The effect of carbon dioxide on the tonic and the rhythmic discharges of expiratory bulbospinal neurones.

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Abstract
Extracellular micro-electrodes were used to measure the responses of expiratory bulbospinal neurons to CO2 in anesthetized, paralyzed cats, ventilated with O2. Simultaneous measurements were made of phrenic nerve and intercostal nerve filament discharges. Hypocapnia produced tonic activity in some of the expiratory neurons and in expiratory filaments but rendered the phrenic and inspiratory filaments silent. A graded excitatory effect of CO2 on tonic activity of both the neurons and the filaments was seen which progressed smoothly and continuously to rhythmic activity as CO2 was increased and to zero as CO2 was decreased. Increases in blood pressure produced effects which were opposite to those produced by CO2, and which had a faster time course. The CO2 response curves of those units showing tonic activity were indistinguishable from the CO2 response curves of those which did not. A mid-line lesion in the medulla interrupted inspiratory activity, converting activity of expiratory bulospinal neurons from periodic to tonic firing patterns. Following such lesions the CO2 threshold for rhythmic excitation of medullary neurones was elevated and the slopes of their CO2 response curves were reduced. These findings confirm the hypothesis by Bainton, Kirkwood and Sears (1978) that bulbospinal respiratory neurons convery both tonic and rhythmic excitation to spinal respiraory motoneurons and that the rhythmic excitation of expiratory muscles derives from a periodic inhibition of expiratory bulbospinal neurons which are subjected to a tonic CO2 dependent excitation which is continuously variable over the physiological range.