The network model of respiratory rhythmogenesis that drives normal breathing (i.e. eupnea) is dependent upon reciprocal inhibitory synaptic connections (e.g. Richter, In Comprehensive human physiology ed. Greger & Windhurst, 1996). Richter has proposed that eupnea is a 3-phase rhythm comprising inspiration, postinspiration (stage I expiration) and expiration (stage II; Richter, 1996). This is reflected in the upper airway: during inspiration the vocal folds dilate to ease air into the lungs whereas they narrow during postinspiration to steady airflow out of the lungs and maintain functional residual capacity. We addressed the role of glycinergic synaptic inhibition within the pontomedullary respiratory network for the maintenance of eupnea, including its modulation of the upper airway, in neonatal and mature rats.

Experiments were performed on arterially perfused in situ working heart-brainstem preparations of both neonatal and mature rats (1 h to 50 d old) at 31 °C. This preparation is decerebrated at the precollicular level and unanaesthetised. We recorded phrenic, hypoglossal and recurrent laryngeal motor activity as well as the intracellular activity of single respiratory neurones with sharp microelectrodes. We also measured airway resistance by recording changes in subglottal pressure (SGP) during constant airflow perfusion of the upper airway in the expiratory direction (see Dutschmann et al. Autonomic Neurosci. 84, 2000).

In both neonatal and mature rats there was rhythmic inspiratory motor activity in phrenic, hypoglossal and recurrent laryngeal nerves. Additionally there was postinspiratory activity in the recurrent laryngeal nerve that was associated with transient increases in SGP. Application of strychnine (0.1–0.5 µm) into the perfusate resulted in a severe reduction of postinspiratory motor activity. Strychnine abolished the inspiratory inhibition in postinspiratory neurones and revealed an underlying synaptic excitatory drive that resulted in an unprecedented inspiratory related burst discharge. Loss of glycine receptor integrity reduced the postinspiratory laryngeal adduction. Paradoxically the glottis started to constrict during the phrenic nerve burst. Since hypoxia is known to depress inhibitory synaptic transmission within the respiratory network (Schmidt et al. J. Physiol. 483, 1995), we gassed the perfusate with isocapnic hypoxia (5% O₂, 5% CO₂and 90% nitrogen). This produced a similar effect to that described for strychnine: loss of postinspiratory motor activity and a paradoxical laryngeal adduction during neural inspiration.

Our studies demonstrate the importance of inhibitory glycinergic transmission within the pontomedullary network for eupnoea and the normal respiratory modulation of the laryngeal muscles. We suggest that prolonged hypoxia could result in upper airway obstruction due to a central re-organisation of the respiratory network.

Studies supported by the British Heart Foundation and the Deutsche Forschungsgemeinschaft.