Abstract
In severe hypoxia, homeostatic mechanisms maintain function of the brainstem respiratory network. We hypothesized that hypoxia involves a transition from neuronal mechanisms of normal breathing (eupnea) to a rudimentary pattern of inspiratory movements (gasping). We provide evidence for hypoxia-driven transformation within the central respiratory oscillator, in which gasping relies on persistent sodium current, whereas eupnea does not depend on this cellular mechanism.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, N.I.H., Intramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Action Potentials / drug effects
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Action Potentials / physiology
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Animals
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Animals, Newborn
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Biological Clocks / drug effects
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Biological Clocks / physiology*
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Brain Stem / drug effects
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Brain Stem / growth & development*
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Hypoxia / physiopathology
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Inhalation / drug effects
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Inhalation / physiology*
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Nerve Net / drug effects
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Nerve Net / growth & development*
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Neural Inhibition / drug effects
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Neural Inhibition / physiology
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Periodicity
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Rats
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Respiratory Center / drug effects
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Respiratory Center / growth & development*
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Sodium Channel Blockers / pharmacology
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Sodium Channels / drug effects
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Sodium Channels / physiology*
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Synaptic Transmission / drug effects
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Synaptic Transmission / physiology
Substances
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Sodium Channel Blockers
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Sodium Channels