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Synaptic transmission and electrophysiological properties of glutamatergic neurons of the Nucleus of Tractus Solitarius of mice submitted to the experimental model of asthma.

Grant number: 23/02346-3
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Effective date (Start): June 01, 2023
Effective date (End): May 31, 2024
Field of knowledge:Biological Sciences - Biophysics - Cellular Biophysics
Principal Investigator:Davi José de Almeida Moraes
Grantee:Enrico Micali Aiello
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil


Asthma accounts for 1 in every 250 deaths around the world. It is an inflammatory disorder defined mainly by periodic and reversible occurrences of airway bronchoconstriction and mucus hypersecretion. The exacerbated inflammatory response, generated by the contact with an allergen, activates sensory fibers in the airways (bronchopulmonary C-fibers) and peripheral chemoreceptors (carotid bodies), which activate the medullary neurons of the Nucleus of Tractus Solitarius (NTS). In response to peripheral information, the NTS neurons act as central sensory integrators for autonomic and respiratory functions. The NTS neurons excite preganglionic parasympathetic medullary motoneurons, more specifically in the Dorsal Motor Nucleus of the Vagus (DMV) and Nucleus Ambiguus (NA), which project to the airways, suggesting their participation in the control of smooth muscles and mucous glands of the airways, being able to generate bronchoconstriction and hypersecretion of mucus in asthmatic conditions. Thus, the Research Project hypothesizes that asthma increases excitatory sensory synaptic transmission and excitability of excitatory neurons (glutamatergic) of the NTS of mice. To test this hypothesis, we will use the whole cell patch clamp technique in medullary slices from control and mice submitted to the experimental model of asthma to evaluate the excitatory synaptic transmission and the electrophysiological properties of the NTS glutamatergic neurons. In addition, the changes in the spontaneous, and evoked by sensory fibers, intracellular [Ca2+] in the NTS glutamatergic neurons will be evaluated using fluorescent microscopy. Clarifying these cellular events in physiological and pathological conditions can help better understand the electrophysiological processes of NTS neurons involved in signaling and controlling bronchoconstriction and mucus secretion in an experimental model of asthma.

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