GABAergic Mechanisms Are Involved in Respiratory Depression Induced by Laryngeal Nerve Stimulation

Article metrics

Abstract 1723 Pulmonary: Control of Breathing Poster Symposium, Tuesday, 5/4

Stimulation of superior laryngeal nerve (SLN) afferents causes apnea in newborn animals. The purpose of this study was to examine the role of GABAergic mechanisms in this reflex induced inhibition of breathing. Experiments were performed in 5-10 day old decerebrate, vagotomized, intubated and paralyzed piglets (n=5). The phrenic nerve response to four levels of electrical SLN stimulation was determined before and after intravenous administration of GABAA receptor blocker bicuculline (0.5 mg/kg). Mean PaCO2 was kept above the apneic threshold, between 35-39 mmHg. SLN stimulation caused significant inhibition of phrenic nerve amplitude and prolongation of expiratory time (TE), that were proportional to the level of stimulation used. TE increased from 0.91±0.11 seconds before stimulation to 10.6±3.1 seconds after maximal electrical stimulation, p< 0.05. Bicuculline reduced the percent inhibition of phrenic nerve amplitude caused by maximal SLN stimulation from 83±9% to 19±19% (before and after bicuculline respectively, p< 0.005). Bicuculline simultaneously abolished the prolongation of TE caused by SLN stimulation. We conclude that the decrease in peak phrenic nerve activity and prolongation of expiratory duration produced by laryngeal nerve stimulation is mediated mainly via GABAergic mechanisms. We speculate that upregulation of GABAergic mechanisms in early postnatal life contributes to the vulnerability of newborns to reflex induced apnea.

Author information

Rights and permissions

Reprints and Permissions

About this article