The responses in respiratory outflow resulting from microstimulation and successive microlesions of the dorsal (DRG) and ventral (VRG) respiratory groups of neurons in the brainstem were studied in anesthetized, paralyzed, artificially ventilated cats. Microstimulation (2 to 120 Hz; 5 to 50 microA; 100 musec pulse duration) at almost every point within the DRG or VRG produced a bilateral short latency inhibition of phrenic nerve activity which had an onset latency of 4 to 9 msec and a duration of 4 to 24 msec. This global stereotyped phrenic inhibition was elicited by single pulses and often was accompanied by a postinhibitory excitation. In 48% (92/193) of the stimulation trials, trains of stimulus pulses during inspiration decreased the duration of inspiration. In 25% of the expiratory microstimulation trials, expiratory duration was increased and in 11%, expiration was shortened markedly by trains of pulses. Single shocks delivered to the right VRG or DRG produced a short latency excitation in the ipsilateral recurrent laryngeal nerve (RRL). This RRL excitation had an onset latency of 2 to 5 msec and a duration of 3 to 15 msec. Evidence suggests that the RRL excitation is due to a paucisynaptic activation of expiratory motoneurons in the caudal VRG. This activation is synchronous with the inhibition of inspiratory neurons in DRG and VRG. Despite the powerful short latency effects of microstimulation in VRG and DRG, extensive bilateral destruction of these neuronal populations had only modest effects on respiratory rhythm, while it decreased (or abolished) respiratory outflow in phrenic and recurrent laryngeal nerves. The combined results of the microstimulation and microlesion portions of this study suggest that a region (or regions) outside of the DRG and VRG might be important in the control of the respiratory pattern and that the DRG and VRG are important in determining the depth of inspiration; their role in generating respiratory rhythm needs to be critically re-examined.