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. 2019 Mar 5;7:24. doi: 10.3389/fcell.2019.00024

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Copyright © 2019 Rodríguez-Iglesias, Sierra and Valero.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Hypothetical mechanisms of microglial regulation of functional maturation of synapses of newborn GCs. (A) Microglia may secrete BDNF, which upregulates the expression of the cotransporter KCC2 in newborn GCs, and increases their inhibitory sensitivity to GABA. (B) Microglia derived TNF-α may increase synaptic efficacy by increasing the AMPA/NMDA ratio. (C) Microglial BDNF may contribute to the enhanced synaptic plasticity of newborn GCs by raising the proportion of GluN2B subunit in NMDA receptors. (D) Microglia secreted BDNF may increase glutamatergic transmission by upregulating the expression of vGlut1 in presynaptic vesicles. BDNF, brain derived neurotrophic factor; Cl, chloride; GC, granule cell; K, potassium; TNF-α, tumor necrosis factor-α; vGlut1, vesicular glutamate transporter 1.