Throughout the brain, astrocytes form networks mediated by gap junction channels that promote the activity of neuronal ensembles. Although their inputs on neuronal information processing are well established, how molecular gap junction channels shape neuronal network patterns remains unclear. Here, using astroglial connexin-deficient mice, in which astrocytes are disconnected and neuronal bursting patterns are abnormal, we show that astrocyte networks strengthen bursting activity via dynamic regulation of extracellular potassium levels, independently of glutamate homeostasis or metabolic support. Using a facilitation-depression model, we identify neuronal afterhyperpolarization as the key parameter underlying bursting pattern regulation by extracellular potassium in mice with disconnected astrocytes. We confirm this prediction experimentally and reveal that astroglial network control of extracellular potassium sustains neuronal afterhyperpolarization via KCNQ voltage-gated K+ channels. Altogether, these data delineate how astroglial gap junctions mechanistically strengthen neuronal population bursts and point to approaches for controlling aberrant activity in neurological diseases.

Department of Cellular Neurophysiology Institute of Experimental Medicine Czech Academy of Sciences Prague Czech Republic

ED386 Ecole Doctorale de Sciences Mathématiques Paris Centre Paris France

Faculty of Medicine Charles University Prague Czech Republic

Group of Data Modeling and Computational Biology Institute of Biology Ecole Normale Superieure CNRS INSERM Université PSL Paris France

Neuroglial Interactions in Cerebral Physiology and Pathologies Center for Interdisciplinary Research in Biology Collège de France CNRS INSERM Labex Memolife Université PSL Paris France

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