Contribution of the sensorial olfactory neurons in the hypercapnia and hypoxia ventilatory response in conscious mice

• Grant number: 21/09377-6
• Support Opportunities: Scholarships in Brazil - Doctorate (Direct)
• Start date: August 01, 2022
• End date: December 31, 2025
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Principal Investigator: Thiago dos Santos Moreira
• Grantee: Phelipe Eduardo Silva
• Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated research grant: 15/23376-1 - Retrotrapezoid nucleus, respiratory chemosensitivity and breathing automaticity, AP.TEM
• Associated scholarship(s): 23/02716-5 - The neural basis of CO2 detection in olfactory neurons, BE.EP.DD

Abstract

The main physiological function of breathing is the maintenance of blood gases (CO2 and O2) homeostasis. For this fine tuning to take place, the Central Nervous System (CNS) must receive refined and accurate information. Among the neural clusters that control respiratory activity, the ventrolateral region of the brainstem, namely the retrotrapezoid nucleus (RTN) are capable of detecting increases in the partial pressure of CO2, composing the process of central chemoreception. It is characteristic of chemoreceptors in addition to their sensitivity to CO2 and pH, an excitatory neurochemical phenotype and projections to the respiratory pattern generator. It is also known that mammals can detect CO2 by the olfactory and taste system. CO2-sensitive olfactory neurons project to a sequence of caudal glomeruli in the olfactory bulb called glomeruli that are anatomically segregated from other olfactory projections, forming a distinct subsystem of the main olfactory system. Ric-8b anosmic mice may reveal a possible contribution of this olfactory chemoreception system to respiratory control modulation. Therefore, our proposal will be to evaluate: a) the ventilatory response to hypercapnia (HCVR) among knock-out mice (cKO) presenting Ric-8b protein deficiency in olfactory bulb neurons and wild-type animals (WT) and b) fos protein expression in the olfactory bulb after a hypercapnia situation in cKO animals for Ric-8b or WT animals. To fulfill our goals, we will use neuroanatomic and neurofunctional techniques. (AU)