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Myelinating satellite oligodendrocytes are integrated in a glial syncytium constraining neuronal high-frequency activity. / Battefeld, Arne; Klooster, Jan; Kole, Maarten H P.

In: Nature Communications, Vol. 7, 2016, p. 11298.

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@article{f3c82d9bc8aa4350bd8fa7deb493a28c,
title = "Myelinating satellite oligodendrocytes are integrated in a glial syncytium constraining neuronal high-frequency activity",
abstract = "Satellite oligodendrocytes (s-OLs) are closely apposed to the soma of neocortical layer 5 pyramidal neurons but their properties and functional roles remain unresolved. Here we show that s-OLs form compact myelin and action potentials of the host neuron evoke precisely timed Ba(2+)-sensitive K(+) inward rectifying (Kir) currents in the s-OL. Unexpectedly, the glial K(+) inward current does not require oligodendrocytic Kir4.1. Action potential-evoked Kir currents are in part mediated by gap-junction coupling with neighbouring OLs and astrocytes that form a syncytium around the pyramidal cell body. Computational modelling predicts that glial Kir constrains the perisomatic [K(+)]o increase most importantly during high-frequency action potentials. Consistent with these predictions neurons with s-OLs showed a reduced probability for action potential burst firing during [K(+)]o elevations. These data suggest that s-OLs are integrated into a glial syncytium for the millisecond rapid K(+) uptake limiting activity-dependent [K(+)]o increase in the perisomatic neuron domain.",
author = "Arne Battefeld and Jan Klooster and Kole, {Maarten H P}",
year = "2016",
doi = "10.1038/ncomms11298",
language = "English",
volume = "7",
pages = "11298",
journal = "Nature Communications",
issn = "2041-1723",

}

RIS

TY - JOUR

T1 - Myelinating satellite oligodendrocytes are integrated in a glial syncytium constraining neuronal high-frequency activity

AU - Battefeld,Arne

AU - Klooster,Jan

AU - Kole,Maarten H P

PY - 2016

Y1 - 2016

N2 - Satellite oligodendrocytes (s-OLs) are closely apposed to the soma of neocortical layer 5 pyramidal neurons but their properties and functional roles remain unresolved. Here we show that s-OLs form compact myelin and action potentials of the host neuron evoke precisely timed Ba(2+)-sensitive K(+) inward rectifying (Kir) currents in the s-OL. Unexpectedly, the glial K(+) inward current does not require oligodendrocytic Kir4.1. Action potential-evoked Kir currents are in part mediated by gap-junction coupling with neighbouring OLs and astrocytes that form a syncytium around the pyramidal cell body. Computational modelling predicts that glial Kir constrains the perisomatic [K(+)]o increase most importantly during high-frequency action potentials. Consistent with these predictions neurons with s-OLs showed a reduced probability for action potential burst firing during [K(+)]o elevations. These data suggest that s-OLs are integrated into a glial syncytium for the millisecond rapid K(+) uptake limiting activity-dependent [K(+)]o increase in the perisomatic neuron domain.

AB - Satellite oligodendrocytes (s-OLs) are closely apposed to the soma of neocortical layer 5 pyramidal neurons but their properties and functional roles remain unresolved. Here we show that s-OLs form compact myelin and action potentials of the host neuron evoke precisely timed Ba(2+)-sensitive K(+) inward rectifying (Kir) currents in the s-OL. Unexpectedly, the glial K(+) inward current does not require oligodendrocytic Kir4.1. Action potential-evoked Kir currents are in part mediated by gap-junction coupling with neighbouring OLs and astrocytes that form a syncytium around the pyramidal cell body. Computational modelling predicts that glial Kir constrains the perisomatic [K(+)]o increase most importantly during high-frequency action potentials. Consistent with these predictions neurons with s-OLs showed a reduced probability for action potential burst firing during [K(+)]o elevations. These data suggest that s-OLs are integrated into a glial syncytium for the millisecond rapid K(+) uptake limiting activity-dependent [K(+)]o increase in the perisomatic neuron domain.

U2 - 10.1038/ncomms11298

DO - 10.1038/ncomms11298

M3 - Article

VL - 7

SP - 11298

JO - Nature Communications

T2 - Nature Communications

JF - Nature Communications

SN - 2041-1723

ER -

ID: 2104816