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Concurrent Blockade of Muscarinic, Neurokinin‐1, and Serotonergic Receptors in the Ventral Respiratory Column of Intact Goats Does Not Affect Breathing
Author(s) -
Muere Clarissa,
Neumueller Suzanne,
Olesiak Samantha,
Miller Justin,
Hodges Matthew,
Pan Lawrence,
Forster Hubert
Publication year - 2015
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.29.1_supplement.1032.12
Subject(s) - serotonergic , muscarinic acetylcholine receptor , chemistry , receptor , excitatory postsynaptic potential , neurokinin a , pharmacology , endocrinology , serotonin , medicine , biology , substance p , biochemistry , neuropeptide
Past and current studies in our laboratory have found that dialyzing antagonists of muscarinic, neurokinin‐1, or serotonergic receptors in the ventral respiratory column (VRC) of intact goats either increases or does not change breathing. However, we found that receptor antagonism alters the effluent dialysate concentration of one or more neuromodulators. These changes may have compensated for disruption of excitatory transmission in the VRC, preventing a decrease in breathing. Thus, we sought to test the hypothesis that simultaneous blockade of all three receptors with a cocktail of antagonists would elicit compensatory changes in multiple neurochemicals, but would ultimately decrease breathing. We dialyzed a cocktail of antagonists of muscarinic, neurokinin‐1, and serotonergic receptors into the VRC of adult goats, and collected the effluent dialysate for quantification of neurochemicals. Breathing was continuously monitored throughout the dialysis period. Data show that breathing is not significantly different (P>0.05, n=5) between time control studies and dialysis of the triple cocktail. Treatment with the cocktail tended to increase effluent substance P and decrease effluent glutamine, glycine, and GABA concentrations. Our results suggest that attenuation of multiple excitatory receptors in the VRC of intact animals may be compensated for by a reduction in inhibitory transmission to maintain a normal level of breathing.