Abstract
When CO2 is lowered to abolish spontaneous respiratory movements (hypocapnic apnoea), expiratory motoneurones show a CO2-dependent, brain stem-mediated tonic discharge. If CO2 is then increased this tonic discharge progressively intensifies until it is rendered periodic by inspiratory-linked inhibition as respiratory rhythm occurs at a critical level of CO2 (refs 1–3). Such results were obtained during oxygen breathing (hyperoxia), hence with minimal excitation of peripheral chemoreceptors. Here we report that in the presence of hypocapnic apnoea, graded oxygen lack (hypoxia) causes a graded discharge of inspiratory motoneurones with graded reciprocal inhibition of the tonic expiratory motoneurone discharge; thus stimulation of peripheral chemoreceptors causes an ‘inspiratory shift’ in the pattern of respiratory motoneurone activation. When O2 is lowered further (or CO2 increased), the onset of respiratory rhythm is now expressed as a periodic, expiratory-phased inhibition of the tonic inspiratory motoneurone discharge. This demonstration that the periodic discharge of both inspiratory and expiratory motoneurones is sculpted from an underlying tonic discharge by reciprocal inhibition allows a new conceptual framework to be advanced. This proposes that the function of the rhythm (pattern) generator is not to cause a phasic excitation of respiratory bulbospinal neurones, as generally assumed previously, but to provide a patterned, phasic inhibition of their tonic excitation by chemical stimuli.
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References
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Sears, T., Berger, A. & Phillipson, E. Reciprocal tonic activation of inspiratory and expiratory motoneurones by chemical drives. Nature 299, 728–730 (1982). https://doi.org/10.1038/299728a0
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DOI: https://doi.org/10.1038/299728a0
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