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Norepinephrine regulates calcium signals and fate of oligodendrocyte precursor cells in the mouse cerebral cortex

Oligodendrocyte precursor cells (OPCs) generate oligodendrocytes, contributing to myelination and myelin repair. OPCs contact axons and respond to neuronal activity, but how the information relayed by the neuronal activity translates into OPC Ca2+ signals, which in turn influence their fate, remains...

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Bibliographische Detailangaben
Hauptverfasser: Fiore, Frédéric (VerfasserIn) , Alhalaseh, Khaleel (VerfasserIn) , Dereddi, Ram (VerfasserIn) , Torres, Felipe Bodaleo (VerfasserIn) , Coban, Ilknur (VerfasserIn) , Harb, Ali (VerfasserIn) , Agarwal, Amit (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 08 December 2023
In: Nature Communications
Year: 2023, Jahrgang: 14, Pages: 1-25
ISSN:2041-1723
DOI:10.1038/s41467-023-43920-w
Online-Zugang:Verlag, kostenfrei, Volltext: https://doi.org/10.1038/s41467-023-43920-w
Verlag, kostenfrei, Volltext: https://www.nature.com/articles/s41467-023-43920-w
Volltext
Verfasserangaben:Frederic Fiore, Khaleel Alhalaseh, Ram R. Dereddi, Felipe Bodaleo Torres, Ilknur Çoban, Ali Harb & Amit Agarwal
Beschreibung
Zusammenfassung:Oligodendrocyte precursor cells (OPCs) generate oligodendrocytes, contributing to myelination and myelin repair. OPCs contact axons and respond to neuronal activity, but how the information relayed by the neuronal activity translates into OPC Ca2+ signals, which in turn influence their fate, remains unknown. We generated transgenic mice for concomitant monitoring of OPCs Ca2+ signals and cell fate using 2-photon microscopy in the somatosensory cortex of awake-behaving mice. Ca2+ signals in OPCs mainly occur within processes and confine to Ca2+ microdomains. A subpopulation of OPCs enhances Ca2+ transients while mice engaged in exploratory locomotion. We found that OPCs responsive to locomotion preferentially differentiate into oligodendrocytes, and locomotion-non-responsive OPCs divide. Norepinephrine mediates locomotion-evoked Ca2+ increases in OPCs by activating α1 adrenergic receptors, and chemogenetic activation of OPCs or noradrenergic neurons promotes OPC differentiation. Hence, we uncovered that for fate decisions OPCs integrate Ca2+ signals, and norepinephrine is a potent regulator of OPC fate.
Beschreibung:Gesehen am 21.02.2024
Beschreibung:Online Resource
ISSN:2041-1723
DOI:10.1038/s41467-023-43920-w

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