In decerebrate cats, stable intracellular recordings were made from 37 laryngeal motoneurones, the membrane potentials of which varied in relation to respiration. These motoneurones were identified as laryngeal since all were antidromically activated by stimulation of the recurrent laryngeal nerve, but in two, the antidromic activity could only be elicited by vagal stimulation (vagotomized cats). The cell bodies were all located within the nucleus ambiguous. Sixteen cells were depolarized during the phrenic burst and were classified as inspiratory laryngeal motoneurones (ILM). They repolarized at end-inspiration and received two successive waves of postsynaptic inhibition during expiration: an early, strong one and a late (end-expiratory), weaker one. The decay of the first wave was related to the duration of postinspiratory phrenic activity. Twenty-one cells depolarized abruptly in early expiration followed by a more-or-less gradual repolarization. They were classified as expiratory laryngeal motoneurones (ELM). All ELM were strongly inhibited during inspiration. Some of them received weak inhibition during end expiratory phase. The rapid and large depolarization observed during early expiration (and consequent maximal discharge frequency) can be explained by two summating mechanisms: a postinhibitory rebound resulting from the removal of inhibition during inspiration, and an excitatory phenomenon of unknown origin. The amplitude of this excitatory phenomenon was largest in cats with the most residual (early expiratory) phrenic activity. To explain the hyperpolarizations occurring in ELM during late expiratory and inspiratory phases and those occurring in ILM during early expiration, we hypothesize that reciprocal inhibition exists between networks controlling ILM and ELM activities or between these motoneurones themselves.(ABSTRACT TRUNCATED AT 250 WORDS)