Studies from our laboratory have documented that hypoxia induces an increase in expiratory activity of rats, which becomes an active process. However, this condition is not due to changes in the electrophysiological properties of ventral medullary expiratory neurons, responsible for the generation of expiration, suggesting that others expiratory neurons could be involved in this change. In this project, we will evaluate whether the final pathway for expiration control, determined by the expiratory motoneurons, are involved in these changes. On the one hand, we intend to investigate the intrinsic electrophysiological membrane properties of these cells under basal conditions and compare them with electrophysiological properties from rats submitted to sustained hypoxia, in which the expiration becomes active. On another hand, molecular biology experiments using single cell RT-qPCR will allow us to evaluate differences in the ion channels genes expressions, which can explain the possible changes in the intrinsic properties of motoneurons in response to hypoxia, and to characterize them using ionic currents records. For this purpose, we will use cellular electrophysiology, essentially, whole cell patch clamp. Microinjections of retrograde tracers in different expiratory muscles will guide us in identifying the cells of interest, as well as to associate intrinsic properties of motoneuron labeled with its medullar lamina. The motoneuron phenotypes will also be analyzed by a neuronal tracer using immunofluorescence techniques. The results to be obtained with this project will help us to understand the mechanisms involved in the changes in the intrinsic properties of motoneurons and their importance to the expiratory muscles activity in sustained hypoxic conditions.
News published in Agência FAPESP Newsletter about the scholarship: