Among the brain structures affected in Schizophrenia is the hippocampus. In addition to structural changes [1], dysfunctions of the synaptic plasticity have also been observed supporting cognitive impairment [2]. To study these phenomena in depth, we aim to develop and match two models of the pathology, computational and experimental. Our work is based on an existing computational hippocampus model [3] and a 3-hits mouse model [4]. For that purpose, we analyze electrophysiological signals recorded with Multi-Electrode Array (MEA) on hippocampal slices to extract synaptic transmission characteristics that can be used in the model. In particular, we are interested in measuring excitatory postsynaptic potentials (EPSP) and neuronal spiking activity to infer plasticity mechanisms. To investigate these mechanisms, we process MEA signals recorded on slices during a high-frequency stimulation (HFS) protocol. It consists in 10 min of basal low-frequency (LF) stimulation of the Schaffer collaterals (a biphasic 100 µs pulse every 20 s at 4000 mV), followed by a one-second high-frequency train (100 Hz) stimulation, succeeded by an additional 20 min basal stimulation. This protocol’s purpose is to induce a long-term potentiation (LTP) observable through EPSP variations. To minimize common noise, line noise, and other external artifacts present on all electrodes, we implemented reference canceling [5]. We filtered the signals, either high-pass (300 Hz) to study spiking activity or low-pass (80 Hz) for LFP/synaptic activity. We categorized the basal stimulations into two sets: those occurring during the first 10 min, before the HFS train, and those starting 3 min after the HFS train. We then computed the means of each set separately on each of the 58 electrode channels and visualized the spatially interpolated activity (Fig 1) to study the effects of the HFS on synaptic and spiking activities mapped on the hippocampus slice. The results show modifications in amplitude, time and space for both responses post-HFS. From there, we aim to deduce anatomical and functional information about the structure, such as the type of cells spiking and their synaptic projections and gains. We are planning to vary the experimentation by using different protocols by changing the stimulation zone and/or the stimulation characteristics to help us further quantify plasticity and extract information that can be used in the computational model.