Introduction: Apneic episodes and consequent hypoxaemia are common features of breathing in high- risk neonates. Apneas of central origin (no respiratory effort) usually terminate with an obstructive component due to collapse of the upper airway. The genioglossus muscle, the main protruder muscle of the tongue, plays a crucial role in maintaining upper airway patency by opposing the negative intra-airway pressure generated during contraction of the diaphragm and by preventing the tongue blocking the oropharyngeal opening. In adults, the respiratory-related activity of the hypoglossal nerve (the motoneurone of the genioglossus) increases during hypoxaemia in order to maintain upper airway patency. However, in neonates it has been shown that the genioglossus muscle during hypoxia is age-related and this increased activity is not sustained. In neonates, little is known about how the hypoglossal motoneurones respond to hypoxaemia and the role of hypoglossal motoneurones during hypoxia in the maintenance of upper airway patency. Aim: The aim of this study was to determine the effects of hypoxaemia on hypoglossal motoneurones in neonates. Methods: Extracellular and intracellular recordings were made from hypoglossal motoneurones in vagotomized and vagi-intact neonatal kittens during normoxia and hypoxia. Results: The results showed: (1) the majority of hypoglossal motoneurones either decreased their discharge frequency or had only a transient increase during hypoxia. (2) During intracellular recordings, the membrane potential showed a sustained depolarisation during hypoxaemia in most cases and respiratory-related rhythmic EPSP activity was reduced in amplitude. The membrane impedance of these motoneurones increased and the excitability was reduced. (3) During upper airway stimulation, the amplitude of the laryngeal-evoked potentials was reduced during hypoxia. Conclusions: My results demonstrate that, in neonates, hypoglossal motoneurone activity is inhibited during hypoxia and the hypoglossal-upper airway reflexes are also inhibited. The probable consequence of such inhibition, for the newborn human infant, would be the failure of the maintenance of upper airway patency, thus leading to obstructive apnea. The mechanisms mediating the inhibition of hypoglossal motoneurones during hypoxia remain to be determined
