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Conditional deletion of Ric‐8B gene in olfactory sensory neurons leads to increased hypercapnic ventilatory response
Author(s) -
Silva Phelipe,
Lyra Cassandra,
Malnic Bettina,
Takakura Ana,
Moreira Thiago
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.01645
Subject(s) - hypercapnia , chemoreceptor , olfactory bulb , neuroscience , olfactory system , olfactory epithelium , brainstem , sensory system , ventilation (architecture) , control of respiration , carotid body , biology , tidal volume , respiratory system , neurochemical , central nervous system , anatomy , electrophysiology , genetics , physics , receptor , thermodynamics
The main physiological function of breathing is the maintenance of blood gases (CO 2 and O 2 ) homeostasis. For this fine tuning to take place, the central nervous system (CNS) must receive refined and accurate information. It is also characteristic of chemoreceptors an excitatory neurochemical phenotype and projections to the respiratory pattern generator. It is also known that rodents can detect CO 2 by the olfactory system. CO 2 ‐sensitive olfactory epithelium neurons (GC‐D+) project to a sequence of caudal glomeruli in the olfactory bulb that are anatomically segregated from other olfactory projections, forming a distinct subsystem of the main olfactory system. Considering that Ric‐8B conditional knock‐out mice are anosmic, and this may reveal a possible contribution of this olfactory chemoreception system to the “classic” chemoreceptors located within the brainstem, our hypothesis is to test the functional consequences of the Ric‐8B gene knock‐out in the olfactory epithelium neurons to the chemosensory control of breathing. Therefore, our proposal is to evaluate baseline and the hypercapnic ventilatory response (HCVR) among Ric‐8B conditional knock‐out mice (cKO) and wild‐type conscious mice. To fulfill our goals, we used the whole‐body pletismography technique. Conscious mice were kept in a sealed chamber whereby ventilatory parameters can be obtained. Hypercapnia was induced by increasing CO 2 up to 7% for 10 minutes. Ventilation (V E ), tidal volume (V T ) and respiratory frequency (f R ) were quantified every 30 seconds of a section of the 10 minutes record period. Hypercapnia (Fi CO2 = 7%) showed a further increase in V E (7628 ± 177, vs. wild‐type: 5759 ± 957 ml/min/g) and V T (22.3 ± 2.7, vs. wild‐type: 17.6 ± 2.1 ml/g), without change in f R (337 ± 62, vs. wild‐type: 324 ± 28 breaths/min) in Ric‐8b compared to wild‐type mice. No significant change was observed in baseline breathing parameters. Our data suggest that the olfactory epithelium sensory neurons chemoreception may also contribute to the process of central chemoreception since lack of Ric‐8B gene in the olfactory epithelium sensory neurons leads to further increase in the ventilatory responses to CO 2.