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J Appl Physiol 99: 1019-1028, 2005; doi:10.1152/japplphysiol.00776.2004
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Superior laryngeal and hypoglossal afferents tonically influence upper airway motor excitability in anesthetized rats

Stephen Ryan and Philip Nolan

Departments of Human Anatomy and Physiology, Conway Institute for Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland

Submitted 23 July 2004 ; accepted in final form 16 March 2005

Upper airway (UA) muscle activity is stimulated by changes in UA transmural pressure and by asphyxia. These responses are reduced by muscle relaxation. We hypothesized that this is due to a change in afferent feedback in the ansa hypoglossi and/or superior laryngeal nerve (SLN). We examined 1) the glossopharyngeal motor responses to UA transmural pressure and asphyxia and 2) how these responses were changed by muscle relaxation in animals where one or both of these afferent pathways had been sectioned bilaterally. Experiments were performed in 24 anesthetized, thoracotomized, artificially ventilated rats. Baseline glossopharyngeal activity and its response to UA transmural pressure and asphyxia were moderately reduced after bilateral section of the ansa hypoglossi (P < 0.05). Conversely, bilateral SLN section increased baseline glossopharyngeal activity, augmented the response to asphyxia, and abolished the response to UA transmural pressure. Muscle relaxation reduced resting glossopharyngeal activity and the response to asphyxia (P < 0.001). This occurred whether or not the ansa hypoglossi, the SLN, or both afferent pathways had been interrupted. We conclude that ansa hypoglossi afferents tonically excite and SLN afferents tonically inhibit UA motor activity. Muscle relaxation depressed UA motor activity after section of the ansa hypoglossi and SLN. This suggests that some or all of the response to muscle relaxation is mediated by alterations in the activity of afferent fibers other than those in the ansa hypoglossi or SLN.

neuromuscular blockade; ansa hypoglossi; superior laryngeal nerve



Address for reprint requests and other correspondence: P. Nolan, Michael Tierney Bldg., Univ. College Dublin, Earlsfort Terrace, Dublin 2, Ireland (E-mail: philip.nolan{at}ucd.ie)




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