Abstract

‘Pre-inspiratory’ neuronal activities in a rostral ventrolateral medullary ‘pre-Bötzinger’ complex have been hypothesized to generate eupnea. Respiratory-modulated neuronal activities were recorded in this region in decerebrate, vagotomized, paralyzed, and ventilated cats, having bilateral carotid sinus nerve sections. As end-tidal partial pressures of carbon dioxide were reduced to hypocapnic levels, all neuronal activities which were tonic or expiratory–inspiratory (‘pre-inspiratory’) either ceased or lost respiratory-modulation. Similarly, most expiratory and inspiratory–expiratory activities did not maintain a phasic discharge. Half of the inspiratory neuronal activities did continue a phasic discharge, which commenced after phrenic activity or became independent of the phrenic rhythm. Results do not support a fundamental role of the ‘pre-Bötzinger’ complex in the neurogenesis of eupnea. Some neuronal activities can establish a phasic discharge in hypocapnia which is independent of the central respiratory rhythm. At normocapnia, this independent discharge is superseded and incorporated into the ponto-medullary respiratory neuronal circuit which generates eupnea.

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