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Purinergic modulation of preBötzinger complex inspiratory rhythm in rodents: the interaction between ATP and adenosine
Author(s) -
Zwicker J. D.,
Rajani V.,
Hahn L. B.,
Funk G. D.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.210930
Subject(s) - purinergic receptor , rhythm , adenosine , purinergic signalling , chemistry , adenosine triphosphate , adenosine triphosphatase , respiration , neuroscience , medicine , biology , adenosine receptor , atpase , anatomy , receptor , biochemistry , enzyme , agonist
Non‐technical summary Hypoxia causes an increase in breathing followed by a secondary depression that is most pronounced, and potentially life‐threatening, in premature infants. Adenosine triphosphate (ATP) is released in brainstem respiratory networks during hypoxia, where it attenuates the secondary respiratory depression. Mechanisms are unknown but likely to be complex because ATP is degraded by enzymes into ADP, which is excitatory, and adenosine (ADO), which is inhibitory. We demonstrate in mouse, like rat, that ATP in the preBötzinger complex (preBötC), a site critical for inspiratory rhythm generation, increases frequency. Unlike rat, this increase is only observed in mouse if ADO receptors are blocked. Differential ATP sensitivity is likely to reflect that ADO is only inhibitory in mouse, and that mouse preBötC enzymes favour ADO production. Thus, purinergic signalling in preBötC networks appears balanced to favour inhibition in mouse but excitation in rat. Knowledge of purinergic signalling increases our understanding of processes underlying respiratory responses to hypoxia.