Neuronal activities underlying inspiratory termination by pneumotaxic mechanisms.

The purpose was to identify and characterize the discharge patterns of pontile neurons which are responsible for the termination of inspiratory activity. Phrenic discharge is prolonged following destruction of neurons at the junction of mesencephalon and pons by neurotoxins. Neuronal activities were recorded in this region in decerebrate, vagotomized, paralyzed and ventilated cats. At normocapnia, neurons had tonic discharge patterns, most of which were linked to phasic periods of phrenic activity. Peak activities occurred in late neural inspiration or early expiration. In hypercapnia, neuronal discharge frequencies did not increase, rather activity became more concentrated during one portion of the respiratory cycle. In severe hypoxia, neuronal activities diminished in parallel with the prolongation of phrenic discharge and establishment of apneusis. During recovery, some neurons transiently acquired phasic, respiratory-modulated discharge patterns. Neuronal activities from neighboring regions did not exhibit comparable changes in hypercapnia or hypoxia. We conclude that rostral pontile neuronal activities are a primary determinant of the reversible and irreversible terminations of eupneic inspiratory activity.