| Grant number: | 09/54888-7 |
| Support Opportunities: | Research Projects - Thematic Grants |
| Duration: | November 01, 2011 - October 31, 2015 |
| Field of knowledge: | Biological Sciences - Physiology - Physiology of Organs and Systems |
| Principal Investigator: | Eduardo Colombari |
| Grantee: | Eduardo Colombari |
| Host Institution: | Faculdade de Odontologia (FOAr). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil |
| Pesquisadores principais: | Thiago dos Santos Moreira |
| Associated grant(s): | 15/14571-5 - 45th Annual Meeting of the Society for Neuroscience - Neuroscience 2015, AR.EXT |
| Associated scholarship(s): | 14/06976-2 - Involvement of serotoninergic mechanisms of the retrotrapezoid nucleus in the sympathetic and respiratory changes induced by intermitente hypoxia,
BP.DR 13/22526-4 - Cholinergic function of commissural nucleus of the solitary tract on cardiorespiratory responses to hypoxia, hypercapnia and pH decrease, BP.DR |
Abstract
Respiration is a physiological process essential to life. The neural circuit that generates the respiratory rhythm and produces the orderly activation of the various respiratory motor outflows (henceforth called central pattern generator, CPG) it is organized at the braistem level. Brain CO2 is almost certainly detected via changes in pH but how pH is detected, where pH is detected and how brain acidification stimulates breathing (the central chemoreflex) are still controversial. A relatively recent theory postulates that central respiratory chemoreception results from the cumulative effect of pH on the CPG itself and many of its tonic drives. The strongest evidence in favor of the specialized chemoreceptor theory came recently from the most ancient approach to neuroscience, namely human pathophysiology. The congenital central hypoventilation syndrome (CCHS), a rare developmental disease caused by mutations of the transcription factor Phox2b is characterized by a virtually complete loss of the central respiratory chemoreception, typically complete sleep apnea but usually maintained breathing during waking and exercise. At this moment, we don't know the real participation of the Phox2b neurons of the RTN in the control of breathing in an animal model without anesthesia. However, in this thematic project our main objective is to understand the cardio-respiratory responses elicted by hypercapnia in conscious rats with specific lesion of the Phox2b neurons in the RTN. To study the cardio-respiratory effects of hypercapnia we will use different experimental methods, which includes pharmacological, eletrophysiological and imunohistochemistry approaches. (AU)
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