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Involvement of the Nucleus Raphe Obscurus (ROb) on CO2 ventilatory response
Author(s) -
Silva Glauber Santos Ferreira,
Giusti Humberto,
Reis Wagner,
Dias Mirela B.,
Gargaglioni Luciane H.,
Branco Luiz G.S.,
Glass Mogens L.
Publication year - 2008
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.22.2_supplement.169
Subject(s) - hypercapnia , nucleus raphe magnus , hyperventilation , chemoreceptor , raphe nuclei , tidal volume , ventilation (architecture) , normocapnia , raphe , anesthesia , hyperpnea , chemistry , central chemoreceptors , ibotenic acid , respiratory system , medicine , acidosis , serotonergic , serotonin , central nervous system , receptor , engineering , mechanical engineering
Background: Several brainstem regions have been recognized as central CO2/pH chemoreceptors, including the medullary raphe region. The specific role of the Nucleus Raphe Obscurus (ROb) in the ventilatory responses to hypercapnia is uncertain, but a prior study suggest that the ROb does not by itself contribute to chemoreception directly, but it has a modulatory role (Li et al., 2006). In the present study, we investigated the involvement of ROb in the ventilatory responses to CO2 by nonspecific lesioning of this nucleus. Methods: Seven days before the experiments, male Wistar rats received microinjections of ibotenic acid (0.4 ìg/0.2 ìL) or vehicle (PBS, 50 mM, pH 7.4) into the ROb. Measurements of ventilation (VE) were performed by the body plethysmograph. Animals were exposed first to humidified room air, followed by 30 min of hypercapnia exposure (7% CO2). Results: Hypercapnia caused hyperventilation and in all groups. ROb lesions decreased ventilatory response to hypercapnia up to 15% [1341.1±67.7 mL.kg‐1.min‐1 (ibotenic acid) vs 1647.8±47.7 mL.kg‐1.min‐1 (vehicle)] due to lower tidal volume (VT) and respiratory frequency (f). Conclusion: The results suggest that ROb exerts an excitatory modulation in CO2‐drive to breathing, acting on VT and f. Financial Support: FAPESP, FAEPA, USP.