Respiratory neuronal activity during apnea and poststimulatory effects of laryngeal origin in the cat

We investigated the behavior of medullary respiratory neurons in cats under pentobarbitone anesthesia, vagotomized, paralysed, and artificially ventil ated to elucidate neural mechanisms underlying apnea and poststimulatory re spiratory depression induced by superior laryngeal nerve (SLN) stimulation Inspiratory neurons were completely inhibited during SLN stimulation and po ststimulatory apnea. During recovery of inspiratory activity, augmenting in spiratory neurons were depressed, decrementing inspiratory neurons were exc ited, and late inspiratory neurons displayed unchanged bursts closely locke d to the end of the inspiratory phase. Augmenting expiratory neurons were e ither silenced or displayed different levels of tonic activity during SLN s timulation; some of them were clearly activated. These expiratory neurons d isplayed activity during poststimulatory apnea, before the onset of the fir st recovery phrenic burst. Postinspiratory or decrementing expiratory neuro ns were activated during SLN stimulation; their discharge continued with a decreasing trend during poststimulatory apnea. The results support the thre e-phase theory of rhythm generation and the view that SLN stimulation provo kes a postinspiratory apnea that could represent the inhibitory component o f respiratory reflexes of laryngeal origin, such as swallowing. In addition , because a subpopulation of augmenting expiratory neurons displays activat ion during SLN stimulation, the hypothesis can be advanced that not only po stinspiratory, or decrementing expiratory neurons, but also augmenting expi ratory neurons may be involved in the genesis of apnea and poststimulatory phenomena. Finally, the increase in the activity of decrementing inspirator y neurons after the end of SLN stimulation may contribute to the generation of poststimulatory respiratory depression by providing an inhibitory input to bulbospinal augmenting inspiratory neurons.