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Cellular and electrophysiological changes in the hippocampus caused by neurodegenerative processes related to neonatal anoxia and temporal lobe epilepsy

Abstract

Neurodegenerative diseases and neuronal disorders cause the loss of specific neuronal subtypes, thus contributing to the clinical changes observed in patients. Neonatal anoxia and temporal lobe epilepsy are important public health problems worldwide, since in addition to the mortality rate, they can cause permanent sequelae, probably related to the imbalance between excitatory and inhibitory neurons. The impact of neonatal anoxia and temporal lobe epilepsy on the balance of excitatory and inhibitory neurons is poorly understood. Also, cell loss in neuronal disorders has been linked to oxidative stress and neuroinflammation. In this project, we intend to evaluate possible changes in interneuron populations in animals submitted to models of neonatal anoxia and temporal lobe epilepsy. Among other approaches, we will assess the impact of NOX2, an essential enzyme in the production of reactive oxygen species (ROS), related to both microglia activation and neuronal plasticity. Electrophysiological analyzes will be performed using records using HD-MEA BioCAM 4096 on hippocampus slices, in addition to electrophysiological records performed in vivo. This project has the support of a network of collaborators involving UCLA, USP, and Humboldt University at Berlin. With this, we intend to contribute to future therapeutic proposals related to cognitive deficits related to neonatal anoxia and temporal lobe epilepsy. (AU)

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