: Initiating and Growing An Axonmentioning

confidence: 99%

Initiating and Growing an Axon

Polleux¹,

Snider²

2010

Cold Spring Harbor Perspectives in Biology

161

127

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The ability of neurons to form a single axon and multiple dendrites underlies the directional flow of information transfer in the central nervous system. Dendrites and axons are molecularly and functionally distinct domains. Dendrites integrate synaptic inputs, triggering the generation of action potentials at the level of the soma. Action potentials then propagate along the axon, which makes presynaptic contacts onto target cells. This article reviews what is known about the cellular and molecular mechanisms underlying the ability of neurons to initiate and extend a single axon during development. Remarkably, neurons can polarize to form a single axon, multiple dendrites, and later establish functional synaptic contacts in reductionist in vitro conditions. This approach became, and remains, the dominant model to study axon initiation and growth and has yielded the identification of many molecules that regulate axon formation in vitro (Dotti et al. 1988). At present, only a few of the genes identified using in vitro approaches have been shown to be required for axon initiation and outgrowth in vivo. In vitro, axon initiation and elongation are largely intrinsic properties of neurons that are established in the absence of relevant extracellular cues. However, the importance of extracellular cues to axon initiation and outgrowth in vivo is emerging as a major theme in neural development (Barnes and Polleux 2009). In this article, we focus our attention on the extracellular cues and signaling pathways required in vivo for axon initiation and axon extension.

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Glia Engulf Degenerating Axons during Developmental Axon Pruning

Cited by 211 publications

References 34 publications

Guidance Molecules in Axon Pruning and Cell Death

Guidance Molecules in Axon Pruning and Cell Death

Stereotyped Axon Pruning via Plexin Signaling Is Associated with Synaptic Complex Elimination in the Hippocampus

Initiating and Growing an Axon

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