Prolonged augmentation of respiratory discharge in hypoglossal motoneurons following superior laryngeal nerve stimulation.

Experiments were conducted to investigate long-lasting effects of brief superior laryngeal nerve (SLN) stimulation on respiratory discharge in the hypoglossal nerve. In paralyzed, decerebrate and artificially ventilated cats, SLN stimulation (Hz, 3-5, s, 3-5 times threshold for inhibition of phrenic nerve discharge) immediately increase hypoglossal activity. Following stimulation, the amplitude of respiratory activity in the hypoglossal nerve was augmented (478 +/- 205%), and slowly decayed to prestimulus levels with a time constant of 106 +/- 16 s. In contrast, phrenic nerve activity was completely inhibited during the SLN stimulation and for several seconds thereafter. After activity resumed, phrenic burst frequency remained depressed (33 +/- 6%). Stimulation of the carotid sinus nerve elicited similar effects on hypoglossal nerve activity. Intracellular recordings from hypoglossal motoneurons indicated that SLN stimulation increased central respiratory drive potentials (CRDPs) following a stimulus train, but had inconsistent effects on resting membrane potential. Intracellular depolarizing current pulses (5-15 nA; 2 s) had no prolonged effects on membrane potential or CRDPs. The possible role of serotonin in prolonged augmentation of hypoglossal activity following SLN stimulation was investigated. Intracellular injection of horseradish peroxidase (HRP) into hypoglossal motoneurons and immunohistochemistry for serotonin revealed some close appositions between serotonin immunoreactive boutons and HRP-labeled neurons, but such appositions were sparse. Pretreatment with methysergide had little effect on prolonged augmentation of hypoglossal discharge following SLN stimulation. These results indicate that: (1) SLN stimulation causes prolonged augmentation of hypoglossal activity probably via increased synaptic inputs to hypoglossal motoneurons; and (2) serotonin is not necessary in the underlying mechanism.