| Grant number: | 14/11101-5 |
| Support Opportunities: | Scholarships in Brazil - Doctorate (Direct) |
| Start date: | October 01, 2014 |
| End date: | May 31, 2018 |
| Field of knowledge: | Biological Sciences - Physiology - Physiology of Organs and Systems |
| Principal Investigator: | Benedito Honorio Machado |
| Grantee: | Ludmila Lima Silveira |
| Host Institution: | Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil |
| Associated research grant: | 13/06077-5 - Changes in the neural networks involved with the generation and control of sympathetic and respiratory activities in different experimental models of hypoxia, AP.TEM |
| Associated scholarship(s): | 17/13720-2 - Effects of minocycline treatment on microglial activation in rats submitted to sustained hypoxia, BE.EP.DD |
Abstract The Nucleus Tractus Solitarius (NTS) is a critical central region for cardiorespiratory control. The neurons in this region receive information from peripheral chemoreceptors, the main sensors of the chemical composition of the blood, and connect to medullary nuclei responsible for the generation and modulation of sympathetic and respiratory activity. In situations of hypoxia, in which the supply of oxygen (O2) to the cells is reduced, the activation of neural pathways can promote chemoreflex responses such as increase in blood pressure and respiratory frequency to reestablish appropriate O2 supply to tissues. The experimental model of Sustained Hypoxia (SH) has been explored in studies from our laboratory in order to promote cardiorespiratory changes in animals similar to humans that move to high altitudes where the partial pressure of O2 is lower. The animals submitted to SH exhibit increased blood pressure. It is known that SH promotes central and peripheral inflammation. Central nervous system inflammation can change neuronal excitability and synaptic activity. Our previous results showed that treatment with the anti-inflammatory minocycline significantly attenuates hypertension promoted by SH. In this project we will study the mechanisms by which this attenuation occurred, especially at the level of the NTS neurons. Using whole cell patch-clamp technique we will investigate if the inflammatory process triggered by SH influences the activity of NTS neurons involved in cardiorespiratory control. (AU) | |
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