|Support type:||Scholarships in Brazil - Doctorate|
|Effective date (Start):||March 01, 2014|
|Effective date (End):||March 31, 2016|
|Field of knowledge:||Biological Sciences - Physiology - Physiology of Organs and Systems|
|Principal Investigator:||Thiago dos Santos Moreira|
|Grantee:||Talita de Melo e Silva|
|Home Institution:||Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil|
In response to a reduction in the partial pressure of O2 (PaO2), peripheral chemoreceptors detect these changes and send information to the CNS in order to elicit brain mobilization to correct the change in homeostasis. Thus, the peripheral chemoreflex is a main element maintainers of cardiorespiratory homeostasis.Information from peripheral chemoreceptors can be distributed to different areas of the CNS, including areas located in the ventrolateral region of the medulla oblongata involved in sympathetic and respiratory control. Under resting conditions, the sympathetic premotor neurons in the ventrolateral medulla are the primary source of sympathetic activity, 70% of these neurons synthesize adrenaline and belong by definition to the C1 neurons. These catecholaminergic projections can promote the activation of hypothalamic neurons, particularly the paraventricular nucleus of the hypothalamus (PVN). Parvocellular neurons of the PVN are involved in cardiovascular control through the innervation of other brain structures involved in the control of sympathetic activity, including the NTS, the catecholaminergic C1 neurons and spinal cord. Studies show that aversive situations are able to promote the production of vasopressin, oxytocin and corticotrophin releasing factor (CRF). From this evidence, it is important to assess whether activation of the peripheral chemoreflex (another important aversive stimulus) activates catecholaminergic neurons located in the ventrolateral medulla which in turn influence the control of the activity of neurons located in the PVN.Moreover, there is evidence of the involvement of an inflammatory process in front of a chronic intermittent hypoxia. Our hypothesis is that hypoxia maintained (3 hours) would be promoting the release of pro-inflammatory factors such as interleukins (IL-1² and IL-6), tumor necrosis factor (TNF ±), which would be essential to promote the activation of the brain pathway C1- PVN.The experiments outlined in this project seek to test these hypotheses and will be performed by anatomical, optogenetic and molecular biology techniques.