High-Frequency Microdomain Ca2+ Transients and Waves during Early Myelin Internode Remodeling.

Arne Battefeld, Marko A. Popovic, Sharon I. de Vries, Maarten H.P. Kole
Cell Reports. 2019-01-01; 26(1): 182-191.e5
DOI: 10.1016/j.celrep.2018.12.039

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1. Cell Rep. 2019 Jan 2;26(1):182-191.e5. doi: 10.1016/j.celrep.2018.12.039.

High-Frequency Microdomain Ca2+ Transients and Waves during Early Myelin
Internode Remodeling.

Battefeld A(1), Popovic MA(2), de Vries SI(2), Kole MHP(3).

Author information:
(1)Department of Axonal Signaling, Netherlands Institute for Neuroscience, Royal
Netherlands Academy of Arts and Sciences, Meibergdreef 47, 1105 BA, Amsterdam,
the Netherlands. Electronic address: .
(2)Department of Axonal Signaling, Netherlands Institute for Neuroscience, Royal
Netherlands Academy of Arts and Sciences, Meibergdreef 47, 1105 BA, Amsterdam,
the Netherlands.
(3)Department of Axonal Signaling, Netherlands Institute for Neuroscience, Royal
Netherlands Academy of Arts and Sciences, Meibergdreef 47, 1105 BA, Amsterdam,
the Netherlands; Cell Biology, Faculty of Science, University of Utrecht,
Padualaan 8, 3584 CH, Utrecht, the Netherlands. Electronic address:
.

Ensheathment of axons by myelin is a highly complex and multi-cellular process.
Cytosolic calcium (Ca2+) changes in the myelin sheath have been implicated in
myelin synthesis, but the source of this Ca2+ and the role of neuronal activity
is not well understood. Using one-photon Ca2+ imaging, we investigated myelin
sheath formation in the mouse somatosensory cortex and found a high rate of
spontaneous microdomain Ca2+ transients and large-amplitude Ca2+ waves
propagating along the internode. The frequency of Ca2+ transients and waves
rapidly declines with maturation and reactivates during remyelination.
Unexpectedly, myelin microdomain Ca2+ transients occur independent of neuronal
action potential generation or network activity but are nearly completely
abolished when the mitochondrial permeability transition pores are blocked. These
findings are supported by the discovery of mitochondria organelles in
non-compacted myelin. Together, the results suggest that myelin microdomain Ca2+
signals are cell-autonomously driven by high activity of mitochondria during
myelin remodeling.

Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.

DOI: 10.1016/j.celrep.2018.12.039
PMCID: PMC6316190
PMID: 30605675

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