Microglial cells are the resident immune cells of the brain. They have mainly been studied under pathological conditions and their functions under physiological conditions are beginning to be understood. In particular, it is now well established that in healthy brain microglia continuously scan the parenchyma and make contacts with synapses and cell bodies of neurons. Recent evidence indicates that the formation and duration of these contacts are regulated by neuronal activity and that these contacts modulate the physiology of neurons. However, the mechanisms governing these neuron-microglia interactions are still far from fully understood, in part due to the difficulty of studying these interactions in real time.The main objective of my thesis was to fill this gap by combining electrophysiological recordings of neuronal activity and calcium imaging of the microglia to dissect the mechanisms governing the real-time response of the microglia to changes in neuronal activity.Using cre / lox technology, we generated Cx3cr1-CreERT2::Pol2ra-GCaMP5-dtTomato mice that express the genetic encoding calcium indicator GCaMP5 with tdTomato specifically in microglia. I first validated the use of this model to study microglial calcium signaling in hippocampal slices. I then induced epileptiform activity pharmacologically and observed an increase in calcium signaling in microglia which consisted of spikes in intracellular calcium at the cell body level, synchronized with bursts of action potentials. These synchronized calcium responses in microglia were due to the release of calcium from intracellular stores and depended on purinergic signaling as they were inhibited by degradation of extracellular ATP / ADP with apyrase and by inhibiting P2Y12 receptors. Purinergic signaling in astrocytes was also enhanced by epileptiform activity, modulated the frequency of neuronal action potential bursts, but did not interfere with synchronized calcium signals in microglia. Finally, my results also showed that the blockade of P2Y12 receptors, and therefore calcium signals in microglia, induced an increase in neuronal activity upon initiation of epileptiform activity.My data reveal a new form of calcium signaling in microglia and demonstrate that microglia respond in real time to increased neuronal activity. They further highlight the importance of purinergic signaling in neuron-microglia interactions. Future studies will be necessary to understand the consequences of this calcium signaling on the functional phenotype of these immune cells.