• Charlotte Bertot, Laurent Groc, and Elena Avignone.
• Université de Bordeaux, Interdisciplinary Institute for Neuroscience, UMR 5297, Centre Broca Nouvelle-Aquitaine, 146 rue Léo Saignat, CS 61292 Case 130, 33076 Bordeaux Cedex, France; CNRS, Interdisciplinary Institute for Neuroscience, UMR 5297, Centre Broca Nouvelle-Aquitaine, 146 rue Léo Saignat, CS 61292 Case 130, 33076 Bordeaux Cedex, France.
• Neuroscience. 2019 May 15; 406: 186-201.

AbstractIn the developing brain, microglial cells play an important role in shaping neuronal circuits. These immune cells communicate with neurons through fractalkine (CX3CL1), a neuronal cytokine that acts on microglial CX3CR1 receptor. Among various functions, this signaling pathway has been implicated in the postnatal maturation of glutamatergic synapses. Although microglial cells are present in the neonate hippocampus when GABA receptor-mediated synaptic transmission and synchronized oscillatory events take place, it remains unknown whether microglial cells tune the establishment of these activities. Using CX3CR1-deficient mice and electrophysiological means, we investigated in CA3 pyramidal neurons the role of the fractalkine signaling in the maturation of GABAA receptor-mediated synaptic currents and giant depolarizing potentials (GDPs), a network activity important for shaping synaptic connections. In CX3CR1-deficient mice, GABAergic currents were slightly altered, whereas the developmental changes of these currents were comparable with wild-type animals. Despite these minor changes in GABAergic transmission, the GDP frequency was strikingly reduced in CX3CR1-deficient mice compared to wild-type, with no change in the GDP shape and ending period. Collectively, it emerges that, in the neonate hippocampus, the fractalkine signaling pathway tunes GDP activities and is marginally involved in the maturation of GABAergic synapses, suggesting that microglial cells have distinct impact on maturing GABAergic, glutamatergic, and network functions.Copyright © 2019 IBRO. Published by Elsevier Ltd. All rights reserved.

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