Publisher Correction: Oligodendrocyte precursor cells engulf synapses during circuit remodeling in mice

Auguste, Yohan S. S.; Ferro, Austin; Kahng, Jessica A.; Xavier, André Machado; Dixon, Jessica R.; Vrudhula, Uma; Nichitiu, Anne-Sarah; Rosado, Daniele; Wee, Tse-Luen; Pedmale, Ullas V.; Cheadle, Lucas

doi:10.1038/s41593-022-01209-z

Cited by 8 publications

(5 citation statements)

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“…Interestingly, removal of OPCs during activity-dependent circuit refinement (7 days post-fertilization) resulted in ectopic RGC neurites and altered visual processing ( Xiao et al, 2022 ). A similar role was then described for OPCs in pruning synapses in the developing mouse visual system ( Auguste et al, 2022b ). Thus, OPCs mediate experience-dependent circuit remodeling in development ( Figure 1D ).…”

Section: Glia As Mediators Of Critical Period Plasticity Viasupporting

confidence: 52%

Glial regulation of critical period plasticity

Starkey,

Horstick,

Ackerman

2023

Front. Cell. Neurosci.

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Animal behavior, from simple to complex, is dependent on the faithful wiring of neurons into functional neural circuits. Neural circuits undergo dramatic experience-dependent remodeling during brief developmental windows called critical periods. Environmental experience during critical periods of plasticity produces sustained changes to circuit function and behavior. Precocious critical period closure is linked to autism spectrum disorders, whereas extended synaptic remodeling is thought to underlie circuit dysfunction in schizophrenia. Thus, resolving the mechanisms that instruct critical period timing is important to our understanding of neurodevelopmental disorders. Control of critical period timing is modulated by neuron-intrinsic cues, yet recent data suggest that some determinants are derived from neighboring glial cells (astrocytes, microglia, and oligodendrocytes). As glia make up 50% of the human brain, understanding how these diverse cells communicate with neurons and with each other to sculpt neural plasticity, especially during specialized critical periods, is essential to our fundamental understanding of circuit development and maintenance.

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Section: Glia As Mediators Of Critical Period Plasticity Viasupporting

confidence: 52%

Glial regulation of critical period plasticity

Starkey,

Horstick,

Ackerman

2023

Front. Cell. Neurosci.

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“…OPCs are the only glial cell type that receives neuronal synapses, which activity was shown to modulate their proliferation, differentiation, and migration and is important for myelination and remyelination (for review, see Moura et al 2022 [25] and Habermacher, Angulo and Benamer 2019 [26]). Recently, OPCs have been shown to phagocytose synapses in the developing and mature mouse visual cortex thus contributing to remodelling of neural circuitries [27]. OPCs are extremely plastic and adapt their program in response to a multitude of signals both in physiological and pathological conditions [28].…”

Section: More Than Oligodendrocyte Progenitor Cellsmentioning

confidence: 99%

“…In agreement with the idea that, upon injury, OPC roles go beyond the generation of new myelinating cells, recent studies have shown that OPCs per se participate in tissue remodelling and healing. Although OPCs were shown to contribute to synapse and axon pruning during normal development, they were also shown to selectively internalize myelin debris through phagocytosis upon injury [27,54,64,65]. Moreover, in the acute phase after brain injury, OPCs release metalloproteinases (e.g., MMP9) which in turn promote blood-brain barrier (BBB) leakage and infiltration of blood-derived cells at lesion site [66].…”

Section: Oligodendroglial Cells Responses To Injurymentioning

confidence: 99%

Oligodendrocyte Progenitors in Glial Scar: A Bet on Remyelination

Marangon,

Castro e Silva,

Cerrato

et al. 2024

Preprint

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Oligodendrocyte progenitor cells (OPCs) represent a subtype of glia giving rise to oligodendrocytes, the myelin forming cells in the central nervous system (CNS). While OPCs are highly proliferating during development, they become relatively quiescent during adulthood, when their fate is strictly influenced by the extracellular context. In traumatic injuries and chronic neurodegenerative conditions including those of autoimmune origin, oligodendrocytes undergo apoptosis, and demyelination starts. Adult OPCs become immediately activated, they migrate at the lesion site and proliferate to replenish the damaged area, but their efficiency is hampered by the presence of a glial scar, a barrier mainly formed by reactive astrocytes, microglia, and the deposition of inhibitory extracellular matrix components. If, on one hand, glial scar limits the lesion spreading, it also blocks tissue regeneration. Therapeutic strategies aimed at reducing astrocyte or microglia activation and shifting them toward a neuroprotective phenotype have been proposed, whereas the role of OPCs has been largely overlooked. In this review, we have considered glial scar from the perspective of OPCs, analysing their behaviour when lesions originate and exploring the potential therapies aimed at sustaining OPCs to efficiently differentiate and promote remyelination.

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“…OPCs are the only glial cell type that receives neuronal synapses, whose activity was shown to modulate their proliferation, differentiation and migration and is important for myelination and remyelination (for review, see [ 30 , 31 ]). Recently, OPCs have been shown to phagocytose synapses in the developing and mature mouse visual cortex, thus contributing to the remodelling of neural circuitries [ 32 ]. These data highlight that OPCs are extremely plastic and adapt their program in response to a multitude of physiological signals [ 33 ].…”

Section: More Than Oligodendrocyte Progenitor Cellsmentioning

confidence: 99%

“…In agreement with the idea that, upon injury, OPC roles go beyond the generation of new myelinating cells, recent studies have shown that OPCs per se participate in tissue remodelling and healing. Although OPCs were shown to contribute to synapse and axon pruning during normal development, they were also shown to selectively internalise myelin debris through phagocytosis upon injury [ 32 , 59 , 71 , 72 ]. Moreover, in the acute phase of white matter injury upon prolonged cerebral hypoperfusion, metalloproteinases (e.g., MMP9) released specifically by OPCs promote blood–brain barrier (BBB) leakage and infiltration of blood-derived cells at the lesion site [ 73 ].…”

Section: Oligodendroglial Cell Responses To Injurymentioning

confidence: 99%

Oligodendrocyte Progenitors in Glial Scar: A Bet on Remyelination

Marangon,

Castro e Silva,

Cerrato

et al. 2024

Cells

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Oligodendrocyte progenitor cells (OPCs) represent a subtype of glia, giving rise to oligodendrocytes, the myelin-forming cells in the central nervous system (CNS). While OPCs are highly proliferative during development, they become relatively quiescent during adulthood, when their fate is strictly influenced by the extracellular context. In traumatic injuries and chronic neurodegenerative conditions, including those of autoimmune origin, oligodendrocytes undergo apoptosis, and demyelination starts. Adult OPCs become immediately activated; they migrate at the lesion site and proliferate to replenish the damaged area, but their efficiency is hampered by the presence of a glial scar—a barrier mainly formed by reactive astrocytes, microglia and the deposition of inhibitory extracellular matrix components. If, on the one hand, a glial scar limits the lesion spreading, it also blocks tissue regeneration. Therapeutic strategies aimed at reducing astrocyte or microglia activation and shifting them toward a neuroprotective phenotype have been proposed, whereas the role of OPCs has been largely overlooked. In this review, we have considered the glial scar from the perspective of OPCs, analysing their behaviour when lesions originate and exploring the potential therapies aimed at sustaining OPCs to efficiently differentiate and promote remyelination.

show abstract

Publisher Correction: Oligodendrocyte precursor cells engulf synapses during circuit remodeling in mice

Cited by 8 publications

References 0 publications

Glial regulation of critical period plasticity

Glial regulation of critical period plasticity

Oligodendrocyte Progenitors in Glial Scar: A Bet on Remyelination

Oligodendrocyte Progenitors in Glial Scar: A Bet on Remyelination

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