The influence of inflamatory process on the activity of nucleus tractus solitarius neurons in juvenile rats submitted to sustained hypoxia

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)