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Noradrenergic modulation of respiratory motor output during tadpole development: role of α‐adrenoceptors
Author(s) -
Fournier Stéphanie,
Kinkead Richard
Publication year - 2006
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.20.5.a1215-d
Subject(s) - bullfrog , ventilation (architecture) , respiratory system , lung , adrenergic receptor , biology , phenylephrine , brainstem , medicine , endocrinology , receptor , chemistry , anatomy , neuroscience , mechanical engineering , blood pressure , engineering
Lung ventilation appears progressively during bullfrog development; however, little is known about the neural mechanisms contributing to the emergence of air breathing in this species. We used an in vitro brainstem preparation from Rana catesbeiana to test the hypothesis that noradrenergic modulation of respiratory related motor output facilitates fictive lung ventilation during development. We first compared the effects of noradrenaline (NA) bath application (conc. = 0.02–10 μM) onto brainstem preparations from pre‐ and post‐metamorphic tadpoles (TK stages VII‐XI and XVIII‐XXIII, respectively) and adult bullfrogs. NA bath application exerted stage‐dependent effects on fictive lung burst frequency which increased in pre‐metamorphic tadpoles but decreased in post‐metamorphic tadpoles and adult bullfrogs. Conversely, NA bath application increased fictive gill ventilation frequency in both tadpole groups. In a second series of experiments, the α 1 and α 2 ‐adrenoceptor agonists phenylephrine (Phe) and clonidine (Clo) were applied onto preparations (conc. = 25–200 μM) to determine whether these receptors mediate these changes in fictive lung and gill ventilation frequency. Data show that, for each stage, α 1 ‐adrenoceptor activation with Phe mimicked well the effects of NA application on lung burst frequency; however, both drugs decreased fictive gill ventilation frequency suggesting that β‐adrenoceptors may mediate this effect. We conclude that noradrenergic modulation of lung ventilation changes during development but does not facilitate lung ventilation in more mature animals. Supported by the Natural Sciences and Engineering Research Council of Canada.