Eupnea of in situ rats persists following blockers of in vitro pacemaker burster activities.

Two groups of intrinsically bursting neurons, linked to respiration, have been identified using in vitro medullary slice preparations. One group is dependent upon a calcium-activated nonspecific cationic current that is blocked by flufanemic acid. This group is hypothesized as essential for eupnea, but not gasping. The second group is dependent upon conductance through persistent sodium channels that is blocked by riluzole. This group is proposed to underlie both eupnea and gasping. In the decerebrate in situ preparation of the juvenile rat, flufanemic acid caused an increase in frequency and a decrease in peak level of the phrenic and vagus nerve activities in both eupnea and gasping. Similar changes in eupnea followed the simultaneous blockades by flufanemic acid and riluzole. However, gasping was eliminated. These results do not support the hypothesis that conductances through either persistent sodium channels or calcium-activated nonspecific cationic channels are essential for the neurogenesis of eupnea. However, gasping does depend upon a conductance through persistent sodium channels.