Abstract
The resting respiratory activity is generated by the synchronized activity of a complex brainstem neural respiratory network, which contains a primary oscillator essential for respiratory rhythmicity. This respiratory oscillator is located within the ventral respiratory column and is composed by pacemaker inspiratory neurons. However, recent studies suggest the presence of a second respiratory oscillator critical for the emergence of active expiratory pattern, as observed in conditions of hypoxia or hypercapnia. This expiratory oscillator is suggested to be located rostral to the ventral respiratory column, ventral to the facial nucleus, in the parafacial respiratory group (pFRG). In addition to its important role for the generation of active expiratory pattern, studies suggest that the respiratory neurons of the pFRG also interact with the neurons involved with the generation of sympathetic activity, contributing for the excitation of sympathetic activity in conditions of hypercapnia. Thereby, it has been proposed that the respiratory neurons of the pFRG play a critical role for the coordinated control of sympathetic and respiratory activities, especially in conditions of metabolic challenges. Nevertheless, some important aspects of the role of pFRG neurons still deserve experimental verification, such as: i) the functional characteristics of the pFRG neurons (chemosensitivity, for example); ii) the synaptic conditions required for the activation of pFRG neurons (excitatory and inhibitory balance); iii) the connectivity of the pFRG neurons with other respiratory neurons, which underlie the generation of active expiratory pattern; and iv) the connectivity with sympathetic neurons, which may contribute to the increase in sympathetic activity coupled with respiratory activity. The clarification of these aspects will be important to verify the neural mechanisms underpinning the generation of active expiration and its coupling with sympathetic nervous system; as well as will contribute for the understanding of the development of cardiorespiratory adaptations induced by the exposure to chronic hypoxia - a condition commonly associated to pathophysiological conditions. Accordingly, in the present study we sought to verify novel concepts about the neural mechanisms responsible for the generation of active expiration and its coupling with sympathetic activity in healthy rats as well as in rats exposed to chronic hypoxia. To this, we will use electrophysiological techniques (nerve and neuronal recordings), immunohistochemical procedures and the experimental model of juvenile rats submitted to chronic hypoxia (10% O2) for 24 h. (AU)
Scientific publications
(11)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
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