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The bullfrog neuroventilatory response to hypercapnia is unaffected by cannabinergic potentiation
Author(s) -
Bajada Nicholas Bradford,
Brundage Cord Michael,
Taylor Barbara E
Publication year - 2010
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.24.1_supplement.1026.3
Subject(s) - bullfrog , long term potentiation , hypercapnia , autoreceptor , hypoxic ventilatory response , neuroscience , cannabinoid receptor , chemistry , agonist , endocannabinoid system , receptor , medicine , endocrinology , biology , respiratory system , acidosis
Cannabinoid type 1 receptors (CB1) are G‐protein coupled receptors widely expressed in the vertebrate CNS. Binding at CB1 autoreceptors on pre‐synaptic neurons reduces GABA release. The hypercapnic ventilatory response (HVR), an increase in ventilatory frequency seen under hypercapnic (high PCO2), may be mediated by a reduction in GABAergic activity. We tested the hypothesis that activation of CB1 autoreceptors suppresses GABAergic inhibition and augments the HVR. Brainstems from juvenile bullfrogs were isolated, and whole‐nerve activity associated with breathing was recorded. Putative breathing was recorded during superfusion with standard artificial cerebrospinal fluid (aCSF) and aCSF containing the non‐selective cannabinoid agonist WIN‐55, 212‐2 (WIN; 100 muM) combined with normocapnic and hypercapnic conditions (1.5 and 5% CO2 respectively; balance O2). WIN significantly increased putative breath frequency. Despite this potentiation there was no significant increase in neuroventilatory frequency during hypercapnia with WIN. These data suggest that, although CB1 receptors may augment neuroventilation, their function does not extend to a modulation of the bullfrog HVR.