Stimulation of the superior laryngeal nerve (SLN) results in
apnea in animals of different species, the mechanism of which is not known. We studied the effect of the
GABA(A) receptor blocker
bicuculline, given intravenously and intracisternally, on
apnea induced by SLN stimulation. Eighteen 5- to 10-day-old piglets were studied:
bicuculline was administered intravenously to nine animals and intracisternally to nine animals. The animals were anesthetized and then decerebrated, vagotomized, ventilated, and paralyzed. The phrenic nerve responses to four levels of electrical SLN stimulation were measured before and after
bicuculline. SLN stimulation caused a significant decrease in phrenic nerve amplitude, phrenic nerve frequency, minute phrenic activity, and inspiratory time (P < 0.01) that was proportional to the level of electrical stimulation. Increased levels of stimulation were more likely to induce
apnea during stimulation that often persisted beyond cessation of the stimulus.
Bicuculline, administered intravenously or intracisternally, decreased the SLN stimulation-induced decrease in phrenic nerve amplitude, minute phrenic activity, and phrenic nerve frequency (P < 0.05).
Bicuculline also reduced SLN-induced
apnea and duration of poststimulation
apnea (P < 0.05). We conclude that centrally mediated GABAergic pathways are involved in laryngeal stimulation-induced
apnea.