Abstract
Synaptic signaling to NG2-expressing oligodendrocyte precursor cells (NG2 cells) could be key to rendering myelination of axons dependent on neuronal activity, but it has remained unclear whether NG2 glial cells integrate and respond to synaptic input. Here we show that NG2 cells perform linear integration of glutamatergic synaptic inputs and respond with increasing dendritic calcium elevations. Synaptic activity induces rapid Ca2+ signals mediated by low-voltage activated Ca2+ channels under strict inhibitory control of voltage-gated A-type K+ channels. Ca2+ signals can be global and originate throughout the cell. However, voltage-gated channels are also found in thin dendrites which act as compartmentalized processing units and generate local calcium transients. Taken together, the activity-dependent control of Ca2+ signals by A-type channels and the global versus local signaling domains make intracellular Ca2+ in NG2 cells a prime signaling molecule to transform neurotransmitter release into activity-dependent myelination.
Article and author information
Author details
Funding
Deutsche Forschungsgemeinschaft (SPP 1757, SFB 1089, DI853/3, INST 1172/15-1)
- Dirk Dietrich
Deutsche Forschungsgemeinschaft (SFB 1089, SCHO820/5)
- Susanne Schoch
Bundesministerium für Bildung und Forschung (01GQ0806)
- Susanne Schoch
BONFOR
- Wenjing Sun
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Animal experimentation: This study was performed in accordance with national and institutional guidelines for the care and use of laboratory animals. Every effort was made to minimize suffering.
Reviewing Editor
- Gary L Westbrook, Vollum Institute, United States
Publication history
- Received: March 23, 2016
- Accepted: September 17, 2016
- Accepted Manuscript published: September 19, 2016 (version 1)
- Version of Record published: October 5, 2016 (version 2)
Copyright
© 2016, Sun et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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