Influence of nasotrigeminal afferents on medullary respiratory neurones and upper airway patency in the rat

Noxious stimulation of the nasal mucosa evokes a nasotrigeminal reflex (diving response), consisting of apnoea, bradycardia and vasoconstriction. However, the central mechanisms underlying the respiratory component remain unclear. Here, we describe the influence of nasotrigeminal stimulation (NS) on different types of ventral medullary respiratory neurotics and upper airway patency in the rat. In an arterially perfused working heart-brainstem preparation (WHBP), NS was induced by either irrigation of the nasal passage with cold saline (100-200 mul) or electrical stimulation of the trigeminal ethmoidal nerve (EN5, 20 Hz, 10 s, 100 mus, 0.5-2 V). Both stimuli evoked apnoea, bradycardia, a pressor response, persistent discharge in the recurrent laryngeal nerve and marked glottal adduction (P<0.001). NS evoked a distinct pattern of response in respiratory neurones: inspiratory (1) neurones ceased firing and hyperpolarized (n=19), while postinspiratory neurones depolarized (n=10) and discharged persistently. The latency of EN5-evoked synaptic responses (excitatory to postinspiratory neurones 12.3 +/- 2.8 ms, n=10; inhibitory to inspiratory neurotics 11.8 +/- 1.9 ms; n=19) was comparable. During the NS-evoked apnoea burst discharges were superimposed on a maintained level of tonic activity recorded from both the recurrent laryngeal nerve (n=4) and some postinspiratory neurotics (n=7). The physiological significance of these apnoeic rhythms is discussed. We conclude that the cardiorespiratory components of the diving response are mediated by activation of distinct sets of postinspiratory respiratory neurones.