A specific GABAergic synapse onto oligodendrocyte precursors does not regulate cortical oligodendrogenesis.
Glia. 2017-08-10; 65(11): 1821-1832
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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.