Involvement of astrocytes/neurons interaction in the brainstem nuclei in autonomic and respiratory changes observed in mice submitted to sustained hypoxia

• Grant number: 24/06385-6
• Support Opportunities: Scholarships in Brazil - Post-Doctoral
• Start date: July 01, 2024
• End date: August 31, 2025
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Benedito Honorio Machado
• Grantee: Luiz Henrique César Vasconcelos
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
• Associated research grant: 18/15957-2 - Astrocytic modulation on brainstem neurons involved with generation and control of sympathetic and respiratory activities in rodents submitted to hypoxia, AP.TEM

Abstract

Recent studies from our laboratory using C57BL/6 mice documented that sustained hypoxia (HM, FiO2 0.1 for 24h) induced significant changes in the respiratory pattern associated with an increase in the parasympathetic component. Previous studies from our laboratory, performed in rats, showed that glial/astrocyte cells in the ventral medulla are involved in the modulation of respiratory and autonomic activities. In this context, it is possible that the neuronal plasticity phenomena observed in the nucleus of the solitary tract (NTS) and in the ventral medulla involved with the generation and modulation of autonomic and respiratory activities after SH in mice are due to changes in astrocytic modulation. The aim of this project is to evaluate the role of astrocytes in the modulation of neural respiratory pathways in the brainstem (NTS and ventral medulla) in the in situ preparation of mice previously submitted to SH. To reach this goal we will evaluate: a) the effects of the metabolic inhibitor of astrocytic activity (Fluorocitrate - FCt) in Wild-Type (WT) C57BL/6 mice submitted to SH, and b) the role of adenosine and A2 receptors in astrocytes in WT mice and knockout mice for A2 receptors (KO/A2) submitted to SH.