In the central nervous system, different brain regions communicate through neural signals. A normal neurophysiological activity is based upon the balance between the excitatory and the inhibitory neuronal networks. However, in certain neurological disorders, an imbalanced activity results due to a decreased inhibitory or exacerbated excitatory drive in neural tissues. So far, the study of such network activity has been achieved with single electrodes/patch clamp technique or low-density microelectrode arrays (MEAs). Towards a better understanding of the underlying features during imbalanced network activity, high-density CMOS MEAs were here used to study the aberrant electrical activity in hippocampal slices and in blind ex vivo retinas. In this thesis, aberrant electrical activity was investigated in organotypic and in acute hippocampal slices. The pharmacologically induced epileptiform-like activity (ELA) in organotypic hippocampal slices revealed propagating local field potentials (LFPs) from dentate gyrus (DG) towards the hippocampal CA3 region. Unexpected and not reported previously p-spikes of the LFPs propagated backwards from CA3 to DG along the same pathway. Also forward and backward propagating LFPs were identified in acute slices. Epileptiform hippocampal activity was compared to the imbalanced activity recorded in photoreceptor degenerated ex vivo mouse retina (rd10 mouse model). High-density recordings revealed local field potentials as well. The quantitative differences in LFP frequency and propagation pattern between hippocampus and retina were investigated and related to morphological differences. Finally, pharmacological experiments revealed that gap junctions and excitatory synaptic transmission are required for the generation of aberrant LFPs in both systems, the hippocampus and the blind retina.