In Vivo regulation of Oligodendrocyte processor cell proliferation and differentiation by the AMPA-receptor Subunit GluA2

T. Chen, B. Kula, B. Nagy, R. Barzan, A. Gall, I. Ehrlich, M. Kukley, Cell Reports 25 (2018) 852–861.e7.

Download
OA 4.46 MB

Journal Article | Published | English
Author
; ; ; ; ; ;
Department
Abstract
The functional role of AMPA receptor (AMPAR)-mediated synaptic signaling between neurons and oligodendrocyte precursor cells (OPCs) remains enigmatic. We modified the properties of AMPARs at axon-OPC synapses in the mouse corpus callosum in vivo during the peak of myelination by targeting the GluA2 subunit. Expression of the unedited (Ca2+ permeable) or the pore-dead GluA2 subunit of AMPARs triggered proliferation of OPCs and reduced their differentiation into oligodendrocytes. Expression of the cytoplasmic C-terminal (GluA2(813-862)) of the GluA2 subunit (C-tail), a modification designed to affect the interaction between GluA2 and AMPAR-binding proteins and to perturb trafficking of GluA2-containing AMPARs, decreased the differentiation of OPCs without affecting their proliferation. These findings suggest that ionotropic and non-ionotropic properties of AMPARs in OPCs, as well as specific aspects of AMPAR-mediated signaling at axon-OPC synapses in the mouse corpus callosum, are important for balancing the response of OPCs to proliferation and differentiation cues. In the brain, oligodendrocyte precursor cells (OPCs) receive glutamatergic AMPA-receptor-mediated synaptic input from neurons. Chen et al. show that modifying AMPA-receptor properties at axon-OPC synapses alters proliferation and differentiation of OPCs. This expands the traditional view of synaptic transmission by suggesting neurons also use synapses to modulate behavior of glia.
Publishing Year
Date Published
2018-10-23
Journal Title
Cell Reports
Acknowledgement
This work was supported by Deutsche Forschungsgemeinschaft (DFG) grant KU2569/1-1 (to M.K.); DFG project EXC307Centre for Integrative Neuroscience (CIN), including grant Pool Project 2011-12 (jointly to M.K. and I.E.); and the Charitable Hertie Foundation (to I.E.). CIN is an Excellence Cluster funded by the DFG within the framework of the Excellence Initiative for 2008–2018. M.K. is supported by the Tistou & Charlotte Kerstan Foundation.
Volume
25
Issue
4
Page
852 - 861.e7
IST-REx-ID

Cite this

Chen T, Kula B, Nagy B, et al. In Vivo regulation of Oligodendrocyte processor cell proliferation and differentiation by the AMPA-receptor Subunit GluA2. Cell Reports. 2018;25(4):852-861.e7. doi:10.1016/j.celrep.2018.09.066
Chen, T., Kula, B., Nagy, B., Barzan, R., Gall, A., Ehrlich, I., & Kukley, M. (2018). In Vivo regulation of Oligodendrocyte processor cell proliferation and differentiation by the AMPA-receptor Subunit GluA2. Cell Reports, 25(4), 852–861.e7. https://doi.org/10.1016/j.celrep.2018.09.066
Chen, Ting, Bartosz Kula, Balint Nagy, Ruxandra Barzan, Andrea Gall, Ingrid Ehrlich, and Maria Kukley. “In Vivo Regulation of Oligodendrocyte Processor Cell Proliferation and Differentiation by the AMPA-Receptor Subunit GluA2.” Cell Reports 25, no. 4 (2018): 852–861.e7. https://doi.org/10.1016/j.celrep.2018.09.066.
T. Chen et al., “In Vivo regulation of Oligodendrocyte processor cell proliferation and differentiation by the AMPA-receptor Subunit GluA2,” Cell Reports, vol. 25, no. 4, p. 852–861.e7, 2018.
Chen T, Kula B, Nagy B, Barzan R, Gall A, Ehrlich I, Kukley M. 2018. In Vivo regulation of Oligodendrocyte processor cell proliferation and differentiation by the AMPA-receptor Subunit GluA2. Cell Reports. 25(4), 852–861.e7.
Chen, Ting, et al. “In Vivo Regulation of Oligodendrocyte Processor Cell Proliferation and Differentiation by the AMPA-Receptor Subunit GluA2.” Cell Reports, vol. 25, no. 4, Elsevier, 2018, p. 852–861.e7, doi:10.1016/j.celrep.2018.09.066.
All files available under the following license(s):
Creative Commons License:
CC-BY-NC-NDCreative Commons Attribution-NonCommercial-NoDerivs (CC BY-NC-ND 4.0)
Main File(s)
File Name
Access Level
OA Open Access
Last Uploaded
2018-12-17T12:42:57Z


Export

Marked Publications

Open Data IST Research Explorer

Search this title in

Google Scholar