Distribution analysis of hippocampal interneurons and electrophysiological changes during the development of rats after neonatal anoxia

• Grant number: 16/16892-6
• Support Opportunities: Scholarships in Brazil - Master
• Effective date (Start): March 01, 2017
• Effective date (End): February 28, 2019
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Acordo de Cooperação: Coordination of Improvement of Higher Education Personnel (CAPES)
• Principal Investigator: Alexandre Hiroaki Kihara
• Grantee: Débora Sterzeck Cardoso
• Host Institution: Centro de Matemática, Computação e Cognição (CMCC). Universidade Federal do ABC (UFABC). Ministério da Educação (Brasil). Santo André , SP, Brazil

Abstract

Neonatal anoxia is an important public health concern worldwide, once besides the high mortality rate it can cause permanent sequelae. The brain is the most susceptible organ to oxygen deprivation, since it demands high energy rate. Among the brain structures, the hippocampus is one of the most sensitive areas to anoxia and is characterized by having a known anatomy and circuits. Its cell variety is largely composed of interneurons, inhibitory cells that form local circuits through synapses with main cells of the hippocampus, thereby controlling the activity and local rhythmicity. Anoxia results in numerous events leading to injury and neuronal death in the hippocampus and can change the connectivity and hippocampal function. However, the impact of anoxia in the balance of excitatory and inhibitory neurons is not well known, as well as the electrophysiological changes resulting from neuronal loss. In this study, we propose to analyze the distribution of populations of calbindin (CB), calretinin (CR) and parvalbumin (PV) -positive interneurons by immunofluorescence and the protein levels by western blot. In addition, we intend to analyze possible electrophysiological changes through records using HD-MEA BioCAM 4096 in hippocampal slices of rats that suffered anoxia during neonatal development (P10 and P30). In this way, we aim to contribute to future therapeutic approaches related to cognitive and learning deficits related to neonatal anoxia. (AU)