Vagal modulation of recurrent laryngeal motoneurone discharge: a thesis presented in partial fulfilment of the requirements for the degree of Master of Science in Physiology at Massey University

Abstract

The larynx has considerable influence on the rate of respiratory airflow, particularly during expiration. The laryngeal muscles are largely controlled by the recurrent laryngeal nerve (RLN) which exhibits respiratory periodicity in its discharge. The effects of the Hering-Breuer inflation reflex, on this periodicity has been studied, but there is little information on the role of the various groups of lung receptors in modulating the patterns of recurrent laryngeal motoneurone (RLM) discharge during # euphoeic breathing.

The purpose of this investigation was to examine the effects of changes in volume-related feedback and other vagal afferent inputs on the activity of RLMs. The discharge patterns of single fibres in the recurrent laryngeal nerve were classified and their responses to pulmonary inflation and deflation before and during pulmonary stretch receptor (PSR) block by sulphur dioxide were compared, using anaesthetized, spontaneously breathing rabbits. On the basis of observations in this study, RLMs were classified into: a) phasic-inspiratory (P-ILMs)

b) tonic-inspiratory (T-Ill!s)

c) phasic-expiratory (P-ELMs)

d) tonic-expiratory (T-ELMs) and their firing patterns were described.

It was found that the frequency and duration of F-ILM discharge in inspiration increased after the inhibition of FSR activity. lung inflation, some RLMs were inhibited whereas others showed either a low-frequency or a high frequency tonic discharge when FSR were intact. During FSR block, lung inflation failed to inhibit phasic F­ ILM discharge. While ILM activity was increased during lung deflation, that of ELM was decreased. These responses persisted in a modified form during FSR block. Breathing through an added dead space increased the frequency of F­ ILM discharge during aspiration. During augmented breaths, the frequency and duration of F-ILM activity greatly exceeded F-ILM activity during normal breaths, whereas the activity of T-ELM was reduced.

Further experiments were carried out on rabbits

during neuromuscular ventilation. With

junction stretch

block receptors

artificial functioning,

simultaneous recordings of the recurrent laryngeal nerve (RLN) and phrenic nerve (FN) showed that the onset of the activities of both nerves occurred during the deflation phase of ventilation. Changing the tidal volume to 50% or 100% of eupnoeic value could not unlink the recurrent laryngeal and phrenic bursts from the deflation phase of the pump cycle. During FSR block, RLN and FN discharges occurred with no set relation to ventilation at spontaneous resting tidal volume. At 100% higher tidal volume, RLN and PN bursts were initiated more frequently by the deflation phase. These timings were changed into a "free-running" pattern by decreasing the tidal volume to half eupnoeic value.

These results suggested that vagal afferents modulate RLM discharge during eupnoeic breathing: PSR inputs terminate ILM discharge whereas RAR activity, which occurs at functional residual capacity, initiates the onset of ILM discharge and extends its activity. The role of RAR is compatible with its effects in shortening ELM activity if the initiation of ILM discharge is considered as a

termination of ELM activity. That RLN and PN responded in almost identical manner to changes in vagal afferent inputs suggests that PSR and RAR may operate through similar central pathways to modulate both neural outputs. The discharge patterns of RLMs and their responses to changes of pulmonary afferent inputs, are probably related to the role of the larynx in regulating upper airway resistance.