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Glia. 2017 Nov;65(11):1821-1832. doi: 10.1002/glia.23197. Epub 2017 Aug 10.

A specific GABAergic synapse onto oligodendrocyte precursors does not regulate cortical oligodendrogenesis.

Author information

1
Laboratory of Neurophysiology and New Microscopies, INSERM U1128, Paris, France.
2
Université Paris Descartes, Sorbonne Paris Cité, France.

Abstract

In the brain, neurons establish bona fide synapses onto oligodendrocyte precursor cells (OPCs), but the function of these neuron-glia synapses remains unresolved. A leading hypothesis suggests that these synapses regulate OPC proliferation and differentiation. However, a causal link between synaptic activity and OPC cellular dynamics is still missing. In the developing somatosensory cortex, OPCs receive a major type of synapse from GABAergic interneurons that is mediated by postsynaptic γ2-containing GABAA receptors. Here we genetically silenced these receptors in OPCs during the critical period of cortical oligodendrogenesis. We found that the inactivation of γ2-mediated synapses does not impact OPC proliferation and differentiation or the propensity of OPCs to myelinate their presynaptic interneurons. However, this inactivation causes a progressive and specific depletion of the OPC pool that lacks γ2-mediated synaptic activity without affecting the oligodendrocyte production. Our results show that, during cortical development, the γ2-mediated interneuron-to-OPC synapses do not play a role in oligodendrogenesis and suggest that these synapses finely tune OPC self-maintenance capacity. They also open the interesting possibility that a particular synaptic signaling onto OPCs plays a specific role in OPC function according to the neurotransmitter released, the identity of presynaptic neurons or the postsynaptic receptors involved.

KEYWORDS:

GABA-A receptors; myelin; oligodendrocyte precursor cells; oligodendrogenesis; somatosensory cortex; synapses

PMID:
28795438
DOI:
10.1002/glia.23197
[Indexed for MEDLINE]

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