This study was undertaken to examine the effects of hypercapnia on the excitability of respiratory motoneurons. The action of CO2 on phrenic (inspiratory) and internal intercostal (expiratory) motoneurons was compared with that exerted on non-respiratory motoneurons of the musculocutaneous nerve. The experiments were performed on spinalized (C1 segment), partially deafferented cats that were exposed to different CO2/O2 mixtures (end-tidal CO2 3 +/- 0.3, 6 +/- 0.5 and 9 +/- 0.5%). Changes in neuronal excitability were assessed by: measuring the amplitudes of antidromic field potentials recorded from a population of motoneurons; analysis of the amplitude and latency of the orthodromic response recorded from a given nerve and evoked by microstimulation within the corresponding motor nucleus; monitoring the membrane potentials during intracellular recordings from phrenic motoneurons; and recording ongoing activity of the phrenic and internal intercostal nerves. Hypercapnia (end-tidal CO2 6 +/- 0.5 or 9 +/- 0.5%) decreased the excitability of phrenic and musculocutaneous motoneurons, the effect being larger at the higher CO2 level. Internal intercostal motoneurons were generally more resistant to the effects of CO2. A depression of their excitability was observed only at end-tidal CO2 9 +/- 0.5%. The decreased excitability of phrenic motoneurons was associated with membrane hyperpolarization. It is concluded that the depressant action of CO2 is present in both respiratory and non-respiratory spinal motoneurons. The action of hypercapnia on respiratory motoneurons may oppose the excitatory effects exerted through specific chemoreflexes.