Alzheimer’s disease (AD) is characterized by a long asymptomatic phase associated with the toxic accumulation of oligomeric form of amyloid-beta peptide (Aβo). One of the first event reported in this phase seems to be a specific hippocampal hyperactivity in both humans and AD mouse model. We highlighted that this early hyperactivity starts with an abnormal increase of calcium activity in astrocytes which affects neighbouring neurons in the hippocampus. We identified an astrocytic calcium channel, transient receptor potential ankyrin-1 (TRPA1), implicated in the Aβo-induced hippocampal hyperactivity. A preclinical assay has been performed in an AD transgenic mouse model showing that a daily pharmacological treatment blocking TRPA1 activation avoids the onset of hippocampal hyperactivity and preserves the structural and functional synaptic integrity during asymptomatic phase, which is enough to prevent mnesic decline. In that context, my objective is to better understand the role of the Aβo-dependent TRPA1 activation in the disruption of neuron-astrocyte interplay. Electrophysiological techniques combined with western-blot and immunofluorescence techniques revealed an increased gliotransmission involving glutamate and D-serine, and a disturbance in the astrocytic glutamate reuptake. These data provide a better understanding of the critical involvement of neuron-astrocyte interplay at the onset of Alzheimer's disease, and how the early destabilized hippocampal network is responsible for creating a pathological vicious circle.