Topic: multi-electrode array

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 character

Focal cortical dysplasia type ll (FCD2) is a congenital brain abnormality characterized by atypical focal brain organizations and dysmorphic neurons, frequently associated with refractory epilepsy. One causative mutation of FCD2 is a gain-of-function mutation in Ras Homologue Enriched in Brain (RHEB), RHEB-p.P37L. Studies on tissue resected from FCD2 patients suggest an elevated NKCC1:KCC2 compared to control tissue. The relative expression of these chloride transporters regulates the chloride reversal potential (ECl). The typical hyperpolarization of ECl during development, due to the upregul

By applying electrical stimulation, retinal prostheses aim to bypass dysfunctional photoreceptors and directly activate retinal ganglion cells (RGCs). Therefore, effective modulation of RGCs is the key step in the development of retinal prostheses. Six cynomolgus monkeys were used: three as a control and the other three as an N-methyl-N-nitrosourea (MNU)-induced retinal degeneration model. The retinal recording was performed using the 8x8 multi-electrode array. Figure shows the electrical stimulation pulses (a), raster plots of RGC spikes (b), and the modulation efficiency score (MES) (c). The

Prodromal network hyperexcitability and mitochondrial dysfunction underly the pathogenesis of various forms of dementia. However, the role of hippocampal hyperexcitability and mitochondria in prodromal dementia with Lewy bodies (DLB) is unclear.We conducted multi-electrode array (MEA) recordings to investigate early hippocampal activity in a transgenic mouse model of DLB which harbours an alanine to proline point mutation (A30P) in the alpha synuclein gene (SNCA), causing overexpression. Hippocampal slices from young pre-symptomatic (2-4 months) male A30P (N = 6 slices/4 mice) and wild-type (W